2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. causal interaction 2 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/32729861/ Histone methyltransferase G9a inhibitor-loaded redox-responsive nanoparticles for pancreatic ductal adenocarcinoma therapy. causal interaction 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/23395645/ Enhancer of Zeste Homolog 2 Silences MicroRNA-218 in Human Pancreatic Ductal Adenocarcinoma Cells by Inducing Formation of Heterochromatin. causal interaction 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/23807219/ Gossypol and an HMT G9a inhibitor act in synergy to induce cell death in pancreatic cancer cells. causal interaction 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. causal interaction 1 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/33639051/ Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2. causal interaction 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/34413625/ Histone Methyltransferases Useful in Gastric Cancer Research. causal interaction 3 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. diagnostic usage 2 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/23395645/ Enhancer of Zeste Homolog 2 Silences MicroRNA-218 in Human Pancreatic Ductal Adenocarcinoma Cells by Inducing Formation of Heterochromatin. diagnostic usage 3 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/30903272/ Robust expression of EZH2 in endocervical neoplastic lesions. diagnostic usage 1 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. diagnostic usage 3 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/33639051/ Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2. diagnostic usage 1 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/34413625/ Histone Methyltransferases Useful in Gastric Cancer Research. diagnostic usage 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. therapeutic application 2 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/32729861/ Histone methyltransferase G9a inhibitor-loaded redox-responsive nanoparticles for pancreatic ductal adenocarcinoma therapy. therapeutic application 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/23395645/ Enhancer of Zeste Homolog 2 Silences MicroRNA-218 in Human Pancreatic Ductal Adenocarcinoma Cells by Inducing Formation of Heterochromatin. therapeutic application 1 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. therapeutic application 1 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. ongoing research 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/19345325/ Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation. ongoing research 1 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/23395645/ Enhancer of Zeste Homolog 2 Silences MicroRNA-218 in Human Pancreatic Ductal Adenocarcinoma Cells by Inducing Formation of Heterochromatin. ongoing research 2 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/30903272/ Robust expression of EZH2 in endocervical neoplastic lesions. ongoing research 2 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. ongoing research 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/33639051/ Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2. ongoing research 3 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/22536950/ A small-molecule probe of the histone methyltransferase G9a induces cellular senescence in pancreatic adenocarcinoma. unassigned - 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/19345325/ Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation. unassigned - 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/20573371/ Implications of enhancer of zeste homologue 2 expression in pancreatic ductal adenocarcinoma. unassigned - 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/30903272/ Robust expression of EZH2 in endocervical neoplastic lesions. unassigned - 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/32729861/ Histone methyltransferase G9a inhibitor-loaded redox-responsive nanoparticles for pancreatic ductal adenocarcinoma therapy. unassigned - 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/23807219/ Gossypol and an HMT G9a inhibitor act in synergy to induce cell death in pancreatic cancer cells. unassigned - 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/33639051/ Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2. unassigned - 2.1.1.355 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/34413625/ Histone Methyltransferases Useful in Gastric Cancer Research. unassigned - 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33223508/ Histone methyltransferase SETD2 inhibits tumor growth via suppressing CXCL1-mediated activation of cell cycle in lung adenocarcinoma. causal interaction 1 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33614250/ Hypoxic tumor-derived exosomal circular RNA SETDB1 promotes invasive growth and EMT via the miR-7/Sp1 axis in lung adenocarcinoma. causal interaction 2 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. causal interaction 3 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/28539837/ Ezh2 Acts as a Tumor Suppressor in Kras-driven Lung Adenocarcinoma. causal interaction 1 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. causal interaction 3 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. diagnostic usage 1 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. diagnostic usage 3 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. therapeutic application 1 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/28539837/ Ezh2 Acts as a Tumor Suppressor in Kras-driven Lung Adenocarcinoma. therapeutic application 3 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33614250/ Hypoxic tumor-derived exosomal circular RNA SETDB1 promotes invasive growth and EMT via the miR-7/Sp1 axis in lung adenocarcinoma. ongoing research 2 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. ongoing research 4 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33223508/ Histone methyltransferase SETD2 inhibits tumor growth via suppressing CXCL1-mediated activation of cell cycle in lung adenocarcinoma. unassigned - 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33614250/ Hypoxic tumor-derived exosomal circular RNA SETDB1 promotes invasive growth and EMT via the miR-7/Sp1 axis in lung adenocarcinoma. unassigned - 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/28539837/ Ezh2 Acts as a Tumor Suppressor in Kras-driven Lung Adenocarcinoma. unassigned - 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. unassigned - 2.1.1.355 Adenocarcinoma of Lung https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. unassigned - 2.1.1.355 Adenoma https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. causal interaction 4 2.1.1.355 Adenoma https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. diagnostic usage 3 2.1.1.355 Adenoma https://pubmed.ncbi.nlm.nih.gov/22863622/ Notch1 counteracts WNT/?-catenin signaling through chromatin modification in colorectal cancer. ongoing research 3 2.1.1.355 Adenoma https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. ongoing research 1 2.1.1.355 Adenoma https://pubmed.ncbi.nlm.nih.gov/22863622/ Notch1 counteracts WNT/?-catenin signaling through chromatin modification in colorectal cancer. unassigned - 2.1.1.355 Adenoma https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. unassigned - 2.1.1.355 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/30668640/ Inhibition of EHMT1/2 rescues synaptic and cognitive functions for Alzheimer's disease. causal interaction 3 2.1.1.355 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/32103178/ Two conserved epigenetic regulators prevent healthy ageing. causal interaction 3 2.1.1.355 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/30668640/ Inhibition of EHMT1/2 rescues synaptic and cognitive functions for Alzheimer's disease. unassigned - 2.1.1.355 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/32103178/ Two conserved epigenetic regulators prevent healthy ageing. unassigned - 2.1.1.355 Anhedonia https://pubmed.ncbi.nlm.nih.gov/20505083/ Setdb1 histone methyltransferase regulates mood-related behaviors and expression of the NMDA receptor subunit NR2B. ongoing research 2 2.1.1.355 Anhedonia https://pubmed.ncbi.nlm.nih.gov/20505083/ Setdb1 histone methyltransferase regulates mood-related behaviors and expression of the NMDA receptor subunit NR2B. unassigned - 2.1.1.355 Anus, Imperforate https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. causal interaction 3 2.1.1.355 Anus, Imperforate https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. therapeutic application 1 2.1.1.355 Anus, Imperforate https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. unassigned - 2.1.1.355 Arthritis, Rheumatoid https://pubmed.ncbi.nlm.nih.gov/21515604/ Expression and function of EZH2 in synovial fibroblasts: epigenetic repression of the Wnt inhibitor SFRP1 in rheumatoid arthritis. ongoing research 3 2.1.1.355 Arthritis, Rheumatoid https://pubmed.ncbi.nlm.nih.gov/21515604/ Expression and function of EZH2 in synovial fibroblasts: epigenetic repression of the Wnt inhibitor SFRP1 in rheumatoid arthritis. unassigned - 2.1.1.355 Asthma https://pubmed.ncbi.nlm.nih.gov/22763435/ An epigenetic silencing pathway controlling T helper 2 cell lineage commitment. therapeutic application 2 2.1.1.355 Asthma https://pubmed.ncbi.nlm.nih.gov/32540493/ An efficient hybrid feature selection method to identify potential biomarkers in common chronic lung inflammatory diseases. therapeutic application 1 2.1.1.355 Asthma https://pubmed.ncbi.nlm.nih.gov/22763435/ An epigenetic silencing pathway controlling T helper 2 cell lineage commitment. ongoing research 2 2.1.1.355 Asthma https://pubmed.ncbi.nlm.nih.gov/22763435/ An epigenetic silencing pathway controlling T helper 2 cell lineage commitment. unassigned - 2.1.1.355 Asthma https://pubmed.ncbi.nlm.nih.gov/32540493/ An efficient hybrid feature selection method to identify potential biomarkers in common chronic lung inflammatory diseases. unassigned - 2.1.1.355 Astrocytoma https://pubmed.ncbi.nlm.nih.gov/34296393/ Histone Mark Profiling in Pediatric Astrocytomas Reveals Prognostic Significance of H3K9 Trimethylation and Histone Methyltransferase SUV39H1. diagnostic usage 3 2.1.1.355 Astrocytoma https://pubmed.ncbi.nlm.nih.gov/34296393/ Histone Mark Profiling in Pediatric Astrocytomas Reveals Prognostic Significance of H3K9 Trimethylation and Histone Methyltransferase SUV39H1. therapeutic application 4 2.1.1.355 Astrocytoma https://pubmed.ncbi.nlm.nih.gov/34296393/ Histone Mark Profiling in Pediatric Astrocytomas Reveals Prognostic Significance of H3K9 Trimethylation and Histone Methyltransferase SUV39H1. ongoing research 3 2.1.1.355 Astrocytoma https://pubmed.ncbi.nlm.nih.gov/34296393/ Histone Mark Profiling in Pediatric Astrocytomas Reveals Prognostic Significance of H3K9 Trimethylation and Histone Methyltransferase SUV39H1. unassigned - 2.1.1.355 Atherosclerosis https://pubmed.ncbi.nlm.nih.gov/34149887/ Pharmacological inhibition of EZH2 by GSK126 decreases atherosclerosis by modulating foam cell formation and monocyte adhesion in apolipoprotein E-deficient mice. causal interaction 1 2.1.1.355 Atherosclerosis https://pubmed.ncbi.nlm.nih.gov/27295295/ Histone Methyltransferase Enhancer of Zeste Homolog 2-Mediated ABCA1 Promoter DNA Methylation Contributes to the Progression of Atherosclerosis. therapeutic application 1 2.1.1.355 Atherosclerosis https://pubmed.ncbi.nlm.nih.gov/34149887/ Pharmacological inhibition of EZH2 by GSK126 decreases atherosclerosis by modulating foam cell formation and monocyte adhesion in apolipoprotein E-deficient mice. therapeutic application 4 2.1.1.355 Atherosclerosis https://pubmed.ncbi.nlm.nih.gov/34149887/ Pharmacological inhibition of EZH2 by GSK126 decreases atherosclerosis by modulating foam cell formation and monocyte adhesion in apolipoprotein E-deficient mice. ongoing research 1 2.1.1.355 Atherosclerosis https://pubmed.ncbi.nlm.nih.gov/27295295/ Histone Methyltransferase Enhancer of Zeste Homolog 2-Mediated ABCA1 Promoter DNA Methylation Contributes to the Progression of Atherosclerosis. unassigned - 2.1.1.355 Atherosclerosis https://pubmed.ncbi.nlm.nih.gov/34149887/ Pharmacological inhibition of EZH2 by GSK126 decreases atherosclerosis by modulating foam cell formation and monocyte adhesion in apolipoprotein E-deficient mice. unassigned - 2.1.1.355 Autoimmune Diseases https://pubmed.ncbi.nlm.nih.gov/24012418/ Histone methyltransferase ash1l suppresses interleukin-6 production and inflammatory autoimmune diseases by inducing the ubiquitin-editing enzyme a20. causal interaction 1 2.1.1.355 Autoimmune Diseases https://pubmed.ncbi.nlm.nih.gov/24012418/ Histone methyltransferase ash1l suppresses interleukin-6 production and inflammatory autoimmune diseases by inducing the ubiquitin-editing enzyme a20. therapeutic application 1 2.1.1.355 Autoimmune Diseases https://pubmed.ncbi.nlm.nih.gov/24012418/ Histone methyltransferase ash1l suppresses interleukin-6 production and inflammatory autoimmune diseases by inducing the ubiquitin-editing enzyme a20. ongoing research 3 2.1.1.355 Autoimmune Diseases https://pubmed.ncbi.nlm.nih.gov/24012418/ Histone methyltransferase ash1l suppresses interleukin-6 production and inflammatory autoimmune diseases by inducing the ubiquitin-editing enzyme a20. unassigned - 2.1.1.355 Avian Leukosis https://pubmed.ncbi.nlm.nih.gov/33363525/ Targeting the Histone Methyltransferase Disruptor of Telomeric Silencing 1-Like Restricts Avian Leukosis Virus Subgroup J Replication by Restoring the Innate Immune Response in Chicken Macrophages. causal interaction 4 2.1.1.355 Avian Leukosis https://pubmed.ncbi.nlm.nih.gov/33363525/ Targeting the Histone Methyltransferase Disruptor of Telomeric Silencing 1-Like Restricts Avian Leukosis Virus Subgroup J Replication by Restoring the Innate Immune Response in Chicken Macrophages. diagnostic usage 3 2.1.1.355 Avian Leukosis https://pubmed.ncbi.nlm.nih.gov/33363525/ Targeting the Histone Methyltransferase Disruptor of Telomeric Silencing 1-Like Restricts Avian Leukosis Virus Subgroup J Replication by Restoring the Innate Immune Response in Chicken Macrophages. therapeutic application 4 2.1.1.355 Avian Leukosis https://pubmed.ncbi.nlm.nih.gov/33363525/ Targeting the Histone Methyltransferase Disruptor of Telomeric Silencing 1-Like Restricts Avian Leukosis Virus Subgroup J Replication by Restoring the Innate Immune Response in Chicken Macrophages. ongoing research 3 2.1.1.355 Bacterial Infections https://pubmed.ncbi.nlm.nih.gov/32887549/ Signatures of selection reveal candidate genes involved in economic traits and cold acclimation in five Swedish cattle breeds. unassigned - 2.1.1.355 Biliary Tract Neoplasms https://pubmed.ncbi.nlm.nih.gov/29133140/ The histone methyltransferase G9a: a new therapeutic target in biliary tract cancer. therapeutic application 4 2.1.1.355 Biliary Tract Neoplasms https://pubmed.ncbi.nlm.nih.gov/29133140/ The histone methyltransferase G9a: a new therapeutic target in biliary tract cancer. unassigned - 2.1.1.355 Blast Crisis https://pubmed.ncbi.nlm.nih.gov/28129457/ Tumor suppressor gene methylation on the short arm of chromosome 1 in chronic myelogenous leukemia. diagnostic usage 3 2.1.1.355 Blast Crisis https://pubmed.ncbi.nlm.nih.gov/28129457/ Tumor suppressor gene methylation on the short arm of chromosome 1 in chronic myelogenous leukemia. ongoing research 2 2.1.1.355 Blast Crisis https://pubmed.ncbi.nlm.nih.gov/28129457/ Tumor suppressor gene methylation on the short arm of chromosome 1 in chronic myelogenous leukemia. unassigned - 2.1.1.355 Blister https://pubmed.ncbi.nlm.nih.gov/20647345/ The CURLY LEAF interacting protein BLISTER controls expression of polycomb-group target genes and cellular differentiation of Arabidopsis thaliana. ongoing research 1 2.1.1.355 Blister https://pubmed.ncbi.nlm.nih.gov/20647345/ The CURLY LEAF interacting protein BLISTER controls expression of polycomb-group target genes and cellular differentiation of Arabidopsis thaliana. unassigned - 2.1.1.355 Bone Marrow Failure Disorders https://pubmed.ncbi.nlm.nih.gov/26909595/ DNA methylation in PRDM8 is indicative for dyskeratosis congenita. causal interaction 3 2.1.1.355 Bone Marrow Failure Disorders https://pubmed.ncbi.nlm.nih.gov/32819411/ PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation. causal interaction 3 2.1.1.355 Bone Marrow Failure Disorders https://pubmed.ncbi.nlm.nih.gov/32819411/ PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation. diagnostic usage 1 2.1.1.355 Bone Marrow Failure Disorders https://pubmed.ncbi.nlm.nih.gov/26909595/ DNA methylation in PRDM8 is indicative for dyskeratosis congenita. unassigned - 2.1.1.355 Bone Marrow Failure Disorders https://pubmed.ncbi.nlm.nih.gov/32819411/ PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation. unassigned - 2.1.1.355 Brain Injuries https://pubmed.ncbi.nlm.nih.gov/34059615/ Post-Treatment Sevoflurane Protects Against Hypoxic-Ischemic Brain Injury in Neonatal Rats by Downregulating Histone Methyltransferase G9a and Upregulating Nuclear Factor Erythroid 2-Related Factor 2 (NRF2). unassigned - 2.1.1.355 Brain Ischemia https://pubmed.ncbi.nlm.nih.gov/25966950/ Inhibition of histone methyltransferases SUV39H1 and G9a leads to neuroprotection in an in vitro model of cerebral ischemia. ongoing research 2 2.1.1.355 Brain Ischemia https://pubmed.ncbi.nlm.nih.gov/25966950/ Inhibition of histone methyltransferases SUV39H1 and G9a leads to neuroprotection in an in vitro model of cerebral ischemia. unassigned - 2.1.1.355 Brain Neoplasms https://pubmed.ncbi.nlm.nih.gov/19618856/ [Epigenetic analyses of brain tumor stem cells] causal interaction 3 2.1.1.355 Brain Neoplasms https://pubmed.ncbi.nlm.nih.gov/28946550/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. causal interaction 4 2.1.1.355 Brain Neoplasms https://pubmed.ncbi.nlm.nih.gov/28946550/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. therapeutic application 4 2.1.1.355 Brain Neoplasms https://pubmed.ncbi.nlm.nih.gov/33279625/ Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases. therapeutic application 4 2.1.1.355 Brain Neoplasms https://pubmed.ncbi.nlm.nih.gov/33279625/ Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases. unassigned - 2.1.1.355 Brain Neoplasms https://pubmed.ncbi.nlm.nih.gov/19618856/ [Epigenetic analyses of brain tumor stem cells] unassigned - 2.1.1.355 Brain Neoplasms https://pubmed.ncbi.nlm.nih.gov/28946550/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21406404/ Histone Methyltransferase EZH2 Induces Akt-Dependent Genomic Instability and BRCA1 Inhibition in Breast Cancer. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23720754/ microRNA-7 suppresses the invasive potential of breast cancer cells and sensitizes cells to DNA damages by targeting histone methyltransferase SET8. causal interaction 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24189459/ Histone methyltransferase SMYD3 promotes MRTF-A-mediated transactivation of MYL9 and migration of MCF-7 breast cancer cells. causal interaction 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24391143/ Kinesin Family Deregulation Coordinated by Bromodomain Protein ANCCA and Histone Methyltransferase MLL for Breast Cancer Cell Growth, Survival, and Tamoxifen Resistance. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25373480/ Histone methyltransferase hSETD1A is a Novel Regulator of Metastasis in Breast Cancer. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26783998/ DOT1L histone methyltransferase regulates the expression of BCAT1 and is involved in sphere formation and cell migration of breast cancer cell lines. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26848522/ The transcription factor GATA1 and the histone methyltransferase SET7 interact to promote VEGF-mediated angiogenesis and tumor growth and predict clinical outcome of breast cancer. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29337058/ EHMT2 is a metastasis regulator in breast cancer. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. causal interaction 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30365075/ The novel prognostic marker, EHMT2, is involved in cell proliferation via HSPD1 regulation in breast cancer. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30483750/ SETDB1 induces epithelial?mesenchymal transition in breast carcinoma by directly binding with Snail promoter. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30775443/ Inhibition of histone methyltransferase DOT1L silences ER? gene and blocks proliferation of antiestrogen-resistant breast cancer cells. causal interaction 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30990809/ Genetic mutational status of genes regulating epigenetics: Role of the histone methyltransferase KMT2D in triple negative breast tumors. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32033749/ RNA-seq based transcriptome analysis of EHMT2 functions in breast cancer. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32765868/ Impact of histone methyltransferase SUV420H2 in breast cancer. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/33129761/ Su(var)3-9, Enhancer of Zeste, and Trithorax Domain-Containing 5 Facilitates Tumor Growth and Pulmonary Metastasis through Up-Regulation of AKT1 Signaling in Breast Cancer. causal interaction 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/18006819/ The lysine 831 of vascular endothelial growth factor receptor 1 is a novel target of methylation by SMYD3. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20556507/ S-adenosylhomocysteine hydrolase inhibition by 3-deazaneplanocin A analogues induces anti-cancer effects in breast cancer cell lines and synergy with both histone deacetylase and HER2 inhibition. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21761357/ In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland: an epigenetic mechanism linking endocrine disruptors to breast cancer. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24491801/ UTX and MLL4 Coordinately Regulate Transcriptional Programs for Cell Proliferation and Invasiveness in Breast Cancer Cells. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24911119/ PRMT2 and ROR? expression are associated with breast cancer survival outcomes. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26840455/ Setdb1, a novel interactor of ?Np63, is involved in breast tumorigenesis. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27399922/ EZH2 Protein Expression and Tumor Response to Neoadjuvant Chemotherapy in Locally Advanced Breast Cancer. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28819251/ G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29926931/ The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis. causal interaction 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29964331/ Inhibition of euchromatin histone-lysine N-methyltransferase 2 sensitizes breast cancer cells to tumor necrosis factor-related apoptosis-inducing ligand through reactive oxygen species-mediated activating transcription factor 4-C/EBP homologous protein-death receptor 5 pathway activation. causal interaction 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31367244/ A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep. causal interaction 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31735020/ Increased Expression of FosB through Reactive Oxygen Species Accumulation Functions as Pro-Apoptotic Protein in Piperlongumine Treated MCF7 Breast Cancer Cells. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32001260/ S-adenosylhomocysteine (AdoHcy)-dependent methyltransferase inhibitor DZNep overcomes breast cancer tamoxifen resistance via induction of NSD2 degradation and suppression of NSD2-driven redox homeostasis. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32292512/ G9a-mediated repression of CDH10 in hypoxia enhances breast tumour cell motility and associates with poor survival outcome. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32895488/ Methylation of EZH2 by PRMT1 regulates its stability and promotes breast cancer metastasis. causal interaction 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. diagnostic usage 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24391143/ Kinesin Family Deregulation Coordinated by Bromodomain Protein ANCCA and Histone Methyltransferase MLL for Breast Cancer Cell Growth, Survival, and Tamoxifen Resistance. diagnostic usage 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26783998/ DOT1L histone methyltransferase regulates the expression of BCAT1 and is involved in sphere formation and cell migration of breast cancer cell lines. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26848522/ The transcription factor GATA1 and the histone methyltransferase SET7 interact to promote VEGF-mediated angiogenesis and tumor growth and predict clinical outcome of breast cancer. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30365075/ The novel prognostic marker, EHMT2, is involved in cell proliferation via HSPD1 regulation in breast cancer. diagnostic usage 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30990809/ Genetic mutational status of genes regulating epigenetics: Role of the histone methyltransferase KMT2D in triple negative breast tumors. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32033749/ RNA-seq based transcriptome analysis of EHMT2 functions in breast cancer. diagnostic usage 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32765868/ Impact of histone methyltransferase SUV420H2 in breast cancer. diagnostic usage 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. diagnostic usage 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/18006819/ The lysine 831 of vascular endothelial growth factor receptor 1 is a novel target of methylation by SMYD3. diagnostic usage 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20556507/ S-adenosylhomocysteine hydrolase inhibition by 3-deazaneplanocin A analogues induces anti-cancer effects in breast cancer cell lines and synergy with both histone deacetylase and HER2 inhibition. diagnostic usage 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22199269/ Histone-modifier gene expression profiles are associated with pathological and clinical outcomes in human breast cancer. diagnostic usage 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24911119/ PRMT2 and ROR? expression are associated with breast cancer survival outcomes. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25499219/ The transcriptional repressor ZBTB4 regulates EZH2 through a MicroRNA-ZBTB4-specificity protein signaling axis. diagnostic usage 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26840455/ Setdb1, a novel interactor of ?Np63, is involved in breast tumorigenesis. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28819251/ G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin. diagnostic usage 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31367244/ A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. diagnostic usage 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31735020/ Increased Expression of FosB through Reactive Oxygen Species Accumulation Functions as Pro-Apoptotic Protein in Piperlongumine Treated MCF7 Breast Cancer Cells. diagnostic usage 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32292512/ G9a-mediated repression of CDH10 in hypoxia enhances breast tumour cell motility and associates with poor survival outcome. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20937768/ Pygo2 associates with MLL2 histone methyltransferase (HMT) and GCN5 histone acetyltransferase (HAT) complexes to augment Wnt target gene expression and breast cancer stem-like cell expansion. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21503890/ Identification of a functional estrogen-responsive enhancer element in the promoter 2 of PRDM2 gene in breast cancer cell lines. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22562246/ Interaction with Suv39H1 is critical for Snail-mediated E-cadherin repression in breast cancer. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22563434/ Dysregulated recruitment of the histone methyltransferase EZH2 to the class II transactivator (CIITA) promoter IV in breast cancer cells. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23720754/ microRNA-7 suppresses the invasive potential of breast cancer cells and sensitizes cells to DNA damages by targeting histone methyltransferase SET8. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. therapeutic application 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24391143/ Kinesin Family Deregulation Coordinated by Bromodomain Protein ANCCA and Histone Methyltransferase MLL for Breast Cancer Cell Growth, Survival, and Tamoxifen Resistance. therapeutic application 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25998860/ The histone methyltransferase EZH2 promotes mammary stem and luminal progenitor cell expansion, metastasis and inhibits estrogen receptor-positive cellular differentiation in a model of basal breast cancer. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26300989/ Dual EZH2 and EHMT2 histone methyltransferase inhibition increases biological efficacy in breast cancer cells. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26783998/ DOT1L histone methyltransferase regulates the expression of BCAT1 and is involved in sphere formation and cell migration of breast cancer cell lines. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26848522/ The transcription factor GATA1 and the histone methyltransferase SET7 interact to promote VEGF-mediated angiogenesis and tumor growth and predict clinical outcome of breast cancer. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28460359/ Synthesis and biological evaluation of benzimidazole derivatives as the G9a Histone Methyltransferase inhibitors that induce autophagy and apoptosis of breast cancer cells. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29337058/ EHMT2 is a metastasis regulator in breast cancer. therapeutic application 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30483750/ SETDB1 induces epithelial?mesenchymal transition in breast carcinoma by directly binding with Snail promoter. therapeutic application 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30545440/ SETDB1 regulates SMAD7 expression for breast cancer metastasis. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30775443/ Inhibition of histone methyltransferase DOT1L silences ER? gene and blocks proliferation of antiestrogen-resistant breast cancer cells. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30990809/ Genetic mutational status of genes regulating epigenetics: Role of the histone methyltransferase KMT2D in triple negative breast tumors. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32033749/ RNA-seq based transcriptome analysis of EHMT2 functions in breast cancer. therapeutic application 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20556507/ S-adenosylhomocysteine hydrolase inhibition by 3-deazaneplanocin A analogues induces anti-cancer effects in breast cancer cell lines and synergy with both histone deacetylase and HER2 inhibition. therapeutic application 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21761357/ In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland: an epigenetic mechanism linking endocrine disruptors to breast cancer. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22199269/ Histone-modifier gene expression profiles are associated with pathological and clinical outcomes in human breast cancer. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25610865/ DBC1/CCAR2 and CCAR1 Are Largely Disordered Proteins that Have Evolved from One Common Ancestor. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26840455/ Setdb1, a novel interactor of ?Np63, is involved in breast tumorigenesis. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28819251/ G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29926931/ The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29964331/ Inhibition of euchromatin histone-lysine N-methyltransferase 2 sensitizes breast cancer cells to tumor necrosis factor-related apoptosis-inducing ligand through reactive oxygen species-mediated activating transcription factor 4-C/EBP homologous protein-death receptor 5 pathway activation. therapeutic application 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31367244/ A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep. therapeutic application 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31735020/ Increased Expression of FosB through Reactive Oxygen Species Accumulation Functions as Pro-Apoptotic Protein in Piperlongumine Treated MCF7 Breast Cancer Cells. therapeutic application 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32001260/ S-adenosylhomocysteine (AdoHcy)-dependent methyltransferase inhibitor DZNep overcomes breast cancer tamoxifen resistance via induction of NSD2 degradation and suppression of NSD2-driven redox homeostasis. therapeutic application 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32292512/ G9a-mediated repression of CDH10 in hypoxia enhances breast tumour cell motility and associates with poor survival outcome. therapeutic application 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. therapeutic application 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/16322686/ Loss of DNA Methylation and Histone H4 Lysine 20 Trimethylation in Human Breast Cancer Cells is Associated with Aberrant Expression of DNA Methyltransferase 1, Suv4-20h2 Histone Methyltransferase and Methyl-Binding Proteins. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20937768/ Pygo2 associates with MLL2 histone methyltransferase (HMT) and GCN5 histone acetyltransferase (HAT) complexes to augment Wnt target gene expression and breast cancer stem-like cell expansion. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21406404/ Histone Methyltransferase EZH2 Induces Akt-Dependent Genomic Instability and BRCA1 Inhibition in Breast Cancer. ongoing research 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21503890/ Identification of a functional estrogen-responsive enhancer element in the promoter 2 of PRDM2 gene in breast cancer cell lines. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22563434/ Dysregulated recruitment of the histone methyltransferase EZH2 to the class II transactivator (CIITA) promoter IV in breast cancer cells. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24189459/ Histone methyltransferase SMYD3 promotes MRTF-A-mediated transactivation of MYL9 and migration of MCF-7 breast cancer cells. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24391143/ Kinesin Family Deregulation Coordinated by Bromodomain Protein ANCCA and Histone Methyltransferase MLL for Breast Cancer Cell Growth, Survival, and Tamoxifen Resistance. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25070049/ MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25373480/ Histone methyltransferase hSETD1A is a Novel Regulator of Metastasis in Breast Cancer. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25998860/ The histone methyltransferase EZH2 promotes mammary stem and luminal progenitor cell expansion, metastasis and inhibits estrogen receptor-positive cellular differentiation in a model of basal breast cancer. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26300989/ Dual EZH2 and EHMT2 histone methyltransferase inhibition increases biological efficacy in breast cancer cells. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26783998/ DOT1L histone methyltransferase regulates the expression of BCAT1 and is involved in sphere formation and cell migration of breast cancer cell lines. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26848522/ The transcription factor GATA1 and the histone methyltransferase SET7 interact to promote VEGF-mediated angiogenesis and tumor growth and predict clinical outcome of breast cancer. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28460359/ Synthesis and biological evaluation of benzimidazole derivatives as the G9a Histone Methyltransferase inhibitors that induce autophagy and apoptosis of breast cancer cells. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30483750/ SETDB1 induces epithelial?mesenchymal transition in breast carcinoma by directly binding with Snail promoter. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30775443/ Inhibition of histone methyltransferase DOT1L silences ER? gene and blocks proliferation of antiestrogen-resistant breast cancer cells. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32765868/ Impact of histone methyltransferase SUV420H2 in breast cancer. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20556507/ S-adenosylhomocysteine hydrolase inhibition by 3-deazaneplanocin A analogues induces anti-cancer effects in breast cancer cell lines and synergy with both histone deacetylase and HER2 inhibition. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22199269/ Histone-modifier gene expression profiles are associated with pathological and clinical outcomes in human breast cancer. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24491801/ UTX and MLL4 Coordinately Regulate Transcriptional Programs for Cell Proliferation and Invasiveness in Breast Cancer Cells. ongoing research 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24911119/ PRMT2 and ROR? expression are associated with breast cancer survival outcomes. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26840455/ Setdb1, a novel interactor of ?Np63, is involved in breast tumorigenesis. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28819251/ G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29926931/ The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31367244/ A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. ongoing research 1 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31693439/ Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31735020/ Increased Expression of FosB through Reactive Oxygen Species Accumulation Functions as Pro-Apoptotic Protein in Piperlongumine Treated MCF7 Breast Cancer Cells. ongoing research 3 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32292512/ G9a-mediated repression of CDH10 in hypoxia enhances breast tumour cell motility and associates with poor survival outcome. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. ongoing research 2 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/16322686/ Loss of DNA Methylation and Histone H4 Lysine 20 Trimethylation in Human Breast Cancer Cells is Associated with Aberrant Expression of DNA Methyltransferase 1, Suv4-20h2 Histone Methyltransferase and Methyl-Binding Proteins. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20937768/ Pygo2 associates with MLL2 histone methyltransferase (HMT) and GCN5 histone acetyltransferase (HAT) complexes to augment Wnt target gene expression and breast cancer stem-like cell expansion. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21503890/ Identification of a functional estrogen-responsive enhancer element in the promoter 2 of PRDM2 gene in breast cancer cell lines. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22562246/ Interaction with Suv39H1 is critical for Snail-mediated E-cadherin repression in breast cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22563434/ Dysregulated recruitment of the histone methyltransferase EZH2 to the class II transactivator (CIITA) promoter IV in breast cancer cells. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25070049/ MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25998860/ The histone methyltransferase EZH2 promotes mammary stem and luminal progenitor cell expansion, metastasis and inhibits estrogen receptor-positive cellular differentiation in a model of basal breast cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26300989/ Dual EZH2 and EHMT2 histone methyltransferase inhibition increases biological efficacy in breast cancer cells. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28460359/ Synthesis and biological evaluation of benzimidazole derivatives as the G9a Histone Methyltransferase inhibitors that induce autophagy and apoptosis of breast cancer cells. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30545440/ SETDB1 regulates SMAD7 expression for breast cancer metastasis. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/22199269/ Histone-modifier gene expression profiles are associated with pathological and clinical outcomes in human breast cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25499219/ The transcriptional repressor ZBTB4 regulates EZH2 through a MicroRNA-ZBTB4-specificity protein signaling axis. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25610865/ DBC1/CCAR2 and CCAR1 Are Largely Disordered Proteins that Have Evolved from One Common Ancestor. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31693439/ Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21406404/ Histone Methyltransferase EZH2 Induces Akt-Dependent Genomic Instability and BRCA1 Inhibition in Breast Cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23720754/ microRNA-7 suppresses the invasive potential of breast cancer cells and sensitizes cells to DNA damages by targeting histone methyltransferase SET8. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24189459/ Histone methyltransferase SMYD3 promotes MRTF-A-mediated transactivation of MYL9 and migration of MCF-7 breast cancer cells. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/25373480/ Histone methyltransferase hSETD1A is a Novel Regulator of Metastasis in Breast Cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29337058/ EHMT2 is a metastasis regulator in breast cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30483750/ SETDB1 induces epithelial?mesenchymal transition in breast carcinoma by directly binding with Snail promoter. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30775443/ Inhibition of histone methyltransferase DOT1L silences ER? gene and blocks proliferation of antiestrogen-resistant breast cancer cells. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/33129761/ Su(var)3-9, Enhancer of Zeste, and Trithorax Domain-Containing 5 Facilitates Tumor Growth and Pulmonary Metastasis through Up-Regulation of AKT1 Signaling in Breast Cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21761357/ In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland: an epigenetic mechanism linking endocrine disruptors to breast cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24491801/ UTX and MLL4 Coordinately Regulate Transcriptional Programs for Cell Proliferation and Invasiveness in Breast Cancer Cells. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27399922/ EZH2 Protein Expression and Tumor Response to Neoadjuvant Chemotherapy in Locally Advanced Breast Cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29926931/ The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/29964331/ Inhibition of euchromatin histone-lysine N-methyltransferase 2 sensitizes breast cancer cells to tumor necrosis factor-related apoptosis-inducing ligand through reactive oxygen species-mediated activating transcription factor 4-C/EBP homologous protein-death receptor 5 pathway activation. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32001260/ S-adenosylhomocysteine (AdoHcy)-dependent methyltransferase inhibitor DZNep overcomes breast cancer tamoxifen resistance via induction of NSD2 degradation and suppression of NSD2-driven redox homeostasis. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32895488/ Methylation of EZH2 by PRMT1 regulates its stability and promotes breast cancer metastasis. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30365075/ The novel prognostic marker, EHMT2, is involved in cell proliferation via HSPD1 regulation in breast cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32765868/ Impact of histone methyltransferase SUV420H2 in breast cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/18006819/ The lysine 831 of vascular endothelial growth factor receptor 1 is a novel target of methylation by SMYD3. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24911119/ PRMT2 and ROR? expression are associated with breast cancer survival outcomes. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30990809/ Genetic mutational status of genes regulating epigenetics: Role of the histone methyltransferase KMT2D in triple negative breast tumors. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/32033749/ RNA-seq based transcriptome analysis of EHMT2 functions in breast cancer. unassigned - 2.1.1.355 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23011637/ The histone methyltransferase Wolf-Hirschhorn syndrome candidate 1-like 1 (WHSC1L1) is involved in human carcinogenesis. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. causal interaction 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25789788/ Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26840455/ Setdb1, a novel interactor of ?Np63, is involved in breast tumorigenesis. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29512765/ Histone methyltransferase KMT5A gene modulates oncogenesis and lipid metabolism of papillary thyroid cancer in vitro. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. causal interaction 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33099471/ Deletion of Histone Methyltransferase G9a Suppresses Mutant Kras-driven Pancreatic Carcinogenesis. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/16497704/ Histone H3 lysine 9 and H4 lysine 20 trimethylation and the expression of Suv4-20h2 and Suv-39h1 histone methyltransferases in hepatocarcinogenesis induced by methyl deficiency in rats. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/17609160/ SET and MYND domain-containing protein 3 decreases sensitivity to dexamethasone and stimulates cell adhesion and migration in NIH3T3 cells. causal interaction 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20039369/ Novobiocin decreases SMYD3 expression and inhibits the migration of MDA-MB-231 human breast cancer cells. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20957523/ Effects of SMYD3 over-expression on cell cycle acceleration and cell proliferation in MDA-MB-231 human breast cancer cells. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21430779/ The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21761357/ In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland: an epigenetic mechanism linking endocrine disruptors to breast cancer. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23557258/ Cancer-associated upregulation of histone H3 lysine 9 trimethylation promotes cell motility in vitro and drives tumor formation in vivo. causal interaction 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24212330/ Cancer-associated fibroblasts enhance the migration ability of ovarian cancer cells by increasing EZH2 expression. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25168426/ Involvement of EZH2, SUV39H1, G9a and associated molecules in pathogenesis of urethane induced mouse lung tumors: potential targets for cancer control. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28418882/ Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29897144/ Surveillance of Retroelement Expression and Nucleic-Acid Immunity by Histone Methyltransferase SETDB1. causal interaction 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29926931/ The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30105513/ Prognostic value of histone marks H3K27me3 and H3K9me3 and modifying enzymes EZH2, SETDB1 and LSD-1 in colorectal cancer. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. causal interaction 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30761216/ Targeting EZH2 in Multiple Myeloma-Multifaceted Anti-Tumor Activity. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31050579/ Fine-tuning AKT kinase activity through direct lysine methylation. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31768101/ Knockdown of SET Domain, Bifurcated 1 suppresses head and neck cancer cell viability and wound-healing ability in vitro. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32062438/ Arsenic and benzo[a]pyrene co-exposure acts synergistically in inducing cancer stem cell-like property and tumorigenesis by epigenetically down-regulating SOCS3 expression. causal interaction 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32291411/ VHL-HIF-2? axis-induced SMYD3 upregulation drives renal cell carcinoma progression via direct trans-activation of EGFR. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. causal interaction 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32391195/ The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. causal interaction 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33339442/ Epigenetic Modifier SETD8 as a Therapeutic Target for High-Grade Serous Ovarian Cancer. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. causal interaction 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23011637/ The histone methyltransferase Wolf-Hirschhorn syndrome candidate 1-like 1 (WHSC1L1) is involved in human carcinogenesis. diagnostic usage 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. diagnostic usage 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. diagnostic usage 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26840455/ Setdb1, a novel interactor of ?Np63, is involved in breast tumorigenesis. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29512765/ Histone methyltransferase KMT5A gene modulates oncogenesis and lipid metabolism of papillary thyroid cancer in vitro. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. diagnostic usage 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33099471/ Deletion of Histone Methyltransferase G9a Suppresses Mutant Kras-driven Pancreatic Carcinogenesis. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. diagnostic usage 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. diagnostic usage 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. diagnostic usage 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24880080/ SMYD2-dependent HSP90 methylation promotes cancer cell proliferation by regulating the chaperone complex formation. diagnostic usage 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. diagnostic usage 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. diagnostic usage 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28418882/ Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer. diagnostic usage 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30105513/ Prognostic value of histone marks H3K27me3 and H3K9me3 and modifying enzymes EZH2, SETDB1 and LSD-1 in colorectal cancer. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32291411/ VHL-HIF-2? axis-induced SMYD3 upregulation drives renal cell carcinoma progression via direct trans-activation of EGFR. diagnostic usage 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. diagnostic usage 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32391195/ The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33339442/ Epigenetic Modifier SETD8 as a Therapeutic Target for High-Grade Serous Ovarian Cancer. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. diagnostic usage 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23011637/ The histone methyltransferase Wolf-Hirschhorn syndrome candidate 1-like 1 (WHSC1L1) is involved in human carcinogenesis. therapeutic application 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. therapeutic application 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. therapeutic application 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. therapeutic application 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25789788/ Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26840455/ Setdb1, a novel interactor of ?Np63, is involved in breast tumorigenesis. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28825595/ Histone methyltransferase SETD2 modulates alternative splicing to inhibit intestinal tumorigenesis. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. therapeutic application 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/16497704/ Histone H3 lysine 9 and H4 lysine 20 trimethylation and the expression of Suv4-20h2 and Suv-39h1 histone methyltransferases in hepatocarcinogenesis induced by methyl deficiency in rats. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/17363582/ The telomerase reverse transcriptase (hTERT) gene is a direct target of the histone methyltransferase SMYD3. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/17609160/ SET and MYND domain-containing protein 3 decreases sensitivity to dexamethasone and stimulates cell adhesion and migration in NIH3T3 cells. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20039369/ Novobiocin decreases SMYD3 expression and inhibits the migration of MDA-MB-231 human breast cancer cells. therapeutic application 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20957523/ Effects of SMYD3 over-expression on cell cycle acceleration and cell proliferation in MDA-MB-231 human breast cancer cells. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21761357/ In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland: an epigenetic mechanism linking endocrine disruptors to breast cancer. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. therapeutic application 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/22552406/ The expression and significance of the enhancer of zeste homolog 2 in lung adenocarcinoma. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24212330/ Cancer-associated fibroblasts enhance the migration ability of ovarian cancer cells by increasing EZH2 expression. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. therapeutic application 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24880080/ SMYD2-dependent HSP90 methylation promotes cancer cell proliferation by regulating the chaperone complex formation. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25168426/ Involvement of EZH2, SUV39H1, G9a and associated molecules in pathogenesis of urethane induced mouse lung tumors: potential targets for cancer control. therapeutic application 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28418882/ Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29926931/ The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis. therapeutic application 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30683853/ Histone methyltransferase NSD2 regulates apoptosis and chemosensitivity in osteosarcoma. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30761216/ Targeting EZH2 in Multiple Myeloma-Multifaceted Anti-Tumor Activity. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31050579/ Fine-tuning AKT kinase activity through direct lysine methylation. therapeutic application 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31768101/ Knockdown of SET Domain, Bifurcated 1 suppresses head and neck cancer cell viability and wound-healing ability in vitro. therapeutic application 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. therapeutic application 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32391195/ The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis. therapeutic application 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. therapeutic application 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33339442/ Epigenetic Modifier SETD8 as a Therapeutic Target for High-Grade Serous Ovarian Cancer. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33742125/ NSD2 promotes tumor angiogenesis through methylating and activating STAT3 protein. therapeutic application 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. therapeutic application 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. therapeutic application 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23011637/ The histone methyltransferase Wolf-Hirschhorn syndrome candidate 1-like 1 (WHSC1L1) is involved in human carcinogenesis. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. ongoing research 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25789788/ Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26840455/ Setdb1, a novel interactor of ?Np63, is involved in breast tumorigenesis. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28825595/ Histone methyltransferase SETD2 modulates alternative splicing to inhibit intestinal tumorigenesis. ongoing research 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. ongoing research 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29512765/ Histone methyltransferase KMT5A gene modulates oncogenesis and lipid metabolism of papillary thyroid cancer in vitro. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. ongoing research 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. ongoing research 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. ongoing research 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. ongoing research 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/17363582/ The telomerase reverse transcriptase (hTERT) gene is a direct target of the histone methyltransferase SMYD3. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/19345325/ Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation. ongoing research 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20039369/ Novobiocin decreases SMYD3 expression and inhibits the migration of MDA-MB-231 human breast cancer cells. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. ongoing research 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20957523/ Effects of SMYD3 over-expression on cell cycle acceleration and cell proliferation in MDA-MB-231 human breast cancer cells. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. ongoing research 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24726141/ The Histone Methyltransferase SMYD2 Methylates PARP1 and Promotes Poly(ADP-ribosyl)ation Activity in Cancer Cells. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25168426/ Involvement of EZH2, SUV39H1, G9a and associated molecules in pathogenesis of urethane induced mouse lung tumors: potential targets for cancer control. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28789418/ Effect of SMYD3 on the microRNA expression profile of MCF-7 breast cancer cells. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29897144/ Surveillance of Retroelement Expression and Nucleic-Acid Immunity by Histone Methyltransferase SETDB1. ongoing research 1 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29926931/ The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30683853/ Histone methyltransferase NSD2 regulates apoptosis and chemosensitivity in osteosarcoma. ongoing research 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32391195/ The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis. ongoing research 3 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33339442/ Epigenetic Modifier SETD8 as a Therapeutic Target for High-Grade Serous Ovarian Cancer. ongoing research 2 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. ongoing research 4 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21932133/ Carcinogenesis of Intraductal Papillary Mucinous Neoplasm of the Pancreas: Loss of MicroRNA-101 Promotes Overexpression of Histone Methyltransferase EZH2. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/22504913/ Environmental estrogens differentially engage the histone methyltransferase EZH2 to increase risk of uterine tumorigenesis. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/22544317/ Role of the SMYD3 histone methyltransferase in tumorigenesis: local or global effects? unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28825595/ Histone methyltransferase SETD2 modulates alternative splicing to inhibit intestinal tumorigenesis. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30300580/ MYC Interacts with the G9a Histone Methyltransferase to Drive Transcriptional Repression and Tumorigenesis. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/16892059/ JAK signaling globally counteracts heterochromatic gene silencing. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/17363582/ The telomerase reverse transcriptase (hTERT) gene is a direct target of the histone methyltransferase SMYD3. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/19345325/ Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21417010/ [Histone methylation and its relationship with cancer]. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/22472464/ Synergistic antileukemic action of a combination of inhibitors of DNA methylation and histone methylation. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/22552406/ The expression and significance of the enhancer of zeste homolog 2 in lung adenocarcinoma. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24726141/ The Histone Methyltransferase SMYD2 Methylates PARP1 and Promotes Poly(ADP-ribosyl)ation Activity in Cancer Cells. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24880080/ SMYD2-dependent HSP90 methylation promotes cancer cell proliferation by regulating the chaperone complex formation. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25266721/ c-Rel regulates Ezh2 expression in activated lymphocytes and malignant lymphoid cells. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/27494834/ GSK3? inactivation promotes the oncogenic functions of EZH2 and enhances methylation of H3K27 in human breast cancers. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/27807891/ Clinicopathological features of primary diffuse large B-cell lymphoma of the central nervous system - strong EZH2 expression implying diagnostic and therapeutic implication. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28739498/ Increased Expression of EZH2 in Merkel Cell Carcinoma Is Associated with Disease Progression and Poorer Prognosis. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28789418/ Effect of SMYD3 on the microRNA expression profile of MCF-7 breast cancer cells. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30683853/ Histone methyltransferase NSD2 regulates apoptosis and chemosensitivity in osteosarcoma. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30952833/ Monomethyltransferase SET8 facilitates hepatocellular carcinoma growth by enhancing aerobic glycolysis. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32015216/ Abnormal overexpression of G9a in melanoma cells promotes cancer progression via upregulation of the Notch1 signaling pathway. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32161011/ EZH2 Downregulation Augments the Effect of Irradiation in Reducing Pancreatic Cancer Cell Proliferation in vitro. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33742125/ NSD2 promotes tumor angiogenesis through methylating and activating STAT3 protein. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34510321/ Novel insights into SMYD2 and SMYD3 inhibitors: from potential anti-tumoural therapy to a variety of new applications. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25789788/ Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/16497704/ Histone H3 lysine 9 and H4 lysine 20 trimethylation and the expression of Suv4-20h2 and Suv-39h1 histone methyltransferases in hepatocarcinogenesis induced by methyl deficiency in rats. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/17609160/ SET and MYND domain-containing protein 3 decreases sensitivity to dexamethasone and stimulates cell adhesion and migration in NIH3T3 cells. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20039369/ Novobiocin decreases SMYD3 expression and inhibits the migration of MDA-MB-231 human breast cancer cells. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20957523/ Effects of SMYD3 over-expression on cell cycle acceleration and cell proliferation in MDA-MB-231 human breast cancer cells. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21430779/ The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/21761357/ In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland: an epigenetic mechanism linking endocrine disruptors to breast cancer. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23557258/ Cancer-associated upregulation of histone H3 lysine 9 trimethylation promotes cell motility in vitro and drives tumor formation in vivo. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/24212330/ Cancer-associated fibroblasts enhance the migration ability of ovarian cancer cells by increasing EZH2 expression. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/25168426/ Involvement of EZH2, SUV39H1, G9a and associated molecules in pathogenesis of urethane induced mouse lung tumors: potential targets for cancer control. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29897144/ Surveillance of Retroelement Expression and Nucleic-Acid Immunity by Histone Methyltransferase SETDB1. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29926931/ The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30761216/ Targeting EZH2 in Multiple Myeloma-Multifaceted Anti-Tumor Activity. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31050579/ Fine-tuning AKT kinase activity through direct lysine methylation. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/31768101/ Knockdown of SET Domain, Bifurcated 1 suppresses head and neck cancer cell viability and wound-healing ability in vitro. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32062438/ Arsenic and benzo[a]pyrene co-exposure acts synergistically in inducing cancer stem cell-like property and tumorigenesis by epigenetically down-regulating SOCS3 expression. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29512765/ Histone methyltransferase KMT5A gene modulates oncogenesis and lipid metabolism of papillary thyroid cancer in vitro. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33099471/ Deletion of Histone Methyltransferase G9a Suppresses Mutant Kras-driven Pancreatic Carcinogenesis. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/30105513/ Prognostic value of histone marks H3K27me3 and H3K9me3 and modifying enzymes EZH2, SETDB1 and LSD-1 in colorectal cancer. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32291411/ VHL-HIF-2? axis-induced SMYD3 upregulation drives renal cell carcinoma progression via direct trans-activation of EGFR. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/28418882/ Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer. unassigned - 2.1.1.355 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/20501857/ Histone methyltransferase gene SETD2 is a novel tumor suppressor gene in clear cell renal cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25634693/ Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma. causal interaction 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27605386/ miR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma. causal interaction 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/30955858/ Histone methyltransferase SMYD2 selective inhibitor LLY-507 in combination with poly ADP ribose polymerase inhibitor has therapeutic potential against high-grade serous ovarian carcinomas. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. causal interaction 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31775874/ Histone methyltransferases EHMT1 and EHMT2 (GLP/G9A) maintain PARP inhibitor resistance in high-grade serous ovarian carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32042619/ Enhancing response to immunotherapy in urothelial carcinoma by targeted inhibition of the histone methyltransferase G9a pathway. causal interaction 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32934721/ The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24079759/ Enhancer of Zeste Homolog 2 Expression Is Associated With Metastasis and Adverse Clinical Outcome in Clear Cell Renal Cell Carcinoma: A Comparative Study and Review of the Literature. causal interaction 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24775604/ Expression of PRMT5 in lung adenocarcinoma and its significance in epithelial-mesenchymal transition. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25672630/ [DZNep raises miR-200c expression to delay the invasion and migration of MGC-803 gastric carcinoma cells]. causal interaction 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/26813693/ Characterization of the Enzymatic Activity of SETDB1 and Its 1:1 Complex with ATF7IP. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. causal interaction 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. causal interaction 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32895488/ Methylation of EZH2 by PRMT1 regulates its stability and promotes breast cancer metastasis. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33626351/ Chromatin dysregulation associated with NSD1 mutation in head and neck squamous cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33910928/ Multilevel Regulation of ?-Catenin Activity by SETD2 Suppresses the Transition from Polycystic Kidney Disease to Clear Cell Renal Cell Carcinoma. causal interaction 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. causal interaction 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. diagnostic usage 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. diagnostic usage 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. diagnostic usage 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. diagnostic usage 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31775874/ Histone methyltransferases EHMT1 and EHMT2 (GLP/G9A) maintain PARP inhibitor resistance in high-grade serous ovarian carcinoma. diagnostic usage 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32934721/ The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. diagnostic usage 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. diagnostic usage 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/22609199/ The enhancer of zeste homolog 2 (EZH2), a potential therapeutic target, is regulated by miR-101 in renal cancer cells. diagnostic usage 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. diagnostic usage 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. diagnostic usage 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24775604/ Expression of PRMT5 in lung adenocarcinoma and its significance in epithelial-mesenchymal transition. diagnostic usage 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. diagnostic usage 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. diagnostic usage 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. diagnostic usage 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. therapeutic application 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25634693/ Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma. therapeutic application 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. therapeutic application 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/28444909/ The histone methyltransferase EZH2 is a therapeutic target in small cell carcinoma of the ovary, hypercalcaemic type. therapeutic application 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/30955858/ Histone methyltransferase SMYD2 selective inhibitor LLY-507 in combination with poly ADP ribose polymerase inhibitor has therapeutic potential against high-grade serous ovarian carcinomas. therapeutic application 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31775874/ Histone methyltransferases EHMT1 and EHMT2 (GLP/G9A) maintain PARP inhibitor resistance in high-grade serous ovarian carcinoma. therapeutic application 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32042619/ Enhancing response to immunotherapy in urothelial carcinoma by targeted inhibition of the histone methyltransferase G9a pathway. therapeutic application 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32934721/ The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. therapeutic application 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33579784/ Histone Methyltransferase NSD3 Is a Lung Squamous Cell Carcinoma Driver. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. therapeutic application 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. therapeutic application 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. therapeutic application 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25672630/ [DZNep raises miR-200c expression to delay the invasion and migration of MGC-803 gastric carcinoma cells]. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/26813693/ Characterization of the Enzymatic Activity of SETDB1 and Its 1:1 Complex with ATF7IP. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. therapeutic application 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. therapeutic application 2 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25634693/ Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma. ongoing research 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. ongoing research 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. ongoing research 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. ongoing research 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32934721/ The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. ongoing research 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/22609199/ The enhancer of zeste homolog 2 (EZH2), a potential therapeutic target, is regulated by miR-101 in renal cancer cells. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. ongoing research 1 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24775604/ Expression of PRMT5 in lung adenocarcinoma and its significance in epithelial-mesenchymal transition. ongoing research 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25672630/ [DZNep raises miR-200c expression to delay the invasion and migration of MGC-803 gastric carcinoma cells]. ongoing research 3 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. ongoing research 4 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/20725992/ Mutated KRAS results in overexpression of DUSP4, a MAP-kinase phosphatase, and SMYD3, a histone methyltransferase, in rectal carcinomas. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/28444909/ The histone methyltransferase EZH2 is a therapeutic target in small cell carcinoma of the ovary, hypercalcaemic type. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33127874/ Histone methyltransferase SET8 is regulated by miR-192/215 and induces oncogene-induced senescence via p53-dependent DNA damage in human gastric carcinoma cells. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33579784/ Histone Methyltransferase NSD3 Is a Lung Squamous Cell Carcinoma Driver. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/20573371/ Implications of enhancer of zeste homologue 2 expression in pancreatic ductal adenocarcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/22609199/ The enhancer of zeste homolog 2 (EZH2), a potential therapeutic target, is regulated by miR-101 in renal cancer cells. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/20501857/ Histone methyltransferase gene SETD2 is a novel tumor suppressor gene in clear cell renal cell carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25634693/ Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27605386/ miR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/30955858/ Histone methyltransferase SMYD2 selective inhibitor LLY-507 in combination with poly ADP ribose polymerase inhibitor has therapeutic potential against high-grade serous ovarian carcinomas. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32042619/ Enhancing response to immunotherapy in urothelial carcinoma by targeted inhibition of the histone methyltransferase G9a pathway. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24079759/ Enhancer of Zeste Homolog 2 Expression Is Associated With Metastasis and Adverse Clinical Outcome in Clear Cell Renal Cell Carcinoma: A Comparative Study and Review of the Literature. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25672630/ [DZNep raises miR-200c expression to delay the invasion and migration of MGC-803 gastric carcinoma cells]. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/26813693/ Characterization of the Enzymatic Activity of SETDB1 and Its 1:1 Complex with ATF7IP. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32895488/ Methylation of EZH2 by PRMT1 regulates its stability and promotes breast cancer metastasis. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33626351/ Chromatin dysregulation associated with NSD1 mutation in head and neck squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33910928/ Multilevel Regulation of ?-Catenin Activity by SETD2 Suppresses the Transition from Polycystic Kidney Disease to Clear Cell Renal Cell Carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/23912631/ Elevated expression of coactivator-associated arginine methyltransferase 1 is associated with early hepatocarcinogenesis. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24775604/ Expression of PRMT5 in lung adenocarcinoma and its significance in epithelial-mesenchymal transition. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31775874/ Histone methyltransferases EHMT1 and EHMT2 (GLP/G9A) maintain PARP inhibitor resistance in high-grade serous ovarian carcinoma. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. unassigned - 2.1.1.355 Carcinoma https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. unassigned - 2.1.1.355 Carcinoma, Adenoid Cystic https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. causal interaction 1 2.1.1.355 Carcinoma, Adenoid Cystic https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Adenoid Cystic https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. ongoing research 4 2.1.1.355 Carcinoma, Adenoid Cystic https://pubmed.ncbi.nlm.nih.gov/31177108/ Knockdown of Histone Methyltransferase WHSC1 Induces Apoptosis and Inhibits Cell Proliferation and Tumorigenesis in Salivary Adenoid Cystic Carcinoma. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/22095217/ A polymorphism at the miR-502 binding site in the 3'-untranslated region of the histone methyltransferase SET8 is associated with hepatocellular carcinoma outcome. causal interaction 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23629948/ Short-Form CDYLb but not long-form CDYLa functions cooperatively with histone methyltransferase G9a in hepatocellular carcinomas. causal interaction 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/24844570/ Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. causal interaction 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. causal interaction 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26765460/ Association of Histone Methyltransferase G9a and Overall Survival After Liver Resection of Patients With Hepatocellular Carcinoma With a Median Observation of 40 Months. causal interaction 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. causal interaction 2 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/27656834/ Knockdown of Histone Methyltransferase hSETD1A Inhibits Progression, Migration, and Invasion in Human Hepatocellular Carcinoma. causal interaction 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/28423509/ Histone lysine methyltransferase G9a is a novel epigenetic target for the treatment of hepatocellular carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. causal interaction 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/29739365/ Histone methyltransferase SETDB1 promotes cells proliferation and migration by interacting withTiam1 in hepatocellular carcinoma. causal interaction 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/32161353/ Downregulation of histone methyltransferase SET8 inhibits progression of hepatocellular carcinoma. causal interaction 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/34069116/ Histone Methyltransferase G9a-Promoted Progression of Hepatocellular Carcinoma Is Targeted by Liver-Specific Hsa-miR-122. causal interaction 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. causal interaction 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/16155568/ A variable number of tandem repeats polymorphism in an E2F-1 binding element in the 5' flanking region of SMYD3 is a risk factor for human cancers. causal interaction 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. causal interaction 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23421437/ Sorafenib suppresses growth and survival of hepatoma cells by accelerating degradation of enhancer of zeste homolog 2. causal interaction 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26336998/ TERT promoter mutations in primary liver tumors. causal interaction 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. causal interaction 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/31654063/ SETD3 is regulated by a couple of microRNAs and plays opposing roles in proliferation and metastasis of hepatocellular carcinoma. causal interaction 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. causal interaction 2 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/33168810/ EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c. causal interaction 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/22095217/ A polymorphism at the miR-502 binding site in the 3'-untranslated region of the histone methyltransferase SET8 is associated with hepatocellular carcinoma outcome. diagnostic usage 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23629948/ Short-Form CDYLb but not long-form CDYLa functions cooperatively with histone methyltransferase G9a in hepatocellular carcinomas. diagnostic usage 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. diagnostic usage 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26765460/ Association of Histone Methyltransferase G9a and Overall Survival After Liver Resection of Patients With Hepatocellular Carcinoma With a Median Observation of 40 Months. diagnostic usage 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. diagnostic usage 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/27656834/ Knockdown of Histone Methyltransferase hSETD1A Inhibits Progression, Migration, and Invasion in Human Hepatocellular Carcinoma. diagnostic usage 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. diagnostic usage 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/30503969/ MicroRNA-621 Acts as a Tumor Radiosensitizer by Directly Targeting SETDB1 in Hepatocellular Carcinoma. diagnostic usage 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/32161353/ Downregulation of histone methyltransferase SET8 inhibits progression of hepatocellular carcinoma. diagnostic usage 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/34069116/ Histone Methyltransferase G9a-Promoted Progression of Hepatocellular Carcinoma Is Targeted by Liver-Specific Hsa-miR-122. diagnostic usage 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. diagnostic usage 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/16155568/ A variable number of tandem repeats polymorphism in an E2F-1 binding element in the 5' flanking region of SMYD3 is a risk factor for human cancers. diagnostic usage 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. diagnostic usage 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. diagnostic usage 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26946844/ [Effect of Basil Polysaccharide on Histone H3K9me2 Methylation and Expression of G9a and JMJD1A in Hepatoma Cells Under Hypoxic Conditions]. diagnostic usage 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/31654063/ SETD3 is regulated by a couple of microRNAs and plays opposing roles in proliferation and metastasis of hepatocellular carcinoma. diagnostic usage 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. diagnostic usage 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23629948/ Short-Form CDYLb but not long-form CDYLa functions cooperatively with histone methyltransferase G9a in hepatocellular carcinomas. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/24844570/ Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. therapeutic application 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/27656834/ Knockdown of Histone Methyltransferase hSETD1A Inhibits Progression, Migration, and Invasion in Human Hepatocellular Carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/28423509/ Histone lysine methyltransferase G9a is a novel epigenetic target for the treatment of hepatocellular carcinoma. therapeutic application 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/29739365/ Histone methyltransferase SETDB1 promotes cells proliferation and migration by interacting withTiam1 in hepatocellular carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/30014490/ Dual targeting of histone methyltransferase G9a and DNA-methyltransferase 1 for the treatment of experimental hepatocellular carcinoma. therapeutic application 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/30503969/ MicroRNA-621 Acts as a Tumor Radiosensitizer by Directly Targeting SETDB1 in Hepatocellular Carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/32161353/ Downregulation of histone methyltransferase SET8 inhibits progression of hepatocellular carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/34069116/ Histone Methyltransferase G9a-Promoted Progression of Hepatocellular Carcinoma Is Targeted by Liver-Specific Hsa-miR-122. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/16155568/ A variable number of tandem repeats polymorphism in an E2F-1 binding element in the 5' flanking region of SMYD3 is a risk factor for human cancers. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/33168810/ EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c. therapeutic application 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. therapeutic application 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/24844570/ Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. ongoing research 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. ongoing research 2 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26765460/ Association of Histone Methyltransferase G9a and Overall Survival After Liver Resection of Patients With Hepatocellular Carcinoma With a Median Observation of 40 Months. ongoing research 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/27656834/ Knockdown of Histone Methyltransferase hSETD1A Inhibits Progression, Migration, and Invasion in Human Hepatocellular Carcinoma. ongoing research 1 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. ongoing research 2 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/16155568/ A variable number of tandem repeats polymorphism in an E2F-1 binding element in the 5' flanking region of SMYD3 is a risk factor for human cancers. ongoing research 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23421437/ Sorafenib suppresses growth and survival of hepatoma cells by accelerating degradation of enhancer of zeste homolog 2. ongoing research 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. ongoing research 2 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26946844/ [Effect of Basil Polysaccharide on Histone H3K9me2 Methylation and Expression of G9a and JMJD1A in Hepatoma Cells Under Hypoxic Conditions]. ongoing research 4 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. ongoing research 2 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. ongoing research 3 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/30014490/ Dual targeting of histone methyltransferase G9a and DNA-methyltransferase 1 for the treatment of experimental hepatocellular carcinoma. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/30503969/ MicroRNA-621 Acts as a Tumor Radiosensitizer by Directly Targeting SETDB1 in Hepatocellular Carcinoma. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26946844/ [Effect of Basil Polysaccharide on Histone H3K9me2 Methylation and Expression of G9a and JMJD1A in Hepatoma Cells Under Hypoxic Conditions]. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/24844570/ Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/28423509/ Histone lysine methyltransferase G9a is a novel epigenetic target for the treatment of hepatocellular carcinoma. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/29739365/ Histone methyltransferase SETDB1 promotes cells proliferation and migration by interacting withTiam1 in hepatocellular carcinoma. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23421437/ Sorafenib suppresses growth and survival of hepatoma cells by accelerating degradation of enhancer of zeste homolog 2. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26336998/ TERT promoter mutations in primary liver tumors. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/33168810/ EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/22095217/ A polymorphism at the miR-502 binding site in the 3'-untranslated region of the histone methyltransferase SET8 is associated with hepatocellular carcinoma outcome. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/26765460/ Association of Histone Methyltransferase G9a and Overall Survival After Liver Resection of Patients With Hepatocellular Carcinoma With a Median Observation of 40 Months. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/31654063/ SETD3 is regulated by a couple of microRNAs and plays opposing roles in proliferation and metastasis of hepatocellular carcinoma. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23629948/ Short-Form CDYLb but not long-form CDYLa functions cooperatively with histone methyltransferase G9a in hepatocellular carcinomas. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/32161353/ Downregulation of histone methyltransferase SET8 inhibits progression of hepatocellular carcinoma. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/34069116/ Histone Methyltransferase G9a-Promoted Progression of Hepatocellular Carcinoma Is Targeted by Liver-Specific Hsa-miR-122. unassigned - 2.1.1.355 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. unassigned - 2.1.1.355 Carcinoma, Merkel Cell https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Merkel Cell https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Merkel Cell https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. unassigned - 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. causal interaction 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. causal interaction 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. causal interaction 1 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. causal interaction 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. causal interaction 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/24775604/ Expression of PRMT5 in lung adenocarcinoma and its significance in epithelial-mesenchymal transition. causal interaction 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. causal interaction 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33298547/ G9a Promotes Invasion and Metastasis of Non-Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-?B Signaling Pathway. causal interaction 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. diagnostic usage 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. diagnostic usage 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. diagnostic usage 1 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. diagnostic usage 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. diagnostic usage 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/24775604/ Expression of PRMT5 in lung adenocarcinoma and its significance in epithelial-mesenchymal transition. diagnostic usage 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. diagnostic usage 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/22925699/ Epigenetic therapy with 3-deazaneplanocin A, an inhibitor of the histone methyltransferase EZH2, inhibits growth of non-small cell lung cancer cells. therapeutic application 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. therapeutic application 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. therapeutic application 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. therapeutic application 1 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. therapeutic application 1 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. therapeutic application 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. therapeutic application 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. ongoing research 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. ongoing research 1 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. ongoing research 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. ongoing research 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. ongoing research 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. ongoing research 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/24775604/ Expression of PRMT5 in lung adenocarcinoma and its significance in epithelial-mesenchymal transition. ongoing research 3 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. ongoing research 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/22925699/ Epigenetic therapy with 3-deazaneplanocin A, an inhibitor of the histone methyltransferase EZH2, inhibits growth of non-small cell lung cancer cells. unassigned - 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/30054425/ A regulatory circuitry comprising TP53, miR-29 family, and SETDB1 in non-small cell lung cancer. unassigned - 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. unassigned - 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33298547/ G9a Promotes Invasion and Metastasis of Non-Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-?B Signaling Pathway. unassigned - 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. unassigned - 2.1.1.355 Carcinoma, Non-Small-Cell Lung https://pubmed.ncbi.nlm.nih.gov/24775604/ Expression of PRMT5 in lung adenocarcinoma and its significance in epithelial-mesenchymal transition. unassigned - 2.1.1.355 Carcinoma, Ovarian Epithelial https://pubmed.ncbi.nlm.nih.gov/33196969/ MiR-520a-3p inhibits malignant progression of epithelial ovarian cancer by targeting SUV39H1 expression. therapeutic application 1 2.1.1.355 Carcinoma, Ovarian Epithelial https://pubmed.ncbi.nlm.nih.gov/33196969/ MiR-520a-3p inhibits malignant progression of epithelial ovarian cancer by targeting SUV39H1 expression. unassigned - 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/20501857/ Histone methyltransferase gene SETD2 is a novel tumor suppressor gene in clear cell renal cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. causal interaction 4 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/33910928/ Multilevel Regulation of ?-Catenin Activity by SETD2 Suppresses the Transition from Polycystic Kidney Disease to Clear Cell Renal Cell Carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. diagnostic usage 4 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/22609199/ The enhancer of zeste homolog 2 (EZH2), a potential therapeutic target, is regulated by miR-101 in renal cancer cells. diagnostic usage 1 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. diagnostic usage 4 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. therapeutic application 4 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/22609199/ The enhancer of zeste homolog 2 (EZH2), a potential therapeutic target, is regulated by miR-101 in renal cancer cells. ongoing research 4 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/22609199/ The enhancer of zeste homolog 2 (EZH2), a potential therapeutic target, is regulated by miR-101 in renal cancer cells. unassigned - 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/20501857/ Histone methyltransferase gene SETD2 is a novel tumor suppressor gene in clear cell renal cell carcinoma. unassigned - 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/33910928/ Multilevel Regulation of ?-Catenin Activity by SETD2 Suppresses the Transition from Polycystic Kidney Disease to Clear Cell Renal Cell Carcinoma. unassigned - 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. unassigned - 2.1.1.355 Carcinoma, Renal Cell https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. unassigned - 2.1.1.355 Carcinoma, Small Cell https://pubmed.ncbi.nlm.nih.gov/28444909/ The histone methyltransferase EZH2 is a therapeutic target in small cell carcinoma of the ovary, hypercalcaemic type. therapeutic application 2 2.1.1.355 Carcinoma, Small Cell https://pubmed.ncbi.nlm.nih.gov/28444909/ The histone methyltransferase EZH2 is a therapeutic target in small cell carcinoma of the ovary, hypercalcaemic type. unassigned - 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. causal interaction 4 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. causal interaction 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. causal interaction 4 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. causal interaction 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/33626351/ Chromatin dysregulation associated with NSD1 mutation in head and neck squamous cell carcinoma. causal interaction 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. diagnostic usage 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. diagnostic usage 4 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. diagnostic usage 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. diagnostic usage 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. diagnostic usage 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. diagnostic usage 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. therapeutic application 2 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/33579784/ Histone Methyltransferase NSD3 Is a Lung Squamous Cell Carcinoma Driver. therapeutic application 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. therapeutic application 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. therapeutic application 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. therapeutic application 1 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. ongoing research 4 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. ongoing research 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. ongoing research 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. ongoing research 3 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. ongoing research 4 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. unassigned - 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/33579784/ Histone Methyltransferase NSD3 Is a Lung Squamous Cell Carcinoma Driver. unassigned - 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/33626351/ Chromatin dysregulation associated with NSD1 mutation in head and neck squamous cell carcinoma. unassigned - 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. unassigned - 2.1.1.355 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24564251/ A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer. unassigned - 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/24247090/ Interplay of chromatin modifications and non-coding RNAs in the heart. causal interaction 3 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/24812277/ Chromatin modifications remodel cardiac gene expression. causal interaction 2 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/25814673/ Histone Methyltransferase SET1 Mediates Angiotensin II-Induced Endothelin-1 Transcription and Cardiac Hypertrophy in Mice. therapeutic application 1 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/31254363/ Protective effect of histone methyltransferase NSD3 on ISO-induced cardiac hypertrophy. therapeutic application 2 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/24812277/ Chromatin modifications remodel cardiac gene expression. therapeutic application 2 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/25814673/ Histone Methyltransferase SET1 Mediates Angiotensin II-Induced Endothelin-1 Transcription and Cardiac Hypertrophy in Mice. ongoing research 2 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/28778944/ Histone Methyltransferase G9a is Required for Cardiomyocyte Homeostasis and Hypertrophy. ongoing research 2 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/25814673/ Histone Methyltransferase SET1 Mediates Angiotensin II-Induced Endothelin-1 Transcription and Cardiac Hypertrophy in Mice. unassigned - 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/31254363/ Protective effect of histone methyltransferase NSD3 on ISO-induced cardiac hypertrophy. unassigned - 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/27668088/ Six1 is down-regulated in end-stage human dilated cardiomyopathy independently of Ezh2. unassigned - 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/28778944/ Histone Methyltransferase G9a is Required for Cardiomyocyte Homeostasis and Hypertrophy. unassigned - 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/24247090/ Interplay of chromatin modifications and non-coding RNAs in the heart. unassigned - 2.1.1.355 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/24812277/ Chromatin modifications remodel cardiac gene expression. unassigned - 2.1.1.355 Cardiomyopathies https://pubmed.ncbi.nlm.nih.gov/29535452/ ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. causal interaction 3 2.1.1.355 Cardiomyopathies https://pubmed.ncbi.nlm.nih.gov/29535452/ ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. diagnostic usage 2 2.1.1.355 Cardiomyopathies https://pubmed.ncbi.nlm.nih.gov/29535452/ ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. therapeutic application 3 2.1.1.355 Cardiomyopathies https://pubmed.ncbi.nlm.nih.gov/31776436/ Correction to: ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. therapeutic application 1 2.1.1.355 Cardiomyopathies https://pubmed.ncbi.nlm.nih.gov/29535452/ ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. ongoing research 4 2.1.1.355 Cardiomyopathies https://pubmed.ncbi.nlm.nih.gov/31776436/ Correction to: ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. unassigned - 2.1.1.355 Cardiomyopathy, Dilated https://pubmed.ncbi.nlm.nih.gov/28805231/ The Histone Methyltransferase Mixed Lineage Leukemia (MLL) 3 May Play a Potential Role on Clinical Dilated Cardiomyopathy. causal interaction 4 2.1.1.355 Cardiomyopathy, Dilated https://pubmed.ncbi.nlm.nih.gov/28805231/ The Histone Methyltransferase Mixed Lineage Leukemia (MLL) 3 May Play a Potential Role on Clinical Dilated Cardiomyopathy. therapeutic application 2 2.1.1.355 Cardiomyopathy, Dilated https://pubmed.ncbi.nlm.nih.gov/25607239/ H3K9 histone methyltransferase G9a ameliorates dilated cardiomyopathy via the downregulation of cell adhesion molecules. ongoing research 3 2.1.1.355 Cardiomyopathy, Dilated https://pubmed.ncbi.nlm.nih.gov/25607239/ H3K9 histone methyltransferase G9a ameliorates dilated cardiomyopathy via the downregulation of cell adhesion molecules. unassigned - 2.1.1.355 Cardiomyopathy, Dilated https://pubmed.ncbi.nlm.nih.gov/28805231/ The Histone Methyltransferase Mixed Lineage Leukemia (MLL) 3 May Play a Potential Role on Clinical Dilated Cardiomyopathy. unassigned - 2.1.1.355 Cardiovascular Diseases https://pubmed.ncbi.nlm.nih.gov/32174799/ EHMT2/G9a Inhibits Aortic Smooth Muscle Cell Death by Suppressing Autophagy Activation. causal interaction 3 2.1.1.355 Cardiovascular Diseases https://pubmed.ncbi.nlm.nih.gov/32174799/ EHMT2/G9a Inhibits Aortic Smooth Muscle Cell Death by Suppressing Autophagy Activation. therapeutic application 4 2.1.1.355 Cardiovascular Diseases https://pubmed.ncbi.nlm.nih.gov/32174799/ EHMT2/G9a Inhibits Aortic Smooth Muscle Cell Death by Suppressing Autophagy Activation. unassigned - 2.1.1.355 Carotid Artery Injuries https://pubmed.ncbi.nlm.nih.gov/31736204/ Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats. causal interaction 4 2.1.1.355 Carotid Artery Injuries https://pubmed.ncbi.nlm.nih.gov/31736204/ Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats. therapeutic application 4 2.1.1.355 Carotid Artery Injuries https://pubmed.ncbi.nlm.nih.gov/31736204/ Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats. ongoing research 2 2.1.1.355 Carotid Artery Injuries https://pubmed.ncbi.nlm.nih.gov/31736204/ Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats. unassigned - 2.1.1.355 Central Nervous System Diseases https://pubmed.ncbi.nlm.nih.gov/33279625/ Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases. therapeutic application 4 2.1.1.355 Central Nervous System Diseases https://pubmed.ncbi.nlm.nih.gov/33279625/ Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases. unassigned - 2.1.1.355 Chagas Disease https://pubmed.ncbi.nlm.nih.gov/8804798/ Antiproliferative effects of delta 24(25) sterol methyl transferase inhibitors on Trypanosoma (Schizotrypanum) cruzi: in vitro and in vivo studies. causal interaction 3 2.1.1.355 Chagas Disease https://pubmed.ncbi.nlm.nih.gov/8804798/ Antiproliferative effects of delta 24(25) sterol methyl transferase inhibitors on Trypanosoma (Schizotrypanum) cruzi: in vitro and in vivo studies. therapeutic application 4 2.1.1.355 Chagas Disease https://pubmed.ncbi.nlm.nih.gov/8804798/ Antiproliferative effects of delta 24(25) sterol methyl transferase inhibitors on Trypanosoma (Schizotrypanum) cruzi: in vitro and in vivo studies. ongoing research 1 2.1.1.355 Chagas Disease https://pubmed.ncbi.nlm.nih.gov/8804798/ Antiproliferative effects of delta 24(25) sterol methyl transferase inhibitors on Trypanosoma (Schizotrypanum) cruzi: in vitro and in vivo studies. unassigned - 2.1.1.355 CHARGE Syndrome https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. causal interaction 3 2.1.1.355 CHARGE Syndrome https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. therapeutic application 1 2.1.1.355 CHARGE Syndrome https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. unassigned - 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/24337160/ Epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A inhibits the growth of cholangiocarcinoma cells. causal interaction 1 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/21450690/ Hepatitis C virus core upregulates the methylation status of the RASSF1A promoter through regulation of SMYD3 in hilar cholangiocarcinoma cells. causal interaction 2 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/25239565/ miR-17-92 cluster promotes cholangiocarcinoma growth: evidence for PTEN as downstream target and IL-6/Stat3 as upstream activator. causal interaction 1 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/25280519/ EZH2 elevates the proliferation of human cholangiocarcinoma cells through the downregulation of RUNX3. causal interaction 1 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/21450690/ Hepatitis C virus core upregulates the methylation status of the RASSF1A promoter through regulation of SMYD3 in hilar cholangiocarcinoma cells. diagnostic usage 1 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/25239565/ miR-17-92 cluster promotes cholangiocarcinoma growth: evidence for PTEN as downstream target and IL-6/Stat3 as upstream activator. diagnostic usage 2 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/24337160/ Epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A inhibits the growth of cholangiocarcinoma cells. therapeutic application 4 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/21450690/ Hepatitis C virus core upregulates the methylation status of the RASSF1A promoter through regulation of SMYD3 in hilar cholangiocarcinoma cells. therapeutic application 1 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/25280519/ EZH2 elevates the proliferation of human cholangiocarcinoma cells through the downregulation of RUNX3. therapeutic application 1 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/21450690/ Hepatitis C virus core upregulates the methylation status of the RASSF1A promoter through regulation of SMYD3 in hilar cholangiocarcinoma cells. ongoing research 3 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/25239565/ miR-17-92 cluster promotes cholangiocarcinoma growth: evidence for PTEN as downstream target and IL-6/Stat3 as upstream activator. ongoing research 2 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/25280519/ EZH2 elevates the proliferation of human cholangiocarcinoma cells through the downregulation of RUNX3. ongoing research 2 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/24337160/ Epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A inhibits the growth of cholangiocarcinoma cells. unassigned - 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/25280519/ EZH2 elevates the proliferation of human cholangiocarcinoma cells through the downregulation of RUNX3. unassigned - 2.1.1.355 Cholangiocarcinoma https://pubmed.ncbi.nlm.nih.gov/25239565/ miR-17-92 cluster promotes cholangiocarcinoma growth: evidence for PTEN as downstream target and IL-6/Stat3 as upstream activator. unassigned - 2.1.1.355 Choline Deficiency https://pubmed.ncbi.nlm.nih.gov/19001366/ Gestational choline supply regulates methylation of histone H3, expression of histone methyltransferases G9a (Kmt1c) and Suv39h1 (Kmt1a), and DNA methylation of their genes in rat fetal liver and brain. unassigned - 2.1.1.355 Chondrosarcoma https://pubmed.ncbi.nlm.nih.gov/24852755/ 3-Deazaneplanocin A (DZNep), an inhibitor of the histone methyltransferase EZH2, induces apoptosis and reduces cell migration in chondrosarcoma cells. causal interaction 4 2.1.1.355 Chondrosarcoma https://pubmed.ncbi.nlm.nih.gov/24852755/ 3-Deazaneplanocin A (DZNep), an inhibitor of the histone methyltransferase EZH2, induces apoptosis and reduces cell migration in chondrosarcoma cells. therapeutic application 4 2.1.1.355 Chondrosarcoma https://pubmed.ncbi.nlm.nih.gov/24852755/ 3-Deazaneplanocin A (DZNep), an inhibitor of the histone methyltransferase EZH2, induces apoptosis and reduces cell migration in chondrosarcoma cells. ongoing research 3 2.1.1.355 Chondrosarcoma https://pubmed.ncbi.nlm.nih.gov/24852755/ 3-Deazaneplanocin A (DZNep), an inhibitor of the histone methyltransferase EZH2, induces apoptosis and reduces cell migration in chondrosarcoma cells. unassigned - 2.1.1.355 Classical Swine Fever https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. causal interaction 4 2.1.1.355 Classical Swine Fever https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. therapeutic application 1 2.1.1.355 Classical Swine Fever https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. ongoing research 2 2.1.1.355 Classical Swine Fever https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. unassigned - 2.1.1.355 Cleft Palate https://pubmed.ncbi.nlm.nih.gov/25677622/ Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. causal interaction 4 2.1.1.355 Cleft Palate https://pubmed.ncbi.nlm.nih.gov/25677622/ Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. therapeutic application 3 2.1.1.355 Cleft Palate https://pubmed.ncbi.nlm.nih.gov/25677622/ Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. ongoing research 4 2.1.1.355 Cleft Palate https://pubmed.ncbi.nlm.nih.gov/25677622/ Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. unassigned - 2.1.1.355 Cockayne Syndrome https://pubmed.ncbi.nlm.nih.gov/31276581/ Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging. causal interaction 3 2.1.1.355 Cockayne Syndrome https://pubmed.ncbi.nlm.nih.gov/17707230/ Activation of RNA polymerase I transcription by cockayne syndrome group B protein and histone methyltransferase G9a. unassigned - 2.1.1.355 Cockayne Syndrome https://pubmed.ncbi.nlm.nih.gov/31276581/ Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging. unassigned - 2.1.1.355 Colitis https://pubmed.ncbi.nlm.nih.gov/32296174/ Gut stem cell necroptosis by genome instability triggers bowel inflammation. causal interaction 4 2.1.1.355 Colitis https://pubmed.ncbi.nlm.nih.gov/34020310/ The histone methyltransferase SETD2 modulates oxidative stress to attenuate experimental colitis. therapeutic application 2 2.1.1.355 Colitis https://pubmed.ncbi.nlm.nih.gov/34020310/ The histone methyltransferase SETD2 modulates oxidative stress to attenuate experimental colitis. ongoing research 2 2.1.1.355 Colitis https://pubmed.ncbi.nlm.nih.gov/24667637/ Methyltransferase G9A regulates T cell differentiation during murine intestinal inflammation. ongoing research 3 2.1.1.355 Colitis https://pubmed.ncbi.nlm.nih.gov/34020310/ The histone methyltransferase SETD2 modulates oxidative stress to attenuate experimental colitis. unassigned - 2.1.1.355 Colitis https://pubmed.ncbi.nlm.nih.gov/24667637/ Methyltransferase G9A regulates T cell differentiation during murine intestinal inflammation. unassigned - 2.1.1.355 Colitis https://pubmed.ncbi.nlm.nih.gov/32296174/ Gut stem cell necroptosis by genome instability triggers bowel inflammation. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23001792/ Inhibition of PRC2 histone methyltransferase activity increases TRAIL-mediated apoptosis sensitivity in human colon cancer cells. causal interaction 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27259240/ Interaction of DNA demethylase and histone methyltransferase upregulates Nrf2 in 5-fluorouracil-resistant colon cancer cells. causal interaction 1 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28913972/ Significance of histone methyltransferase SETDB1 expression in colon adenocarcinoma. causal interaction 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23588203/ Pharmacological inhibition of polycomb repressive complex-2 activity induces apoptosis in human colon cancer stem cells. causal interaction 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24184908/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. causal interaction 3 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24322755/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. causal interaction 3 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25361163/ Regulation of Wnt signaling target gene expression by the histone methyltransferase DOT1L. causal interaction 3 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25535899/ EZH2 inhibition enhances the efficacy of an EGFR inhibitor in suppressing colon cancer cells. causal interaction 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30257334/ KDM5c inhibits multidrug resistance of colon cancer cell line by down-regulating ABCC1. causal interaction 2 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. causal interaction 1 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28913972/ Significance of histone methyltransferase SETDB1 expression in colon adenocarcinoma. diagnostic usage 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30257334/ KDM5c inhibits multidrug resistance of colon cancer cell line by down-regulating ABCC1. diagnostic usage 3 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. diagnostic usage 1 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23001792/ Inhibition of PRC2 histone methyltransferase activity increases TRAIL-mediated apoptosis sensitivity in human colon cancer cells. therapeutic application 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27259240/ Interaction of DNA demethylase and histone methyltransferase upregulates Nrf2 in 5-fluorouracil-resistant colon cancer cells. therapeutic application 1 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28913972/ Significance of histone methyltransferase SETDB1 expression in colon adenocarcinoma. therapeutic application 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23588203/ Pharmacological inhibition of polycomb repressive complex-2 activity induces apoptosis in human colon cancer stem cells. therapeutic application 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24184908/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. therapeutic application 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24322755/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. therapeutic application 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25361163/ Regulation of Wnt signaling target gene expression by the histone methyltransferase DOT1L. therapeutic application 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25535899/ EZH2 inhibition enhances the efficacy of an EGFR inhibitor in suppressing colon cancer cells. therapeutic application 2 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. therapeutic application 2 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30257334/ KDM5c inhibits multidrug resistance of colon cancer cell line by down-regulating ABCC1. therapeutic application 3 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. therapeutic application 1 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23001792/ Inhibition of PRC2 histone methyltransferase activity increases TRAIL-mediated apoptosis sensitivity in human colon cancer cells. ongoing research 3 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28913972/ Significance of histone methyltransferase SETDB1 expression in colon adenocarcinoma. ongoing research 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22863622/ Notch1 counteracts WNT/?-catenin signaling through chromatin modification in colorectal cancer. ongoing research 3 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23588203/ Pharmacological inhibition of polycomb repressive complex-2 activity induces apoptosis in human colon cancer stem cells. ongoing research 3 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25361163/ Regulation of Wnt signaling target gene expression by the histone methyltransferase DOT1L. ongoing research 1 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30257334/ KDM5c inhibits multidrug resistance of colon cancer cell line by down-regulating ABCC1. ongoing research 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. ongoing research 4 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22863622/ Notch1 counteracts WNT/?-catenin signaling through chromatin modification in colorectal cancer. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23001792/ Inhibition of PRC2 histone methyltransferase activity increases TRAIL-mediated apoptosis sensitivity in human colon cancer cells. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27259240/ Interaction of DNA demethylase and histone methyltransferase upregulates Nrf2 in 5-fluorouracil-resistant colon cancer cells. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23588203/ Pharmacological inhibition of polycomb repressive complex-2 activity induces apoptosis in human colon cancer stem cells. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24184908/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24322755/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25361163/ Regulation of Wnt signaling target gene expression by the histone methyltransferase DOT1L. unassigned - 2.1.1.355 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25535899/ EZH2 inhibition enhances the efficacy of an EGFR inhibitor in suppressing colon cancer cells. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/17657744/ Association of the SUV39H1 histone methyltransferase with the DNA methyltransferase 1 at mRNA expression level in primary colorectal cancer. causal interaction 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/27020509/ NSD1 encoding a histone methyltransferase exhibits frameshift mutations in colorectal cancers. causal interaction 2 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/30105513/ Prognostic value of histone marks H3K27me3 and H3K9me3 and modifying enzymes EZH2, SETDB1 and LSD-1 in colorectal cancer. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31090199/ KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation. causal interaction 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31306481/ Histone Methyltransferase SETDB1 Promotes Colorectal Cancer Proliferation through the STAT1-CCND1/CDK6 Axis. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. causal interaction 2 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. causal interaction 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/19843671/ Genetic Variants of Methyl Metabolizing Enzymes and Epigenetic Regulators: Associations with Promoter CpG Island Hypermethylation in Colorectal Cancer. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/23001792/ Inhibition of PRC2 histone methyltransferase activity increases TRAIL-mediated apoptosis sensitivity in human colon cancer cells. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/23557258/ Cancer-associated upregulation of histone H3 lysine 9 trimethylation promotes cell motility in vitro and drives tumor formation in vivo. causal interaction 2 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/25549357/ EZH2 regulates cofilin activity and colon cancer cell migration by targeting ITGA2 gene. causal interaction 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/30850015/ Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33323965/ G9a controls pluripotent-like identity and tumor-initiating function in human colorectal cancer. causal interaction 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/17657744/ Association of the SUV39H1 histone methyltransferase with the DNA methyltransferase 1 at mRNA expression level in primary colorectal cancer. diagnostic usage 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. diagnostic usage 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/30105513/ Prognostic value of histone marks H3K27me3 and H3K9me3 and modifying enzymes EZH2, SETDB1 and LSD-1 in colorectal cancer. diagnostic usage 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31090199/ KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation. diagnostic usage 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31306481/ Histone Methyltransferase SETDB1 Promotes Colorectal Cancer Proliferation through the STAT1-CCND1/CDK6 Axis. diagnostic usage 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. diagnostic usage 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. diagnostic usage 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. diagnostic usage 1 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/19843671/ Genetic Variants of Methyl Metabolizing Enzymes and Epigenetic Regulators: Associations with Promoter CpG Island Hypermethylation in Colorectal Cancer. diagnostic usage 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. diagnostic usage 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33323965/ G9a controls pluripotent-like identity and tumor-initiating function in human colorectal cancer. diagnostic usage 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31090199/ KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation. therapeutic application 2 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. therapeutic application 2 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. therapeutic application 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33469000/ Histone methyltransferase WHSC1 inhibits colorectal cancer cell apoptosis via targeting anti-apoptotic BCL2. therapeutic application 2 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. therapeutic application 1 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/19843671/ Genetic Variants of Methyl Metabolizing Enzymes and Epigenetic Regulators: Associations with Promoter CpG Island Hypermethylation in Colorectal Cancer. therapeutic application 1 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/23001792/ Inhibition of PRC2 histone methyltransferase activity increases TRAIL-mediated apoptosis sensitivity in human colon cancer cells. therapeutic application 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/25549357/ EZH2 regulates cofilin activity and colon cancer cell migration by targeting ITGA2 gene. therapeutic application 1 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/30850015/ Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming. therapeutic application 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/17657744/ Association of the SUV39H1 histone methyltransferase with the DNA methyltransferase 1 at mRNA expression level in primary colorectal cancer. ongoing research 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. ongoing research 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31090199/ KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation. ongoing research 2 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31896605/ Network Inference Analysis Identifies SETDB1 as a Key Regulator for Reverting Colorectal Cancer Cells into Differentiated Normal-Like Cells. ongoing research 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. ongoing research 2 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. ongoing research 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33469000/ Histone methyltransferase WHSC1 inhibits colorectal cancer cell apoptosis via targeting anti-apoptotic BCL2. ongoing research 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/19843671/ Genetic Variants of Methyl Metabolizing Enzymes and Epigenetic Regulators: Associations with Promoter CpG Island Hypermethylation in Colorectal Cancer. ongoing research 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/22863622/ Notch1 counteracts WNT/?-catenin signaling through chromatin modification in colorectal cancer. ongoing research 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/23001792/ Inhibition of PRC2 histone methyltransferase activity increases TRAIL-mediated apoptosis sensitivity in human colon cancer cells. ongoing research 3 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. ongoing research 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31896605/ Network Inference Analysis Identifies SETDB1 as a Key Regulator for Reverting Colorectal Cancer Cells into Differentiated Normal-Like Cells. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33469000/ Histone methyltransferase WHSC1 inhibits colorectal cancer cell apoptosis via targeting anti-apoptotic BCL2. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/22863622/ Notch1 counteracts WNT/?-catenin signaling through chromatin modification in colorectal cancer. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/27020509/ NSD1 encoding a histone methyltransferase exhibits frameshift mutations in colorectal cancers. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/23001792/ Inhibition of PRC2 histone methyltransferase activity increases TRAIL-mediated apoptosis sensitivity in human colon cancer cells. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/23557258/ Cancer-associated upregulation of histone H3 lysine 9 trimethylation promotes cell motility in vitro and drives tumor formation in vivo. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/25549357/ EZH2 regulates cofilin activity and colon cancer cell migration by targeting ITGA2 gene. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/30850015/ Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/17657744/ Association of the SUV39H1 histone methyltransferase with the DNA methyltransferase 1 at mRNA expression level in primary colorectal cancer. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/30105513/ Prognostic value of histone marks H3K27me3 and H3K9me3 and modifying enzymes EZH2, SETDB1 and LSD-1 in colorectal cancer. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/31306481/ Histone Methyltransferase SETDB1 Promotes Colorectal Cancer Proliferation through the STAT1-CCND1/CDK6 Axis. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33323965/ G9a controls pluripotent-like identity and tumor-initiating function in human colorectal cancer. unassigned - 2.1.1.355 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/17431393/ SMYD3 tandem repeats polymorphism is not associated with the occurrence and metastasis of hepatocellular carcinoma in a Chinese population. unassigned - 2.1.1.355 Coronary Disease https://pubmed.ncbi.nlm.nih.gov/30190170/ Novel epigenetic-sensitive clinical challenges both in type 1 and type 2 diabetes. ongoing research 1 2.1.1.355 Coronary Disease https://pubmed.ncbi.nlm.nih.gov/30190170/ Novel epigenetic-sensitive clinical challenges both in type 1 and type 2 diabetes. unassigned - 2.1.1.355 COVID-19 https://pubmed.ncbi.nlm.nih.gov/34299101/ COVID-19 in Children: Expressions of Type I/II/III Interferons, TRIM28, SETDB1, and Endogenous Retroviruses in Mild and Severe Cases. causal interaction 4 2.1.1.355 COVID-19 https://pubmed.ncbi.nlm.nih.gov/33236014/ Novel gene-specific translation mechanism of dysregulated, chronic inflammation reveals promising, multifaceted COVID-19 therapeutics. causal interaction 4 2.1.1.355 COVID-19 https://pubmed.ncbi.nlm.nih.gov/34299101/ COVID-19 in Children: Expressions of Type I/II/III Interferons, TRIM28, SETDB1, and Endogenous Retroviruses in Mild and Severe Cases. diagnostic usage 3 2.1.1.355 COVID-19 https://pubmed.ncbi.nlm.nih.gov/34299101/ COVID-19 in Children: Expressions of Type I/II/III Interferons, TRIM28, SETDB1, and Endogenous Retroviruses in Mild and Severe Cases. therapeutic application 1 2.1.1.355 COVID-19 https://pubmed.ncbi.nlm.nih.gov/34299101/ COVID-19 in Children: Expressions of Type I/II/III Interferons, TRIM28, SETDB1, and Endogenous Retroviruses in Mild and Severe Cases. ongoing research 1 2.1.1.355 COVID-19 https://pubmed.ncbi.nlm.nih.gov/33236014/ Novel gene-specific translation mechanism of dysregulated, chronic inflammation reveals promising, multifaceted COVID-19 therapeutics. unassigned - 2.1.1.355 Crohn Disease https://pubmed.ncbi.nlm.nih.gov/32296174/ Gut stem cell necroptosis by genome instability triggers bowel inflammation. causal interaction 4 2.1.1.355 Crohn Disease https://pubmed.ncbi.nlm.nih.gov/32296174/ Gut stem cell necroptosis by genome instability triggers bowel inflammation. unassigned - 2.1.1.355 Cysts https://pubmed.ncbi.nlm.nih.gov/18493619/ dSETDB1 and SU(VAR)3-9 sequentially function during germline-stem cell differentiation in Drosophila melanogaster. therapeutic application 1 2.1.1.355 Cysts https://pubmed.ncbi.nlm.nih.gov/28605118/ Histone methyltransferase 1 regulates the encystation process in the parasite Giardia lamblia. ongoing research 2 2.1.1.355 Cysts https://pubmed.ncbi.nlm.nih.gov/18493619/ dSETDB1 and SU(VAR)3-9 sequentially function during germline-stem cell differentiation in Drosophila melanogaster. unassigned - 2.1.1.355 Cysts https://pubmed.ncbi.nlm.nih.gov/28605118/ Histone methyltransferase 1 regulates the encystation process in the parasite Giardia lamblia. unassigned - 2.1.1.355 Diabetes Mellitus https://pubmed.ncbi.nlm.nih.gov/25472959/ Adverse epigenetic signatures by histone methyltransferase set7 contribute to vascular dysfunction in patients with type 2 diabetes mellitus. causal interaction 3 2.1.1.355 Diabetes Mellitus https://pubmed.ncbi.nlm.nih.gov/25472959/ Adverse epigenetic signatures by histone methyltransferase set7 contribute to vascular dysfunction in patients with type 2 diabetes mellitus. unassigned - 2.1.1.355 Diabetes Mellitus, Type 1 https://pubmed.ncbi.nlm.nih.gov/34220961/ Type 1 Diabetes and the HLA Region: Genetic Association Besides Classical HLA Class II Genes. causal interaction 3 2.1.1.355 Diabetes Mellitus, Type 1 https://pubmed.ncbi.nlm.nih.gov/21896933/ Genetic examination of SETD7 and SUV39H1/H2 methyltransferases and the risk of diabetes complications in patients with type 1 diabetes. diagnostic usage 3 2.1.1.355 Diabetes Mellitus, Type 1 https://pubmed.ncbi.nlm.nih.gov/21896933/ Genetic examination of SETD7 and SUV39H1/H2 methyltransferases and the risk of diabetes complications in patients with type 1 diabetes. ongoing research 3 2.1.1.355 Diabetes Mellitus, Type 1 https://pubmed.ncbi.nlm.nih.gov/27582499/ Histone H2AK119 and H2BK120 Monoubiquitination Modulate SET7/9 and SUV39H1 in Type 1 Diabetes Induced Renal Fibrosis. unassigned - 2.1.1.355 Diabetes Mellitus, Type 1 https://pubmed.ncbi.nlm.nih.gov/21896933/ Genetic examination of SETD7 and SUV39H1/H2 methyltransferases and the risk of diabetes complications in patients with type 1 diabetes. unassigned - 2.1.1.355 Diabetes Mellitus, Type 1 https://pubmed.ncbi.nlm.nih.gov/34220961/ Type 1 Diabetes and the HLA Region: Genetic Association Besides Classical HLA Class II Genes. unassigned - 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/25472959/ Adverse epigenetic signatures by histone methyltransferase set7 contribute to vascular dysfunction in patients with type 2 diabetes mellitus. causal interaction 3 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/28663191/ The Histone Methyltransferase MLL1 Directs Macrophage-Mediated Inflammation in Wound Healing and Is Altered in a Murine Model of Obesity and Type 2 Diabetes. causal interaction 3 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/23826075/ Mutations in Mll2, an H3K4 methyltransferase, result in insulin resistance and impaired glucose tolerance in mice. causal interaction 4 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/28663191/ The Histone Methyltransferase MLL1 Directs Macrophage-Mediated Inflammation in Wound Healing and Is Altered in a Murine Model of Obesity and Type 2 Diabetes. therapeutic application 1 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/23826075/ Mutations in Mll2, an H3K4 methyltransferase, result in insulin resistance and impaired glucose tolerance in mice. therapeutic application 1 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/23826075/ Mutations in Mll2, an H3K4 methyltransferase, result in insulin resistance and impaired glucose tolerance in mice. ongoing research 2 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/25472959/ Adverse epigenetic signatures by histone methyltransferase set7 contribute to vascular dysfunction in patients with type 2 diabetes mellitus. unassigned - 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/28663191/ The Histone Methyltransferase MLL1 Directs Macrophage-Mediated Inflammation in Wound Healing and Is Altered in a Murine Model of Obesity and Type 2 Diabetes. unassigned - 2.1.1.355 Diabetes Mellitus, Type 2 https://pubmed.ncbi.nlm.nih.gov/23826075/ Mutations in Mll2, an H3K4 methyltransferase, result in insulin resistance and impaired glucose tolerance in mice. unassigned - 2.1.1.355 Diabetes, Gestational https://pubmed.ncbi.nlm.nih.gov/25614281/ Gestational Diabetes Mellitus Impairs Fetal Endothelial Cell Functions Through a Mechanism Involving MicroRNA-101 and Histone Methyltransferase Enhancer of Zester Homolog-2. unassigned - 2.1.1.355 Diabetic Cardiomyopathies https://pubmed.ncbi.nlm.nih.gov/33097254/ MALAT1-mediated recruitment of the histone methyltransferase EZH2 to the microRNA-22 promoter leads to cardiomyocyte apoptosis in diabetic cardiomyopathy. unassigned - 2.1.1.355 Down Syndrome https://pubmed.ncbi.nlm.nih.gov/28861129/ Genome-wide DNA methylation analysis in blood cells from patients with Werner syndrome. causal interaction 4 2.1.1.355 Down Syndrome https://pubmed.ncbi.nlm.nih.gov/32819411/ PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation. causal interaction 3 2.1.1.355 Down Syndrome https://pubmed.ncbi.nlm.nih.gov/32819411/ PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation. diagnostic usage 1 2.1.1.355 Down Syndrome https://pubmed.ncbi.nlm.nih.gov/28861129/ Genome-wide DNA methylation analysis in blood cells from patients with Werner syndrome. unassigned - 2.1.1.355 Down Syndrome https://pubmed.ncbi.nlm.nih.gov/32819411/ PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation. unassigned - 2.1.1.355 Dyskeratosis Congenita https://pubmed.ncbi.nlm.nih.gov/26909595/ DNA methylation in PRDM8 is indicative for dyskeratosis congenita. causal interaction 3 2.1.1.355 Dyskeratosis Congenita https://pubmed.ncbi.nlm.nih.gov/28861129/ Genome-wide DNA methylation analysis in blood cells from patients with Werner syndrome. causal interaction 4 2.1.1.355 Dyskeratosis Congenita https://pubmed.ncbi.nlm.nih.gov/26909595/ DNA methylation in PRDM8 is indicative for dyskeratosis congenita. unassigned - 2.1.1.355 Dyskeratosis Congenita https://pubmed.ncbi.nlm.nih.gov/28861129/ Genome-wide DNA methylation analysis in blood cells from patients with Werner syndrome. unassigned - 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29396090/ Generalized dystonia associated with mutation in the histone methyltransferase gene KMT2B (DYT28) and white matter abnormalities. causal interaction 2 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29289525/ Review of the phenotype of early-onset generalised progressive dystonia due to mutations in KMT2B. causal interaction 4 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29653907/ Phenotype variability and allelic heterogeneity in KMT2B-Associated disease. causal interaction 1 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/31338059/ Identification of Novel KMT2B Variants in Chinese Dystonia Patients via Whole-Exome Sequencing. causal interaction 3 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29289525/ Review of the phenotype of early-onset generalised progressive dystonia due to mutations in KMT2B. diagnostic usage 2 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/31338059/ Identification of Novel KMT2B Variants in Chinese Dystonia Patients via Whole-Exome Sequencing. diagnostic usage 3 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/27839873/ Haploinsufficiency of KMT2B, Encoding the Lysine-Specific Histone Methyltransferase 2B, Results in Early-Onset Generalized Dystonia. therapeutic application 2 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/27992417/ Mutations in the histone methyltransferase gene KMT2B cause complex early-onset dystonia. therapeutic application 1 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/28546572/ Corrigendum: Mutations in the histone methyltransferase gene KMT2B cause complex early-onset dystonia. therapeutic application 1 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29289525/ Review of the phenotype of early-onset generalised progressive dystonia due to mutations in KMT2B. therapeutic application 4 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29653907/ Phenotype variability and allelic heterogeneity in KMT2B-Associated disease. therapeutic application 1 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/31338059/ Identification of Novel KMT2B Variants in Chinese Dystonia Patients via Whole-Exome Sequencing. therapeutic application 1 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/33300088/ Identification of a novel de novo KMT2B variant in a Greek dystonia patient via exome sequencing genotype-phenotype correlations of all published cases. therapeutic application 1 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/27839873/ Haploinsufficiency of KMT2B, Encoding the Lysine-Specific Histone Methyltransferase 2B, Results in Early-Onset Generalized Dystonia. unassigned - 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/27992417/ Mutations in the histone methyltransferase gene KMT2B cause complex early-onset dystonia. unassigned - 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/28546572/ Corrigendum: Mutations in the histone methyltransferase gene KMT2B cause complex early-onset dystonia. unassigned - 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/33300088/ Identification of a novel de novo KMT2B variant in a Greek dystonia patient via exome sequencing genotype-phenotype correlations of all published cases. unassigned - 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29396090/ Generalized dystonia associated with mutation in the histone methyltransferase gene KMT2B (DYT28) and white matter abnormalities. unassigned - 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29653907/ Phenotype variability and allelic heterogeneity in KMT2B-Associated disease. unassigned - 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/29289525/ Review of the phenotype of early-onset generalised progressive dystonia due to mutations in KMT2B. unassigned - 2.1.1.355 Dystonia https://pubmed.ncbi.nlm.nih.gov/31338059/ Identification of Novel KMT2B Variants in Chinese Dystonia Patients via Whole-Exome Sequencing. unassigned - 2.1.1.355 Encephalomyelitis https://pubmed.ncbi.nlm.nih.gov/30367633/ Circulating EZH2-positive T cells are decreased in multiple sclerosis patients. unassigned - 2.1.1.355 Encephalomyelitis, Autoimmune, Experimental https://pubmed.ncbi.nlm.nih.gov/30367633/ Circulating EZH2-positive T cells are decreased in multiple sclerosis patients. unassigned - 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/25613390/ The H3K9 Methyltransferase G9a Represses E-cadherin and is Associated with Myometrial Invasion in Endometrial Cancer. causal interaction 4 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/28418882/ Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer. causal interaction 3 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/28418882/ Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer. diagnostic usage 1 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/28418882/ Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer. therapeutic application 4 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/28910750/ Analysis of methylation profiling data of hyperplasia and primary and metastatic endometrial cancers. unassigned - 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/25613390/ The H3K9 Methyltransferase G9a Represses E-cadherin and is Associated with Myometrial Invasion in Endometrial Cancer. unassigned - 2.1.1.355 Endometrial Neoplasms https://pubmed.ncbi.nlm.nih.gov/28418882/ Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer. unassigned - 2.1.1.355 Endometriosis https://pubmed.ncbi.nlm.nih.gov/29408993/ Effects of histone methyltransferase inhibition in endometriosis. causal interaction 3 2.1.1.355 Endometriosis https://pubmed.ncbi.nlm.nih.gov/29408993/ Effects of histone methyltransferase inhibition in endometriosis. therapeutic application 4 2.1.1.355 Endometriosis https://pubmed.ncbi.nlm.nih.gov/32651901/ Inhibition of Histone Methyltransferase EZH2 Suppresses Endometriotic Vesicle Development in a Rat Model of Endometriosis. therapeutic application 4 2.1.1.355 Endometriosis https://pubmed.ncbi.nlm.nih.gov/29408993/ Effects of histone methyltransferase inhibition in endometriosis. ongoing research 3 2.1.1.355 Endometriosis https://pubmed.ncbi.nlm.nih.gov/32651901/ Inhibition of Histone Methyltransferase EZH2 Suppresses Endometriotic Vesicle Development in a Rat Model of Endometriosis. ongoing research 4 2.1.1.355 Endometriosis https://pubmed.ncbi.nlm.nih.gov/32651901/ Inhibition of Histone Methyltransferase EZH2 Suppresses Endometriotic Vesicle Development in a Rat Model of Endometriosis. unassigned - 2.1.1.355 Endometriosis https://pubmed.ncbi.nlm.nih.gov/29408993/ Effects of histone methyltransferase inhibition in endometriosis. unassigned - 2.1.1.355 Epilepsy https://pubmed.ncbi.nlm.nih.gov/27106595/ An atypical 12q24.31 microdeletion implicates six genes including a histone demethylase KDM2B and a histone methyltransferase SETD1B in syndromic intellectual disability. therapeutic application 1 2.1.1.355 Epilepsy https://pubmed.ncbi.nlm.nih.gov/27106595/ An atypical 12q24.31 microdeletion implicates six genes including a histone demethylase KDM2B and a histone methyltransferase SETD1B in syndromic intellectual disability. unassigned - 2.1.1.355 Esophageal Squamous Cell Carcinoma https://pubmed.ncbi.nlm.nih.gov/27605386/ miR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma. causal interaction 2 2.1.1.355 Esophageal Squamous Cell Carcinoma https://pubmed.ncbi.nlm.nih.gov/27605386/ miR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma. unassigned - 2.1.1.355 Foot-and-Mouth Disease https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. therapeutic application 4 2.1.1.355 Foot-and-Mouth Disease https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. ongoing research 4 2.1.1.355 Foot-and-Mouth Disease https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. unassigned - 2.1.1.355 Friedreich Ataxia https://pubmed.ncbi.nlm.nih.gov/33028632/ Inhibition of the SUV4-20 H1 histone methyltransferase increases frataxin expression in Friedreich's ataxia patient cells. causal interaction 3 2.1.1.355 Friedreich Ataxia https://pubmed.ncbi.nlm.nih.gov/33028632/ Inhibition of the SUV4-20 H1 histone methyltransferase increases frataxin expression in Friedreich's ataxia patient cells. unassigned - 2.1.1.355 Ganglioglioma https://pubmed.ncbi.nlm.nih.gov/21681934/ Constitutional tandem duplication of 9q34 that truncates EHMT1 in a child with ganglioglioma. therapeutic application 1 2.1.1.355 Ganglioglioma https://pubmed.ncbi.nlm.nih.gov/21681934/ Constitutional tandem duplication of 9q34 that truncates EHMT1 in a child with ganglioglioma. unassigned - 2.1.1.355 Gastrointestinal Diseases https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Gastrointestinal Diseases https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Genetic Diseases, Inborn https://pubmed.ncbi.nlm.nih.gov/33387673/ Broad neurodevelopmental features and cortical anomalies associated with a novel de novo KMT2A variant in Wiedemann-Steiner syndrome. causal interaction 2 2.1.1.355 Genetic Diseases, Inborn https://pubmed.ncbi.nlm.nih.gov/30063093/ Pulmonary hypertension in patients with 9q34.3 microdeletion-associated Kleefstra syndrome. unassigned - 2.1.1.355 Genetic Diseases, Inborn https://pubmed.ncbi.nlm.nih.gov/34357686/ Kleefstra syndrome: Recurrence in siblings due to a paternal mosaic mutation. unassigned - 2.1.1.355 Genetic Diseases, Inborn https://pubmed.ncbi.nlm.nih.gov/33387673/ Broad neurodevelopmental features and cortical anomalies associated with a novel de novo KMT2A variant in Wiedemann-Steiner syndrome. unassigned - 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/33059737/ SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway. causal interaction 4 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/34447744/ Epigenetic Deregulation of the Histone Methyltransferase KMT5B Contributes to Malignant Transformation in Glioblastoma. causal interaction 2 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. causal interaction 3 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/31367244/ A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep. causal interaction 1 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/31367244/ A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep. diagnostic usage 3 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/33059737/ SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway. therapeutic application 4 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. therapeutic application 1 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. therapeutic application 2 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/31367244/ A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep. therapeutic application 4 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/33059737/ SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway. ongoing research 2 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/31367244/ A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep. ongoing research 2 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/28737508/ Targeting NEK2 attenuates glioblastoma growth and radioresistance by destabilizing histone methyltransferase EZH2. unassigned - 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/32870163/ Targeting NEK2 attenuates glioblastoma growth and radioresistance by destabilizing histone methyltransferase EZH2. unassigned - 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/33044225/ Targeting NEK2 attenuates glioblastoma growth and radioresistance by destabilizing histone methyltransferase EZH2. unassigned - 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. unassigned - 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/33059737/ SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway. unassigned - 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/34447744/ Epigenetic Deregulation of the Histone Methyltransferase KMT5B Contributes to Malignant Transformation in Glioblastoma. unassigned - 2.1.1.355 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/30450051/ Pre-treatment or Post-treatment of Human Glioma Cells With BIX01294, the Inhibitor of Histone Methyltransferase G9a, Sensitizes Cells to Temozolomide. causal interaction 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/20946108/ ENHANCER OF ZESTE 2 (EZH2) IS UP-REGULATED IN MALIGNANT GLIOMAS AND IN GLIOMA STEM-LIKE CELLS. causal interaction 3 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/23763996/ Cancer Stem Cells Activate STAT3 the EZ Way. causal interaction 3 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/23943221/ Role of Histone Lysine Methyltransferases SUV39H1 and SETDB1 in Gliomagenesis: Modulation of Cell Proliferation, Migration, and Colony Formation. causal interaction 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25602259/ Emerging role of linker histone variant H1x as a biomarker with prognostic value in astrocytic gliomas. A multivariate analysis including trimethylation of H3K9 and H4K20. causal interaction 2 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25996283/ EGFR promoter exhibits dynamic histone modifications and binding of ASH2L and P300 in human germinal matrix and gliomas. causal interaction 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/28623138/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. causal interaction 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/28946550/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. causal interaction 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/23763996/ Cancer Stem Cells Activate STAT3 the EZ Way. diagnostic usage 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/23943221/ Role of Histone Lysine Methyltransferases SUV39H1 and SETDB1 in Gliomagenesis: Modulation of Cell Proliferation, Migration, and Colony Formation. diagnostic usage 3 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25996283/ EGFR promoter exhibits dynamic histone modifications and binding of ASH2L and P300 in human germinal matrix and gliomas. diagnostic usage 2 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/24833465/ Histone methyltransferase G9a and H3K9 dimethylation inhibit the self-renewal of glioma cancer stem cells. therapeutic application 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/27934912/ BIX01294, an inhibitor of histone methyltransferase, induces autophagy-dependent differentiation of glioma stem-like cells. therapeutic application 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/30450051/ Pre-treatment or Post-treatment of Human Glioma Cells With BIX01294, the Inhibitor of Histone Methyltransferase G9a, Sensitizes Cells to Temozolomide. therapeutic application 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/23943221/ Role of Histone Lysine Methyltransferases SUV39H1 and SETDB1 in Gliomagenesis: Modulation of Cell Proliferation, Migration, and Colony Formation. therapeutic application 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25602259/ Emerging role of linker histone variant H1x as a biomarker with prognostic value in astrocytic gliomas. A multivariate analysis including trimethylation of H3K9 and H4K20. therapeutic application 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/28445939/ Epigenetic therapy with inhibitors of histone methylation suppresses DNA damage signaling and increases glioma cell radiosensitivity. therapeutic application 2 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/28946550/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. therapeutic application 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/33363140/ EZH2-Inhibited MicroRNA-454-3p Promotes M2 Macrophage Polarization in Glioma. therapeutic application 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/20018718/ Epigenetic inactivation of the Sotos overgrowth syndrome gene histone methyltransferase NSD1 in human neuroblastoma and glioma. ongoing research 2 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25046371/ Epigenetic modification in gliomas: role of the histone methyltransferase EZH2. ongoing research 2 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/27470408/ TCH1036, a indeno[1,2-c]quinoline derivative, potentially inhibited the growth of human brain malignant glioma (GBM) 8401 cells via suppression of the expression of Suv39h1 and PARP. ongoing research 3 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/27934912/ BIX01294, an inhibitor of histone methyltransferase, induces autophagy-dependent differentiation of glioma stem-like cells. ongoing research 2 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/30450051/ Pre-treatment or Post-treatment of Human Glioma Cells With BIX01294, the Inhibitor of Histone Methyltransferase G9a, Sensitizes Cells to Temozolomide. ongoing research 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/31636512/ Histone methyltransferase SUV39H2 regulates cell growth and chemosensitivity in glioma via regulation of hedgehog signaling. ongoing research 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/20946108/ ENHANCER OF ZESTE 2 (EZH2) IS UP-REGULATED IN MALIGNANT GLIOMAS AND IN GLIOMA STEM-LIKE CELLS. ongoing research 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/23943221/ Role of Histone Lysine Methyltransferases SUV39H1 and SETDB1 in Gliomagenesis: Modulation of Cell Proliferation, Migration, and Colony Formation. ongoing research 2 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25996283/ EGFR promoter exhibits dynamic histone modifications and binding of ASH2L and P300 in human germinal matrix and gliomas. ongoing research 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/28623138/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. ongoing research 1 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/20018718/ Epigenetic inactivation of the Sotos overgrowth syndrome gene histone methyltransferase NSD1 in human neuroblastoma and glioma. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/24833465/ Histone methyltransferase G9a and H3K9 dimethylation inhibit the self-renewal of glioma cancer stem cells. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25046371/ Epigenetic modification in gliomas: role of the histone methyltransferase EZH2. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/27470408/ TCH1036, a indeno[1,2-c]quinoline derivative, potentially inhibited the growth of human brain malignant glioma (GBM) 8401 cells via suppression of the expression of Suv39h1 and PARP. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/27934912/ BIX01294, an inhibitor of histone methyltransferase, induces autophagy-dependent differentiation of glioma stem-like cells. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/31636512/ Histone methyltransferase SUV39H2 regulates cell growth and chemosensitivity in glioma via regulation of hedgehog signaling. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/26902498/ Pygo2 functions as a prognostic factor for glioma due to its up-regulation of H3K4me3 and promotion of MLL1/MLL2 complex recruitment. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/28445939/ Epigenetic therapy with inhibitors of histone methylation suppresses DNA damage signaling and increases glioma cell radiosensitivity. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/31429770/ A central role for MeCP2 in the epigenetic repression of miR-200c during epithelial-to-mesenchymal transition of glioma. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/33363140/ EZH2-Inhibited MicroRNA-454-3p Promotes M2 Macrophage Polarization in Glioma. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/30450051/ Pre-treatment or Post-treatment of Human Glioma Cells With BIX01294, the Inhibitor of Histone Methyltransferase G9a, Sensitizes Cells to Temozolomide. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/20946108/ ENHANCER OF ZESTE 2 (EZH2) IS UP-REGULATED IN MALIGNANT GLIOMAS AND IN GLIOMA STEM-LIKE CELLS. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25602259/ Emerging role of linker histone variant H1x as a biomarker with prognostic value in astrocytic gliomas. A multivariate analysis including trimethylation of H3K9 and H4K20. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/28623138/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/28946550/ HP1? is highly expressed in glioma cells and facilitates cell proliferation and survival. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/23763996/ Cancer Stem Cells Activate STAT3 the EZ Way. unassigned - 2.1.1.355 Glioma https://pubmed.ncbi.nlm.nih.gov/25996283/ EGFR promoter exhibits dynamic histone modifications and binding of ASH2L and P300 in human germinal matrix and gliomas. unassigned - 2.1.1.355 Graft vs Host Disease https://pubmed.ncbi.nlm.nih.gov/24141370/ The histone methyltransferase Ezh2 is a crucial epigenetic regulator of allogeneic T-cell responses mediating graft-versus-host disease. unassigned - 2.1.1.355 Graft vs Host Disease https://pubmed.ncbi.nlm.nih.gov/34206082/ Analysis of Relationships between Immune Checkpoint and Methylase Gene Polymorphisms and Outcomes after Unrelated Bone Marrow Transplantation. unassigned - 2.1.1.355 Growth Hormone-Secreting Pituitary Adenoma https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. causal interaction 4 2.1.1.355 Growth Hormone-Secreting Pituitary Adenoma https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. diagnostic usage 4 2.1.1.355 Growth Hormone-Secreting Pituitary Adenoma https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. therapeutic application 1 2.1.1.355 Growth Hormone-Secreting Pituitary Adenoma https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. ongoing research 4 2.1.1.355 Head and Neck Neoplasms https://pubmed.ncbi.nlm.nih.gov/21532618/ The tumor suppressor gene rap1GAP is silenced by miR-101-mediated EZH2 overexpression in invasive squamous cell carcinoma. therapeutic application 1 2.1.1.355 Head and Neck Neoplasms https://pubmed.ncbi.nlm.nih.gov/21532618/ The tumor suppressor gene rap1GAP is silenced by miR-101-mediated EZH2 overexpression in invasive squamous cell carcinoma. unassigned - 2.1.1.355 Hearing Loss https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. causal interaction 3 2.1.1.355 Hearing Loss https://pubmed.ncbi.nlm.nih.gov/30710318/ Inhibition of Histone Methyltransferase G9a Attenuates Noise-Induced Cochlear Synaptopathy and Hearing Loss. therapeutic application 1 2.1.1.355 Hearing Loss https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. therapeutic application 1 2.1.1.355 Hearing Loss https://pubmed.ncbi.nlm.nih.gov/30710318/ Inhibition of Histone Methyltransferase G9a Attenuates Noise-Induced Cochlear Synaptopathy and Hearing Loss. ongoing research 4 2.1.1.355 Hearing Loss https://pubmed.ncbi.nlm.nih.gov/30710318/ Inhibition of Histone Methyltransferase G9a Attenuates Noise-Induced Cochlear Synaptopathy and Hearing Loss. unassigned - 2.1.1.355 Hearing Loss https://pubmed.ncbi.nlm.nih.gov/24705355/ CHARGE and Kabuki syndromes: A phenotypic and molecular link. unassigned - 2.1.1.355 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/31746096/ G9?-dependent histone H3K9me3 hypomethylation promotes overexpression of cardiomyogenesis-related genes in foetal mice. causal interaction 2 2.1.1.355 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/31746096/ G9?-dependent histone H3K9me3 hypomethylation promotes overexpression of cardiomyogenesis-related genes in foetal mice. therapeutic application 3 2.1.1.355 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/31746096/ G9?-dependent histone H3K9me3 hypomethylation promotes overexpression of cardiomyogenesis-related genes in foetal mice. unassigned - 2.1.1.355 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Heart Diseases https://pubmed.ncbi.nlm.nih.gov/28560987/ The promising therapeutic agents for heart diseases: Histone Methyltransferase inhibitors. causal interaction 3 2.1.1.355 Heart Diseases https://pubmed.ncbi.nlm.nih.gov/28560987/ The promising therapeutic agents for heart diseases: Histone Methyltransferase inhibitors. therapeutic application 4 2.1.1.355 Heart Diseases https://pubmed.ncbi.nlm.nih.gov/28560987/ The promising therapeutic agents for heart diseases: Histone Methyltransferase inhibitors. unassigned - 2.1.1.355 Heart Failure https://pubmed.ncbi.nlm.nih.gov/27663768/ The chromatin-binding protein Smyd1 restricts adult mammalian heart growth. causal interaction 4 2.1.1.355 Heart Failure https://pubmed.ncbi.nlm.nih.gov/27663768/ The chromatin-binding protein Smyd1 restricts adult mammalian heart growth. therapeutic application 4 2.1.1.355 Heart Failure https://pubmed.ncbi.nlm.nih.gov/28051130/ The histone 3 lysine 9 methyltransferase inhibitor chaetocin improves prognosis in a rat model of high salt diet-induced heart failure. therapeutic application 4 2.1.1.355 Heart Failure https://pubmed.ncbi.nlm.nih.gov/27663768/ The chromatin-binding protein Smyd1 restricts adult mammalian heart growth. ongoing research 3 2.1.1.355 Heart Failure https://pubmed.ncbi.nlm.nih.gov/28051130/ The histone 3 lysine 9 methyltransferase inhibitor chaetocin improves prognosis in a rat model of high salt diet-induced heart failure. ongoing research 4 2.1.1.355 Heart Failure https://pubmed.ncbi.nlm.nih.gov/28051130/ The histone 3 lysine 9 methyltransferase inhibitor chaetocin improves prognosis in a rat model of high salt diet-induced heart failure. unassigned - 2.1.1.355 Heart Failure https://pubmed.ncbi.nlm.nih.gov/27663768/ The chromatin-binding protein Smyd1 restricts adult mammalian heart growth. unassigned - 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34266924/ The Benzene Hematotoxic and Reactive Metabolite 1,4-Benzoquinone Impairs the Activity of the Histone Methyltransferase SET Domain Containing 2 (SETD2) and Causes Aberrant Histone H3 Lysine 36 Trimethylation (H3K36me3). causal interaction 4 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34531375/ PRMT5 regulates cell pyroptosis by silencing CASP1 in multiple myeloma. causal interaction 2 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. therapeutic application 4 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. ongoing research 3 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34531375/ PRMT5 regulates cell pyroptosis by silencing CASP1 in multiple myeloma. ongoing research 1 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25149548/ Diffuse large B-cell lymphoma with histone H3 trimethylation at lysine 27: another poor prognostic phenotype independent of c-Myc/Bcl2 coexpression. unassigned - 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/26314470/ [Advances of Researches on the Role of Histone Modification in Hematological Neoplasms]. unassigned - 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. unassigned - 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34266924/ The Benzene Hematotoxic and Reactive Metabolite 1,4-Benzoquinone Impairs the Activity of the Histone Methyltransferase SET Domain Containing 2 (SETD2) and Causes Aberrant Histone H3 Lysine 36 Trimethylation (H3K36me3). unassigned - 2.1.1.355 Hematologic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34531375/ PRMT5 regulates cell pyroptosis by silencing CASP1 in multiple myeloma. unassigned - 2.1.1.355 Hepatitis https://pubmed.ncbi.nlm.nih.gov/34479991/ Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2. causal interaction 1 2.1.1.355 Hepatitis https://pubmed.ncbi.nlm.nih.gov/34479991/ Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2. therapeutic application 1 2.1.1.355 Hepatitis https://pubmed.ncbi.nlm.nih.gov/34479991/ Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2. ongoing research 2 2.1.1.355 Hepatitis https://pubmed.ncbi.nlm.nih.gov/34479991/ Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2. unassigned - 2.1.1.355 Hepatitis B https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. causal interaction 2 2.1.1.355 Hepatitis B https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. diagnostic usage 3 2.1.1.355 Hepatitis B https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. ongoing research 2 2.1.1.355 Hepatitis B https://pubmed.ncbi.nlm.nih.gov/26143443/ HBx relieves chromatin-mediated transcriptional repression of hepatitis B viral cccDNA involving SETDB1 histone methyltransferase. unassigned - 2.1.1.355 Hepatitis B https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. unassigned - 2.1.1.355 Hepatitis B, Chronic https://pubmed.ncbi.nlm.nih.gov/29238036/ Identification of additional EHMT2 variant associated with the risk of chronic hepatitis B by GWAS follow-up study. causal interaction 3 2.1.1.355 Hepatitis B, Chronic https://pubmed.ncbi.nlm.nih.gov/24465836/ Genetic association of human leukocyte antigens with chronicity or resolution of hepatitis B infection in thai population. causal interaction 3 2.1.1.355 Hepatitis B, Chronic https://pubmed.ncbi.nlm.nih.gov/29238036/ Identification of additional EHMT2 variant associated with the risk of chronic hepatitis B by GWAS follow-up study. diagnostic usage 1 2.1.1.355 Hepatitis B, Chronic https://pubmed.ncbi.nlm.nih.gov/24465836/ Genetic association of human leukocyte antigens with chronicity or resolution of hepatitis B infection in thai population. unassigned - 2.1.1.355 Hepatitis B, Chronic https://pubmed.ncbi.nlm.nih.gov/29238036/ Identification of additional EHMT2 variant associated with the risk of chronic hepatitis B by GWAS follow-up study. unassigned - 2.1.1.355 Herpes Simplex https://pubmed.ncbi.nlm.nih.gov/26015494/ Barrier-to-Autointegration Factor 1 (BAF/BANF1) Promotes Association of the SETD1A Histone Methyltransferase with Herpes Simplex Virus Immediate-Early Gene Promoters. causal interaction 1 2.1.1.355 Herpes Simplex https://pubmed.ncbi.nlm.nih.gov/26015494/ Barrier-to-Autointegration Factor 1 (BAF/BANF1) Promotes Association of the SETD1A Histone Methyltransferase with Herpes Simplex Virus Immediate-Early Gene Promoters. therapeutic application 1 2.1.1.355 Herpes Simplex https://pubmed.ncbi.nlm.nih.gov/26015494/ Barrier-to-Autointegration Factor 1 (BAF/BANF1) Promotes Association of the SETD1A Histone Methyltransferase with Herpes Simplex Virus Immediate-Early Gene Promoters. ongoing research 1 2.1.1.355 Herpes Simplex https://pubmed.ncbi.nlm.nih.gov/26015494/ Barrier-to-Autointegration Factor 1 (BAF/BANF1) Promotes Association of the SETD1A Histone Methyltransferase with Herpes Simplex Virus Immediate-Early Gene Promoters. unassigned - 2.1.1.355 Huntington Disease https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Huntington Disease https://pubmed.ncbi.nlm.nih.gov/33279625/ Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases. therapeutic application 4 2.1.1.355 Huntington Disease https://pubmed.ncbi.nlm.nih.gov/33771089/ Modulation of SETDB1 activity by APQ ameliorates heterochromatin condensation, motor function, and neuropathology in a Huntington's disease mouse model. ongoing research 1 2.1.1.355 Huntington Disease https://pubmed.ncbi.nlm.nih.gov/33771089/ Modulation of SETDB1 activity by APQ ameliorates heterochromatin condensation, motor function, and neuropathology in a Huntington's disease mouse model. unassigned - 2.1.1.355 Huntington Disease https://pubmed.ncbi.nlm.nih.gov/33279625/ Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases. unassigned - 2.1.1.355 Huntington Disease https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Hyperalgesia https://pubmed.ncbi.nlm.nih.gov/27483126/ Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity. causal interaction 4 2.1.1.355 Hyperalgesia https://pubmed.ncbi.nlm.nih.gov/27483126/ Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity. diagnostic usage 2 2.1.1.355 Hyperalgesia https://pubmed.ncbi.nlm.nih.gov/27483126/ Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity. therapeutic application 4 2.1.1.355 Hyperalgesia https://pubmed.ncbi.nlm.nih.gov/27483126/ Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity. ongoing research 2 2.1.1.355 Hyperglycemia https://pubmed.ncbi.nlm.nih.gov/31467597/ High blood sugar levels but not diabetes mellitus significantly enhance oxaliplatin chemoresistance in patients with stage III colorectal cancer receiving adjuvant FOLFOX6 chemotherapy. causal interaction 4 2.1.1.355 Hyperglycemia https://pubmed.ncbi.nlm.nih.gov/31467597/ High blood sugar levels but not diabetes mellitus significantly enhance oxaliplatin chemoresistance in patients with stage III colorectal cancer receiving adjuvant FOLFOX6 chemotherapy. therapeutic application 1 2.1.1.355 Hyperglycemia https://pubmed.ncbi.nlm.nih.gov/31467597/ High blood sugar levels but not diabetes mellitus significantly enhance oxaliplatin chemoresistance in patients with stage III colorectal cancer receiving adjuvant FOLFOX6 chemotherapy. unassigned - 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/27483126/ Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity. causal interaction 4 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/32670741/ N6-Methyladenosine Demethylase FTO Contributes to Neuropathic Pain by Stabilizing G9a Expression in Primary Sensory Neurons. causal interaction 1 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/34383386/ Downregulation of a Dorsal Root Ganglion-Specifically Enriched Long Noncoding RNA is Required for Neuropathic Pain by Negatively Regulating RALY-Triggered Ehmt2 Expression. causal interaction 2 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/27483126/ Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity. diagnostic usage 2 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/23861670/ Histone methyltransferase DOT1L drives recovery of gene expression after a genotoxic attack. therapeutic application 1 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/27483126/ Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity. therapeutic application 4 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/23861670/ Histone methyltransferase DOT1L drives recovery of gene expression after a genotoxic attack. ongoing research 1 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/27483126/ Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury-induced Nociceptive Hypersensitivity. ongoing research 2 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/29635344/ Histone H3 lysine 36 methyltransferase mobilizes NER factors to regulate tolerance against alkylation damage in fission yeast. ongoing research 2 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/23861670/ Histone methyltransferase DOT1L drives recovery of gene expression after a genotoxic attack. unassigned - 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/29635344/ Histone H3 lysine 36 methyltransferase mobilizes NER factors to regulate tolerance against alkylation damage in fission yeast. unassigned - 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/32670741/ N6-Methyladenosine Demethylase FTO Contributes to Neuropathic Pain by Stabilizing G9a Expression in Primary Sensory Neurons. unassigned - 2.1.1.355 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/34383386/ Downregulation of a Dorsal Root Ganglion-Specifically Enriched Long Noncoding RNA is Required for Neuropathic Pain by Negatively Regulating RALY-Triggered Ehmt2 Expression. unassigned - 2.1.1.355 Hypertension https://pubmed.ncbi.nlm.nih.gov/32616020/ Genomic analysis of the domestication and post-Spanish conquest evolution of the llama and alpaca. causal interaction 1 2.1.1.355 Hypertension https://pubmed.ncbi.nlm.nih.gov/32616020/ Genomic analysis of the domestication and post-Spanish conquest evolution of the llama and alpaca. unassigned - 2.1.1.355 Hypertrichosis https://pubmed.ncbi.nlm.nih.gov/30014449/ RNA Sequencing and Pathway Analysis Identify Important Pathways Involved in Hypertrichosis and Intellectual Disability in Patients with Wiedemann-Steiner Syndrome. causal interaction 1 2.1.1.355 Hypertrichosis https://pubmed.ncbi.nlm.nih.gov/33387673/ Broad neurodevelopmental features and cortical anomalies associated with a novel de novo KMT2A variant in Wiedemann-Steiner syndrome. causal interaction 2 2.1.1.355 Hypertrichosis https://pubmed.ncbi.nlm.nih.gov/30014449/ RNA Sequencing and Pathway Analysis Identify Important Pathways Involved in Hypertrichosis and Intellectual Disability in Patients with Wiedemann-Steiner Syndrome. unassigned - 2.1.1.355 Hypertrichosis https://pubmed.ncbi.nlm.nih.gov/33387673/ Broad neurodevelopmental features and cortical anomalies associated with a novel de novo KMT2A variant in Wiedemann-Steiner syndrome. unassigned - 2.1.1.355 Hypogonadism https://pubmed.ncbi.nlm.nih.gov/30370152/ Hypogonadotropic Hypogonadism and Kleefstra Syndrome due to a Pathogenic Variant in the EHMT1 Gene: An Underrecognized Association. causal interaction 2 2.1.1.355 Hypogonadism https://pubmed.ncbi.nlm.nih.gov/25228647/ Setdb1 is required for germline development and silencing of H3K9me3-marked endogenous retroviruses in primordial germ cells. causal interaction 4 2.1.1.355 Hypogonadism https://pubmed.ncbi.nlm.nih.gov/30370152/ Hypogonadotropic Hypogonadism and Kleefstra Syndrome due to a Pathogenic Variant in the EHMT1 Gene: An Underrecognized Association. unassigned - 2.1.1.355 Hypogonadism https://pubmed.ncbi.nlm.nih.gov/25228647/ Setdb1 is required for germline development and silencing of H3K9me3-marked endogenous retroviruses in primordial germ cells. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. causal interaction 4 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/21450690/ Hepatitis C virus core upregulates the methylation status of the RASSF1A promoter through regulation of SMYD3 in hilar cholangiocarcinoma cells. causal interaction 2 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/22194464/ SMYD3 promotes cancer invasion by epigenetic upregulation of the metalloproteinase MMP-9. causal interaction 4 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/26255971/ Host genetic variants influencing the clinical course of hepatitis B virus infection. causal interaction 2 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/29170282/ Histone methyltransferase SUV39H1 participates in host defense by methylating mycobacterial histone-like protein HupB. causal interaction 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/29624717/ SIRT3 restricts hepatitis B virus transcription and replication through epigenetic regulation of covalently closed circular DNA involving suppressor of variegation 3-9 homolog 1 and SET domain containing 1A histone methyltransferases. causal interaction 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. causal interaction 2 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. causal interaction 4 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/34299101/ COVID-19 in Children: Expressions of Type I/II/III Interferons, TRIM28, SETDB1, and Endogenous Retroviruses in Mild and Severe Cases. causal interaction 4 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/21450690/ Hepatitis C virus core upregulates the methylation status of the RASSF1A promoter through regulation of SMYD3 in hilar cholangiocarcinoma cells. diagnostic usage 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/21669218/ Testosterone response of hepatic gene expression in female mice having acquired testosterone-unresponsive immunity to Plasmodium chabaudi malaria. diagnostic usage 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/26255971/ Host genetic variants influencing the clinical course of hepatitis B virus infection. diagnostic usage 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. diagnostic usage 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/34299101/ COVID-19 in Children: Expressions of Type I/II/III Interferons, TRIM28, SETDB1, and Endogenous Retroviruses in Mild and Severe Cases. diagnostic usage 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. therapeutic application 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/21450690/ Hepatitis C virus core upregulates the methylation status of the RASSF1A promoter through regulation of SMYD3 in hilar cholangiocarcinoma cells. therapeutic application 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/22194464/ SMYD3 promotes cancer invasion by epigenetic upregulation of the metalloproteinase MMP-9. therapeutic application 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/29170282/ Histone methyltransferase SUV39H1 participates in host defense by methylating mycobacterial histone-like protein HupB. therapeutic application 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/29624717/ SIRT3 restricts hepatitis B virus transcription and replication through epigenetic regulation of covalently closed circular DNA involving suppressor of variegation 3-9 homolog 1 and SET domain containing 1A histone methyltransferases. therapeutic application 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/34299101/ COVID-19 in Children: Expressions of Type I/II/III Interferons, TRIM28, SETDB1, and Endogenous Retroviruses in Mild and Severe Cases. therapeutic application 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. ongoing research 2 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/21450690/ Hepatitis C virus core upregulates the methylation status of the RASSF1A promoter through regulation of SMYD3 in hilar cholangiocarcinoma cells. ongoing research 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/22194464/ SMYD3 promotes cancer invasion by epigenetic upregulation of the metalloproteinase MMP-9. ongoing research 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/23733190/ Nitric oxide and KLF4 protein epigenetically modify class II transactivator to repress major histocompatibility complex II expression during Mycobacterium bovis bacillus Calmette-Guerin infection. ongoing research 3 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/31682228/ IFI16, a nuclear innate immune DNA sensor, mediates epigenetic silencing of herpesvirus genomes by its association with H3K9 methyltransferases SUV39H1 and GLP. ongoing research 2 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. ongoing research 2 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. ongoing research 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/34299101/ COVID-19 in Children: Expressions of Type I/II/III Interferons, TRIM28, SETDB1, and Endogenous Retroviruses in Mild and Severe Cases. ongoing research 1 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/21669218/ Testosterone response of hepatic gene expression in female mice having acquired testosterone-unresponsive immunity to Plasmodium chabaudi malaria. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/23733190/ Nitric oxide and KLF4 protein epigenetically modify class II transactivator to repress major histocompatibility complex II expression during Mycobacterium bovis bacillus Calmette-Guerin infection. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/24478419/ Transcriptional Derepression of the ERVWE1 Locus following Influenza A Virus Infection. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/31682228/ IFI16, a nuclear innate immune DNA sensor, mediates epigenetic silencing of herpesvirus genomes by its association with H3K9 methyltransferases SUV39H1 and GLP. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/22194464/ SMYD3 promotes cancer invasion by epigenetic upregulation of the metalloproteinase MMP-9. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/29170282/ Histone methyltransferase SUV39H1 participates in host defense by methylating mycobacterial histone-like protein HupB. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/29624717/ SIRT3 restricts hepatitis B virus transcription and replication through epigenetic regulation of covalently closed circular DNA involving suppressor of variegation 3-9 homolog 1 and SET domain containing 1A histone methyltransferases. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/26255971/ Host genetic variants influencing the clinical course of hepatitis B virus infection. unassigned - 2.1.1.355 Infections https://pubmed.ncbi.nlm.nih.gov/32514521/ Signal activation of hepatitis B virus-related hepatocarcinogenesis by upregulation of SUV39h1. unassigned - 2.1.1.355 Infertility https://pubmed.ncbi.nlm.nih.gov/32642764/ Prdm9 inter-subspecific interactions in hybrid male sterility of house mouse. diagnostic usage 3 2.1.1.355 Infertility https://pubmed.ncbi.nlm.nih.gov/28294943/ A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress. therapeutic application 1 2.1.1.355 Infertility https://pubmed.ncbi.nlm.nih.gov/32642764/ Prdm9 inter-subspecific interactions in hybrid male sterility of house mouse. therapeutic application 1 2.1.1.355 Infertility https://pubmed.ncbi.nlm.nih.gov/32642764/ Prdm9 inter-subspecific interactions in hybrid male sterility of house mouse. ongoing research 1 2.1.1.355 Infertility https://pubmed.ncbi.nlm.nih.gov/28294943/ A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress. unassigned - 2.1.1.355 Infertility https://pubmed.ncbi.nlm.nih.gov/32642764/ Prdm9 inter-subspecific interactions in hybrid male sterility of house mouse. unassigned - 2.1.1.355 Infertility, Male https://pubmed.ncbi.nlm.nih.gov/30071651/ PRDM Histone Methyltransferase mRNA Levels Increase in Response to Curative Hormone Treatment for Cryptorchidism-Dependent Male Infertility. causal interaction 2 2.1.1.355 Infertility, Male https://pubmed.ncbi.nlm.nih.gov/30071651/ PRDM Histone Methyltransferase mRNA Levels Increase in Response to Curative Hormone Treatment for Cryptorchidism-Dependent Male Infertility. therapeutic application 3 2.1.1.355 Infertility, Male https://pubmed.ncbi.nlm.nih.gov/30071651/ PRDM Histone Methyltransferase mRNA Levels Increase in Response to Curative Hormone Treatment for Cryptorchidism-Dependent Male Infertility. unassigned - 2.1.1.355 Inflammatory Bowel Diseases https://pubmed.ncbi.nlm.nih.gov/27909059/ The Role of the Histone Methyltransferase Enhancer of Zeste Homolog 2 (EZH2) in the Pathobiological Mechanisms Underlying Inflammatory Bowel Disease (IBD). causal interaction 1 2.1.1.355 Inflammatory Bowel Diseases https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Inflammatory Bowel Diseases https://pubmed.ncbi.nlm.nih.gov/27909059/ The Role of the Histone Methyltransferase Enhancer of Zeste Homolog 2 (EZH2) in the Pathobiological Mechanisms Underlying Inflammatory Bowel Disease (IBD). unassigned - 2.1.1.355 Inflammatory Bowel Diseases https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Influenza, Human https://pubmed.ncbi.nlm.nih.gov/24478419/ Transcriptional Derepression of the ERVWE1 Locus following Influenza A Virus Infection. unassigned - 2.1.1.355 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/24196706/ EHMT1 controls brown adipose cell fate and thermogenesis through the PRDM16 complex. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/18814864/ Epigenetic regulation in human brain-focus on histone lysine methylation. causal interaction 2 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/21245904/ Epigenetic regulation of learning and memory by Drosophila EHMT/G9a. causal interaction 4 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/23175442/ Hippocampal dysfunction in the Euchromatin histone methyltransferase 1 heterozygous knockout mouse model for Kleefstra syndrome. causal interaction 1 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/25400900/ Exon resequencing of H3K9 methyltransferase complex genes, EHMT1, EHTM2 and WIZ, in Japanese autism subjects. causal interaction 1 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/27767173/ Euchromatin histone methyltransferase 1 regulates cortical neuronal network development. causal interaction 3 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28071689/ Haploinsufficiency of EHMT1 improves pattern separation and increases hippocampal cell proliferation. causal interaction 3 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28361100/ A novel de novo frameshift deletion in EHMT1 in a patient with Kleefstra Syndrome results in decreased H3K9 dimethylation. causal interaction 1 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29554304/ Increased H3K9 methylation and impaired expression of Protocadherins are associated with the cognitive dysfunctions of the Kleefstra syndrome. causal interaction 3 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29753921/ De novo loss-of-function variants of ASH1L are associated with an emergent neurodevelopmental disorder. causal interaction 2 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/30014449/ RNA Sequencing and Pathway Analysis Identify Important Pathways Involved in Hypertrichosis and Intellectual Disability in Patients with Wiedemann-Steiner Syndrome. causal interaction 1 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/31465303/ Precocious neuronal differentiation and disrupted oxygen responses in Kabuki syndrome. causal interaction 3 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/31914384/ Distinct Pathogenic Genes Causing Intellectual Disability and Autism Exhibit a Common Neuronal Network Hyperactivity Phenotype. causal interaction 3 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/32531423/ The Object Space Task reveals increased expression of cumulative memory in a mouse model of Kleefstra syndrome. causal interaction 3 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/34258564/ Derepression of inflammation-related genes link to microglia activation and neural maturation defect in a mouse model of Kleefstra syndrome. causal interaction 1 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/27767173/ Euchromatin histone methyltransferase 1 regulates cortical neuronal network development. diagnostic usage 3 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29753921/ De novo loss-of-function variants of ASH1L are associated with an emergent neurodevelopmental disorder. diagnostic usage 3 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/27106595/ An atypical 12q24.31 microdeletion implicates six genes including a histone demethylase KDM2B and a histone methyltransferase SETD1B in syndromic intellectual disability. therapeutic application 1 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/30171419/ Identification of protoberberine alkaloids as novel histone methyltransferase G9a inhibitors by structure-based virtual screening. therapeutic application 1 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/27106595/ An atypical 12q24.31 microdeletion implicates six genes including a histone demethylase KDM2B and a histone methyltransferase SETD1B in syndromic intellectual disability. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29069077/ Functional convergence of histone methyltransferases EHMT1 and KMT2C involved in intellectual disability and autism spectrum disorder. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/19896504/ Reduced exploration, increased anxiety, and altered social behavior: Autistic-like features of euchromatin histone methyltransferase 1 heterozygous knockout mice. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/24906019/ Transcriptional consequences of 16p11.2 deletion and duplication in mouse cortex and multiplex autism families. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/27123477/ Reversible white matter lesions associated with mutant EHMT1 and Kleefstra syndrome. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29203834/ Molecular and cellular issues of KMT2A variants involved in Wiedemann-Steiner syndrome. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/30171419/ Identification of protoberberine alkaloids as novel histone methyltransferase G9a inhibitors by structure-based virtual screening. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/30655503/ Setd5 haploinsufficiency alters neuronal network connectivity and leads to autistic-like behaviors in mice. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/32975655/ EHMT1 regulates Parvalbumin-positive interneuron development and GABAergic input in sensory cortical areas. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/34010111/ First episode of psychosis in Kleefstra syndrome: a case report. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/18814864/ Epigenetic regulation in human brain-focus on histone lysine methylation. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/21245904/ Epigenetic regulation of learning and memory by Drosophila EHMT/G9a. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/23175442/ Hippocampal dysfunction in the Euchromatin histone methyltransferase 1 heterozygous knockout mouse model for Kleefstra syndrome. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/25400900/ Exon resequencing of H3K9 methyltransferase complex genes, EHMT1, EHTM2 and WIZ, in Japanese autism subjects. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28071689/ Haploinsufficiency of EHMT1 improves pattern separation and increases hippocampal cell proliferation. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28361100/ A novel de novo frameshift deletion in EHMT1 in a patient with Kleefstra Syndrome results in decreased H3K9 dimethylation. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29554304/ Increased H3K9 methylation and impaired expression of Protocadherins are associated with the cognitive dysfunctions of the Kleefstra syndrome. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/30014449/ RNA Sequencing and Pathway Analysis Identify Important Pathways Involved in Hypertrichosis and Intellectual Disability in Patients with Wiedemann-Steiner Syndrome. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/31465303/ Precocious neuronal differentiation and disrupted oxygen responses in Kabuki syndrome. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/31914384/ Distinct Pathogenic Genes Causing Intellectual Disability and Autism Exhibit a Common Neuronal Network Hyperactivity Phenotype. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/32531423/ The Object Space Task reveals increased expression of cumulative memory in a mouse model of Kleefstra syndrome. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/34258564/ Derepression of inflammation-related genes link to microglia activation and neural maturation defect in a mouse model of Kleefstra syndrome. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/27767173/ Euchromatin histone methyltransferase 1 regulates cortical neuronal network development. unassigned - 2.1.1.355 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29753921/ De novo loss-of-function variants of ASH1L are associated with an emergent neurodevelopmental disorder. unassigned - 2.1.1.355 Intestinal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33349639/ The epigenetic regulator Mll1 is required for Wnt-driven intestinal tumorigenesis and cancer stemness. therapeutic application 1 2.1.1.355 Intestinal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33349639/ The epigenetic regulator Mll1 is required for Wnt-driven intestinal tumorigenesis and cancer stemness. ongoing research 3 2.1.1.355 Intestinal Neoplasms https://pubmed.ncbi.nlm.nih.gov/33349639/ The epigenetic regulator Mll1 is required for Wnt-driven intestinal tumorigenesis and cancer stemness. unassigned - 2.1.1.355 Ischemic Stroke https://pubmed.ncbi.nlm.nih.gov/34472033/ The progress of research on histone methylation in ischemic stroke pathogenesis. causal interaction 3 2.1.1.355 Ischemic Stroke https://pubmed.ncbi.nlm.nih.gov/34472033/ The progress of research on histone methylation in ischemic stroke pathogenesis. therapeutic application 4 2.1.1.355 Ischemic Stroke https://pubmed.ncbi.nlm.nih.gov/34472033/ The progress of research on histone methylation in ischemic stroke pathogenesis. unassigned - 2.1.1.355 Kidney Diseases https://pubmed.ncbi.nlm.nih.gov/33679454/ Histone Methyltransferase EZH2: A Potential Therapeutic Target for Kidney Diseases. causal interaction 3 2.1.1.355 Kidney Diseases https://pubmed.ncbi.nlm.nih.gov/33679454/ Histone Methyltransferase EZH2: A Potential Therapeutic Target for Kidney Diseases. therapeutic application 4 2.1.1.355 Kidney Diseases https://pubmed.ncbi.nlm.nih.gov/34102281/ The H3K9 histone methyltransferase G9a modulates renal ischemia reperfusion injury by targeting Sirt1. unassigned - 2.1.1.355 Kidney Diseases https://pubmed.ncbi.nlm.nih.gov/33679454/ Histone Methyltransferase EZH2: A Potential Therapeutic Target for Kidney Diseases. unassigned - 2.1.1.355 Kidney Neoplasms https://pubmed.ncbi.nlm.nih.gov/34336110/ Histone Methyltransferase G9a Promotes the Development of Renal Cancer through Epigenetic Silencing of Tumor Suppressor Gene SPINK5. ongoing research 2 2.1.1.355 Kidney Neoplasms https://pubmed.ncbi.nlm.nih.gov/34336110/ Histone Methyltransferase G9a Promotes the Development of Renal Cancer through Epigenetic Silencing of Tumor Suppressor Gene SPINK5. unassigned - 2.1.1.355 Lafora Disease https://pubmed.ncbi.nlm.nih.gov/22961547/ Early-onset Lafora body disease. causal interaction 4 2.1.1.355 Lafora Disease https://pubmed.ncbi.nlm.nih.gov/22961547/ Early-onset Lafora body disease. therapeutic application 1 2.1.1.355 Lafora Disease https://pubmed.ncbi.nlm.nih.gov/22961547/ Early-onset Lafora body disease. ongoing research 2 2.1.1.355 Lafora Disease https://pubmed.ncbi.nlm.nih.gov/22961547/ Early-onset Lafora body disease. unassigned - 2.1.1.355 Language Development Disorders https://pubmed.ncbi.nlm.nih.gov/22890305/ Human subtelomeric copy number gains suggest a DNA replication mechanism for formation: beyond breakage-fusion-bridge for telomere stabilization. causal interaction 1 2.1.1.355 Language Development Disorders https://pubmed.ncbi.nlm.nih.gov/22890305/ Human subtelomeric copy number gains suggest a DNA replication mechanism for formation: beyond breakage-fusion-bridge for telomere stabilization. unassigned - 2.1.1.355 Language Disorders https://pubmed.ncbi.nlm.nih.gov/34010111/ First episode of psychosis in Kleefstra syndrome: a case report. unassigned - 2.1.1.355 Leiomyoma https://pubmed.ncbi.nlm.nih.gov/25922306/ The Mechanism and Function of Epigenetics in Uterine Leiomyoma Development. causal interaction 3 2.1.1.355 Leiomyoma https://pubmed.ncbi.nlm.nih.gov/25922306/ The Mechanism and Function of Epigenetics in Uterine Leiomyoma Development. diagnostic usage 1 2.1.1.355 Leiomyoma https://pubmed.ncbi.nlm.nih.gov/25922306/ The Mechanism and Function of Epigenetics in Uterine Leiomyoma Development. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. causal interaction 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23400519/ Improved therapeutic effect against leukemia by a combination of the histone methyltransferase inhibitor chaetocin and the histone deacetylase inhibitor trichostatin A. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24832370/ Euchromatic histone methyltransferase 2 inhibitor, BIX-01294, sensitizes human promyelocytic leukemia HL-60 and NB4 cells to growth inhibition and differentiation. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/26147105/ The Histone Methyltransferase Inhibitor A-366 Uncovers a Role for G9a/GLP in the Epigenetics of Leukemia. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27151440/ PRDM16 Suppresses MLL1r Leukemia via Intrinsic Histone Methyltransferase Activity. causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27393948/ Discovery of novel small molecule inhibitors of lysine methyltransferase G9a and their mechanism in leukemia cell lines. causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28805231/ The Histone Methyltransferase Mixed Lineage Leukemia (MLL) 3 May Play a Potential Role on Clinical Dilated Cardiomyopathy. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/16239140/ The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20230194/ Targeting DOT1L action and interactions in leukemia: the role of DOT1L in transformation and development. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20445327/ Clathrin Assembly Lymphoid Myeloid Leukemia-AF10-positive Acute Leukemias: A Report of 2 Cases with a Review of the Literature. causal interaction 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20861184/ Histone Methyltransferase MLL1 Regulates MDR1 Transcription and Chemoresistance. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21921037/ Dual functions of histone-lysine N-methyltransferase Setdb1 protein at promyelocytic leukemia-nuclear body (PML-NB): maintaining PML-NB structure and regulating the expression of its associated genes. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22046413/ Human RNA polymerase II-association factor 1 (hPaf1/PD2) regulates histone methylation and chromatin remodeling in pancreatic cancer. causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22543272/ Gene-specific patterns of coregulator requirements by estrogen receptor-? in breast cancer cells. causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22566624/ Genome-wide association and functional studies identify the DOT1L gene to be involved in cartilage thickness and hip osteoarthritis. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23448241/ Substituted purine and 7-deazapurine compounds as modulators of epigenetic enzymes: a patent evaluation (WO2012075381). causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23484697/ [Effect of SUV39H1 siRNA Silence on Apoptosis and Proliferation of Acute Myelogenous Leukemia KG-1 Cell Line]. causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23782009/ Regulated nuclear entry of over-expressed Setdb1. causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23795283/ Synthesis, Activity and Metabolic Stability of Non-Ribose Containing Inhibitors of Histone Methyltransferase DOT1L. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23826075/ Mutations in Mll2, an H3K4 methyltransferase, result in insulin resistance and impaired glucose tolerance in mice. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24240169/ KMT2D maintains neoplastic cell proliferation and global histone H3 lysine 4 monomethylation. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24415392/ Nonclinical pharmacokinetics and metabolism of EPZ-5676, a novel DOT1L histone methyltransferase inhibitor. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27154821/ ASH1L Links Histone H3 Lysine 36 Dimethylation to MLL Leukemia. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27259240/ Interaction of DNA demethylase and histone methyltransferase upregulates Nrf2 in 5-fluorouracil-resistant colon cancer cells. causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27434826/ Identification of phenoxyacetamide derivatives as novel DOT1L inhibitors via docking screening and molecular dynamics simulation. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28337327/ Discovery of Potent, Selective, and Structurally Novel Dot1L Inhibitors by a Fragment Linking Approach. causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29142068/ Pharmacologic Inhibition of the Menin-MLL Interaction Leads to Transcriptional Repression of causal interaction 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29627316/ KMT2D Mutation Is Associated With Poor Prognosis in Non-Small-Cell Lung Cancer. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/30385408/ MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity. causal interaction 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/31558673/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32437908/ Epigenetic regulation of protein translation in KMT2A-rearranged AML. causal interaction 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32814769/ Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32889036/ Epigenetic priming by EHMT1/EHMT2 in acute lymphoblastic leukemia induces TP53 and TP73 overexpression and promotes cell death. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33054052/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33162400/ SUV39H1 is a New Client Protein of Hsp90 Degradated by Chaetocin as a Novel C-Terminal Inhibitor of Hsp90. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33497867/ Inhibition of Dot1L Alleviates Fulminant Hepatitis Through Myeloid-Derived Suppressor Cells. causal interaction 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33606679/ Cyp33 binds AU-rich RNA motifs via an extended interface that competitively disrupts the gene repressive Cyp33-MLL1 interaction in vitro. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33990599/ Discovery of first-in-class inhibitors of ASH1L histone methyltransferase with anti-leukemic activity. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/34500733/ Synthesis and Biological Activity of a Cytostatic Inhibitor of MLLr Leukemia Targeting the DOT1L Protein. causal interaction 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23597465/ [Experimental study of SUV39H1 gene specific siRNA in human leukemia cell line]. diagnostic usage 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24612037/ Inhibition of histone methyltransferase EZH2 depletes leukemia stem cell of mixed lineage leukemia fusion leukemia through upregulation of p16. diagnostic usage 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27151440/ PRDM16 Suppresses MLL1r Leukemia via Intrinsic Histone Methyltransferase Activity. diagnostic usage 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20230194/ Targeting DOT1L action and interactions in leukemia: the role of DOT1L in transformation and development. diagnostic usage 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21979880/ Anti-leukemia activity of chaetocin via death receptor-dependent apoptosis and dual modulation of the histone methyl-transferase SUV39H1. diagnostic usage 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22046413/ Human RNA polymerase II-association factor 1 (hPaf1/PD2) regulates histone methylation and chromatin remodeling in pancreatic cancer. diagnostic usage 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. diagnostic usage 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27154821/ ASH1L Links Histone H3 Lysine 36 Dimethylation to MLL Leukemia. diagnostic usage 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29627316/ KMT2D Mutation Is Associated With Poor Prognosis in Non-Small-Cell Lung Cancer. diagnostic usage 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/30385408/ MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity. diagnostic usage 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/31558673/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. diagnostic usage 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32549764/ SETDB2 promoted breast cancer stem cell maintenance by interaction with and stabilization of ?Np63? protein. diagnostic usage 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32814769/ Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer. diagnostic usage 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. diagnostic usage 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33054052/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. diagnostic usage 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/34083515/ A KDM4A-PAF1-mediated epigenomic network is essential for acute myeloid leukemia cell self-renewal and survival. diagnostic usage 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23400519/ Improved therapeutic effect against leukemia by a combination of the histone methyltransferase inhibitor chaetocin and the histone deacetylase inhibitor trichostatin A. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23597465/ [Experimental study of SUV39H1 gene specific siRNA in human leukemia cell line]. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24832370/ Euchromatic histone methyltransferase 2 inhibitor, BIX-01294, sensitizes human promyelocytic leukemia HL-60 and NB4 cells to growth inhibition and differentiation. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/26147105/ The Histone Methyltransferase Inhibitor A-366 Uncovers a Role for G9a/GLP in the Epigenetics of Leukemia. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27151440/ PRDM16 Suppresses MLL1r Leukemia via Intrinsic Histone Methyltransferase Activity. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27393948/ Discovery of novel small molecule inhibitors of lysine methyltransferase G9a and their mechanism in leukemia cell lines. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28805231/ The Histone Methyltransferase Mixed Lineage Leukemia (MLL) 3 May Play a Potential Role on Clinical Dilated Cardiomyopathy. therapeutic application 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/18566324/ DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/18598942/ Menin critically links MLL proteins with LEDGF on cancer-associated target genes. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/19318494/ Transcriptional activation of the mixed lineage leukemia-p27Kip1 pathway by a somatostatin analogue. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20230194/ Targeting DOT1L action and interactions in leukemia: the role of DOT1L in transformation and development. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20861184/ Histone Methyltransferase MLL1 Regulates MDR1 Transcription and Chemoresistance. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21427230/ Lysine methyltransferase G9a is required for de novo DNA methylation and the establishment, but not the maintenance, of proviral silencing. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21921037/ Dual functions of histone-lysine N-methyltransferase Setdb1 protein at promyelocytic leukemia-nuclear body (PML-NB): maintaining PML-NB structure and regulating the expression of its associated genes. therapeutic application 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21979880/ Anti-leukemia activity of chaetocin via death receptor-dependent apoptosis and dual modulation of the histone methyl-transferase SUV39H1. therapeutic application 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22046413/ Human RNA polymerase II-association factor 1 (hPaf1/PD2) regulates histone methylation and chromatin remodeling in pancreatic cancer. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22867873/ Chromatin modifications as therapeutic targets in MLL-rearranged leukemia. therapeutic application 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23448241/ Substituted purine and 7-deazapurine compounds as modulators of epigenetic enzymes: a patent evaluation (WO2012075381). therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23484697/ [Effect of SUV39H1 siRNA Silence on Apoptosis and Proliferation of Acute Myelogenous Leukemia KG-1 Cell Line]. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23795283/ Synthesis, Activity and Metabolic Stability of Non-Ribose Containing Inhibitors of Histone Methyltransferase DOT1L. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23801631/ Potent inhibition of DOT1L as treatment of MLL-fusion leukemia. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23826075/ Mutations in Mll2, an H3K4 methyltransferase, result in insulin resistance and impaired glucose tolerance in mice. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23868976/ Promoter occupancy of MLL1 histone methyltransferase seems to specify the proliferative and apoptotic functions of E2F1 in a tumour microenvironment. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24100017/ Elements of the Polycomb repressor SU(Z)12 needed for histone H3-K27 methylation, the interface with E(Z), and in vivo function. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24240169/ KMT2D maintains neoplastic cell proliferation and global histone H3 lysine 4 monomethylation. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24415392/ Nonclinical pharmacokinetics and metabolism of EPZ-5676, a novel DOT1L histone methyltransferase inhibitor. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/25751424/ NAD(+)-SIRT1 control of H3K4 trimethylation through circadian deacetylation of MLL1. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/26541578/ Design of a fluorescent ligand targeting the S-adenosylmethionine binding site of the histone methyltransferase MLL1. therapeutic application 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27116709/ Structure-based design and synthesis of small molecular inhibitors disturbing the interaction of MLL1-WDR5. therapeutic application 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27154821/ ASH1L Links Histone H3 Lysine 36 Dimethylation to MLL Leukemia. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27219490/ Reprogramming of the Epigenome by MLL1 Links Early-Life Environmental Exposures to Prostate Cancer Risk. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27259240/ Interaction of DNA demethylase and histone methyltransferase upregulates Nrf2 in 5-fluorouracil-resistant colon cancer cells. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27434826/ Identification of phenoxyacetamide derivatives as novel DOT1L inhibitors via docking screening and molecular dynamics simulation. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27563394/ Optimization of a Fragment-Based Screening Hit toward Potent DOT1L Inhibitors Interacting in an Induced Binding Pocket. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27705736/ MLL translocation in two castration-resistant prostate cancer patients. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28229434/ Preclinical Pharmacokinetics and Pharmacodynamics of Pinometostat (EPZ-5676), a First-in-Class, Small Molecule S-Adenosyl Methionine Competitive Inhibitor of DOT1L. therapeutic application 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28337327/ Discovery of Potent, Selective, and Structurally Novel Dot1L Inhibitors by a Fragment Linking Approach. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28609655/ MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28733487/ The STAT4/MLL1 Epigenetic Axis Regulates the Antimicrobial Functions of Murine Macrophages. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29142068/ Pharmacologic Inhibition of the Menin-MLL Interaction Leads to Transcriptional Repression of therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29228680/ Long noncoding RNA MIAT promotes non-small cell lung cancer proliferation and metastasis through MMP9 activation. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29627316/ KMT2D Mutation Is Associated With Poor Prognosis in Non-Small-Cell Lung Cancer. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/30385408/ MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity. therapeutic application 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/31263570/ Mixed-lineage leukemia protein 2 suppresses ciliary assembly by the modulation of actin dynamics and vesicle transport. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/31558673/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. therapeutic application 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32059151/ MLL1 combined with GSK3 and MAP2K inhibition improves the development of in vitro-fertilized embryos. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32151962/ MLL1 promotes migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis by activating the TRIF/NF-?B signaling pathway via H3K4me3 enrichment in the TLR4 promoter region. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32266022/ lncRNA MIAT promotes cell invasion and migration in esophageal cancer. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32598934/ ROR? autoregulates its transcription via MLL4-associated enhancer remodeling in the liver. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32814769/ Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer. therapeutic application 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. therapeutic application 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33054052/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. therapeutic application 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33151904/ Decreased mixed lineage leukemia 1 is involved in endometriosis-related infertility. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33162400/ SUV39H1 is a New Client Protein of Hsp90 Degradated by Chaetocin as a Novel C-Terminal Inhibitor of Hsp90. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33606679/ Cyp33 binds AU-rich RNA motifs via an extended interface that competitively disrupts the gene repressive Cyp33-MLL1 interaction in vitro. therapeutic application 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/34500733/ Synthesis and Biological Activity of a Cytostatic Inhibitor of MLLr Leukemia Targeting the DOT1L Protein. therapeutic application 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/15464450/ MLL: a histone methyltransferase disrupted in leukemia. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22801367/ Negative Regulation of JAK2 by H3K9 Methyltransferase G9a in Leukemia. ongoing research 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23597465/ [Experimental study of SUV39H1 gene specific siRNA in human leukemia cell line]. ongoing research 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24612037/ Inhibition of histone methyltransferase EZH2 depletes leukemia stem cell of mixed lineage leukemia fusion leukemia through upregulation of p16. ongoing research 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24832370/ Euchromatic histone methyltransferase 2 inhibitor, BIX-01294, sensitizes human promyelocytic leukemia HL-60 and NB4 cells to growth inhibition and differentiation. ongoing research 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/25765655/ H3K9 methyltransferase G9a negatively regulates UHRF1 transcription during leukemia cell differentiation. ongoing research 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27393948/ Discovery of novel small molecule inhibitors of lysine methyltransferase G9a and their mechanism in leukemia cell lines. ongoing research 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20230194/ Targeting DOT1L action and interactions in leukemia: the role of DOT1L in transformation and development. ongoing research 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20332322/ MLL-rearranged B lymphoblastic leukemias selectively express the immunoregulatory carbohydrate-binding protein galectin-1. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. ongoing research 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21979880/ Anti-leukemia activity of chaetocin via death receptor-dependent apoptosis and dual modulation of the histone methyl-transferase SUV39H1. ongoing research 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22046413/ Human RNA polymerase II-association factor 1 (hPaf1/PD2) regulates histone methylation and chromatin remodeling in pancreatic cancer. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23484697/ [Effect of SUV39H1 siRNA Silence on Apoptosis and Proliferation of Acute Myelogenous Leukemia KG-1 Cell Line]. ongoing research 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23801631/ Potent inhibition of DOT1L as treatment of MLL-fusion leukemia. ongoing research 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23826075/ Mutations in Mll2, an H3K4 methyltransferase, result in insulin resistance and impaired glucose tolerance in mice. ongoing research 2 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23868976/ Promoter occupancy of MLL1 histone methyltransferase seems to specify the proliferative and apoptotic functions of E2F1 in a tumour microenvironment. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24240169/ KMT2D maintains neoplastic cell proliferation and global histone H3 lysine 4 monomethylation. ongoing research 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. ongoing research 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27268279/ KAT8 Regulates Androgen Signaling in Prostate Cancer Cells. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28609655/ MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29627316/ KMT2D Mutation Is Associated With Poor Prognosis in Non-Small-Cell Lung Cancer. ongoing research 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/30385408/ MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity. ongoing research 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/31558673/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. ongoing research 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32792914/ Mixed Lineage Leukemia 1 Promoted Neuron Apoptosis in Ischemic Penumbra via Regulating ASK-1/TNF-? Complex. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33054052/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. ongoing research 4 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. ongoing research 3 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33326791/ The Histone Methyltransferase DOT1L Is Essential for Humoral Immune Responses. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33990599/ Discovery of first-in-class inhibitors of ASH1L histone methyltransferase with anti-leukemic activity. ongoing research 1 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/15464450/ MLL: a histone methyltransferase disrupted in leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22801367/ Negative Regulation of JAK2 by H3K9 Methyltransferase G9a in Leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23597465/ [Experimental study of SUV39H1 gene specific siRNA in human leukemia cell line]. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24612037/ Inhibition of histone methyltransferase EZH2 depletes leukemia stem cell of mixed lineage leukemia fusion leukemia through upregulation of p16. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/25765655/ H3K9 methyltransferase G9a negatively regulates UHRF1 transcription during leukemia cell differentiation. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/7915232/ The protein encoded by the Drosophila position-effect variegation suppressor gene Su(var)3-9 combines domains of antagonistic regulators of homeotic gene complexes. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/12957285/ Dimerization contributes to oncogenic activation of MLL chimeras in acute leukemias. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/15199122/ Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/15941828/ Global and Hox-specific roles for the MLL1 methyltransferase. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/17942707/ Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/17942719/ Prefrontal dysfunction in schizophrenia involves mixed-lineage leukemia 1-regulated histone methylation at GABAergic gene promoters. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/18566324/ DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/18598942/ Menin critically links MLL proteins with LEDGF on cancer-associated target genes. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/19318494/ Transcriptional activation of the mixed lineage leukemia-p27Kip1 pathway by a somatostatin analogue. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/19956800/ Misguided transcriptional elongation causes mixed lineage leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20332322/ MLL-rearranged B lymphoblastic leukemias selectively express the immunoregulatory carbohydrate-binding protein galectin-1. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21427230/ Lysine methyltransferase G9a is required for de novo DNA methylation and the establishment, but not the maintenance, of proviral silencing. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21836617/ Hypoxia-induced mixed-lineage leukemia 1 regulates glioma stem cell tumorigenic potential. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21979880/ Anti-leukemia activity of chaetocin via death receptor-dependent apoptosis and dual modulation of the histone methyl-transferase SUV39H1. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22772991/ The epigenetic control of E-box and Myc-dependent chromatin modifications regulate the licensing of lamin B2 origin during cell cycle. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22867873/ Chromatin modifications as therapeutic targets in MLL-rearranged leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23648481/ MEN1 is a melanoma tumor suppressor that preserves genomic integrity by stimulating transcription of genes that promote homologous recombination-directed DNA repair. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23728610/ MicroRNAs mark in the MLL-rearranged leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23744037/ An MLL-dependent network sustains hematopoiesis. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23801631/ Potent inhibition of DOT1L as treatment of MLL-fusion leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23868976/ Promoter occupancy of MLL1 histone methyltransferase seems to specify the proliferative and apoptotic functions of E2F1 in a tumour microenvironment. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24100017/ Elements of the Polycomb repressor SU(Z)12 needed for histone H3-K27 methylation, the interface with E(Z), and in vivo function. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24130829/ Solution NMR structure and histone binding of the PHD domain of human MLL5. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/25751424/ NAD(+)-SIRT1 control of H3K4 trimethylation through circadian deacetylation of MLL1. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/26541578/ Design of a fluorescent ligand targeting the S-adenosylmethionine binding site of the histone methyltransferase MLL1. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27116709/ Structure-based design and synthesis of small molecular inhibitors disturbing the interaction of MLL1-WDR5. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27219490/ Reprogramming of the Epigenome by MLL1 Links Early-Life Environmental Exposures to Prostate Cancer Risk. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27268279/ KAT8 Regulates Androgen Signaling in Prostate Cancer Cells. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27563394/ Optimization of a Fragment-Based Screening Hit toward Potent DOT1L Inhibitors Interacting in an Induced Binding Pocket. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27563395/ Discovery of Novel Dot1L Inhibitors through a Structure-Based Fragmentation Approach. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27610619/ Loss of Mll3 Catalytic Function Promotes Aberrant Myelopoiesis. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27705736/ MLL translocation in two castration-resistant prostate cancer patients. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28229434/ Preclinical Pharmacokinetics and Pharmacodynamics of Pinometostat (EPZ-5676), a First-in-Class, Small Molecule S-Adenosyl Methionine Competitive Inhibitor of DOT1L. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28447382/ Quantitative proteomic analysis of EZH2 inhibition in acute myeloid leukemia reveals the targets and pathways that precede the induction of cell death. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28609655/ MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28663576/ SETD2 and histone H3 lysine 36 methylation deficiency in advanced systemic mastocytosis. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28733487/ The STAT4/MLL1 Epigenetic Axis Regulates the Antimicrobial Functions of Murine Macrophages. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29228680/ Long noncoding RNA MIAT promotes non-small cell lung cancer proliferation and metastasis through MMP9 activation. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/30710046/ Histone Methylation Directs Myeloid TLR4 Expression and Regulates Wound Healing following Cutaneous Tissue Injury. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/31263570/ Mixed-lineage leukemia protein 2 suppresses ciliary assembly by the modulation of actin dynamics and vesicle transport. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/31527241/ A higher-order configuration of the heterodimeric DOT1L-AF10 coiled-coil domains potentiates their leukemogenenic activity. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32059151/ MLL1 combined with GSK3 and MAP2K inhibition improves the development of in vitro-fertilized embryos. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32151962/ MLL1 promotes migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis by activating the TRIF/NF-?B signaling pathway via H3K4me3 enrichment in the TLR4 promoter region. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32266022/ lncRNA MIAT promotes cell invasion and migration in esophageal cancer. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32549764/ SETDB2 promoted breast cancer stem cell maintenance by interaction with and stabilization of ?Np63? protein. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32598934/ ROR? autoregulates its transcription via MLL4-associated enhancer remodeling in the liver. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32792914/ Mixed Lineage Leukemia 1 Promoted Neuron Apoptosis in Ischemic Penumbra via Regulating ASK-1/TNF-? Complex. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33151904/ Decreased mixed lineage leukemia 1 is involved in endometriosis-related infertility. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33326791/ The Histone Methyltransferase DOT1L Is Essential for Humoral Immune Responses. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/34083515/ A KDM4A-PAF1-mediated epigenomic network is essential for acute myeloid leukemia cell self-renewal and survival. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23400519/ Improved therapeutic effect against leukemia by a combination of the histone methyltransferase inhibitor chaetocin and the histone deacetylase inhibitor trichostatin A. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24832370/ Euchromatic histone methyltransferase 2 inhibitor, BIX-01294, sensitizes human promyelocytic leukemia HL-60 and NB4 cells to growth inhibition and differentiation. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/26147105/ The Histone Methyltransferase Inhibitor A-366 Uncovers a Role for G9a/GLP in the Epigenetics of Leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27393948/ Discovery of novel small molecule inhibitors of lysine methyltransferase G9a and their mechanism in leukemia cell lines. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28805231/ The Histone Methyltransferase Mixed Lineage Leukemia (MLL) 3 May Play a Potential Role on Clinical Dilated Cardiomyopathy. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/16239140/ The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20445327/ Clathrin Assembly Lymphoid Myeloid Leukemia-AF10-positive Acute Leukemias: A Report of 2 Cases with a Review of the Literature. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20599755/ The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/20861184/ Histone Methyltransferase MLL1 Regulates MDR1 Transcription and Chemoresistance. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/21921037/ Dual functions of histone-lysine N-methyltransferase Setdb1 protein at promyelocytic leukemia-nuclear body (PML-NB): maintaining PML-NB structure and regulating the expression of its associated genes. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22543272/ Gene-specific patterns of coregulator requirements by estrogen receptor-? in breast cancer cells. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/22566624/ Genome-wide association and functional studies identify the DOT1L gene to be involved in cartilage thickness and hip osteoarthritis. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23448241/ Substituted purine and 7-deazapurine compounds as modulators of epigenetic enzymes: a patent evaluation (WO2012075381). unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23484697/ [Effect of SUV39H1 siRNA Silence on Apoptosis and Proliferation of Acute Myelogenous Leukemia KG-1 Cell Line]. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23782009/ Regulated nuclear entry of over-expressed Setdb1. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23795283/ Synthesis, Activity and Metabolic Stability of Non-Ribose Containing Inhibitors of Histone Methyltransferase DOT1L. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/23826075/ Mutations in Mll2, an H3K4 methyltransferase, result in insulin resistance and impaired glucose tolerance in mice. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24240169/ KMT2D maintains neoplastic cell proliferation and global histone H3 lysine 4 monomethylation. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/24415392/ Nonclinical pharmacokinetics and metabolism of EPZ-5676, a novel DOT1L histone methyltransferase inhibitor. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27259240/ Interaction of DNA demethylase and histone methyltransferase upregulates Nrf2 in 5-fluorouracil-resistant colon cancer cells. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27434826/ Identification of phenoxyacetamide derivatives as novel DOT1L inhibitors via docking screening and molecular dynamics simulation. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/28337327/ Discovery of Potent, Selective, and Structurally Novel Dot1L Inhibitors by a Fragment Linking Approach. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/29142068/ Pharmacologic Inhibition of the Menin-MLL Interaction Leads to Transcriptional Repression of unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32437908/ Epigenetic regulation of protein translation in KMT2A-rearranged AML. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32889036/ Epigenetic priming by EHMT1/EHMT2 in acute lymphoblastic leukemia induces TP53 and TP73 overexpression and promotes cell death. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33162400/ SUV39H1 is a New Client Protein of Hsp90 Degradated by Chaetocin as a Novel C-Terminal Inhibitor of Hsp90. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33497867/ Inhibition of Dot1L Alleviates Fulminant Hepatitis Through Myeloid-Derived Suppressor Cells. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33606679/ Cyp33 binds AU-rich RNA motifs via an extended interface that competitively disrupts the gene repressive Cyp33-MLL1 interaction in vitro. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33990599/ Discovery of first-in-class inhibitors of ASH1L histone methyltransferase with anti-leukemic activity. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/34500733/ Synthesis and Biological Activity of a Cytostatic Inhibitor of MLLr Leukemia Targeting the DOT1L Protein. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27151440/ PRDM16 Suppresses MLL1r Leukemia via Intrinsic Histone Methyltransferase Activity. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/27154821/ ASH1L Links Histone H3 Lysine 36 Dimethylation to MLL Leukemia. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/32814769/ Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer. unassigned - 2.1.1.355 Leukemia https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. unassigned - 2.1.1.355 Leukemia, Erythroblastic, Acute https://pubmed.ncbi.nlm.nih.gov/26320100/ EHMT1 and EHMT2 inhibition induces fetal hemoglobin expression. causal interaction 2 2.1.1.355 Leukemia, Erythroblastic, Acute https://pubmed.ncbi.nlm.nih.gov/33407944/ The histone methyltransferase inhibitor A-366 enhances hemoglobin expression in erythroleukemia cells upon co-exposure with chemical inducers in culture. therapeutic application 1 2.1.1.355 Leukemia, Erythroblastic, Acute https://pubmed.ncbi.nlm.nih.gov/16652147/ RUNX1 associates with histone deacetylases and SUV39H1 to repress transcription. therapeutic application 1 2.1.1.355 Leukemia, Erythroblastic, Acute https://pubmed.ncbi.nlm.nih.gov/26320100/ EHMT1 and EHMT2 inhibition induces fetal hemoglobin expression. therapeutic application 4 2.1.1.355 Leukemia, Erythroblastic, Acute https://pubmed.ncbi.nlm.nih.gov/33407944/ The histone methyltransferase inhibitor A-366 enhances hemoglobin expression in erythroleukemia cells upon co-exposure with chemical inducers in culture. unassigned - 2.1.1.355 Leukemia, Erythroblastic, Acute https://pubmed.ncbi.nlm.nih.gov/16652147/ RUNX1 associates with histone deacetylases and SUV39H1 to repress transcription. unassigned - 2.1.1.355 Leukemia, Erythroblastic, Acute https://pubmed.ncbi.nlm.nih.gov/26320100/ EHMT1 and EHMT2 inhibition induces fetal hemoglobin expression. unassigned - 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/27191993/ The histone methyltransferase EZH2 as a novel prosurvival factor in clinically aggressive chronic lymphocytic leukemia. causal interaction 3 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/28833505/ Aberrant levels of SUV39H1 and SUV39H2 methyltransferase are associated with genomic instability in chronic lymphocytic leukemia. causal interaction 3 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/25131810/ Overexpression of EZH2 associates with a poor prognosis in chronic lymphocytic leukemia. causal interaction 4 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/28833505/ Aberrant levels of SUV39H1 and SUV39H2 methyltransferase are associated with genomic instability in chronic lymphocytic leukemia. diagnostic usage 1 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/25131810/ Overexpression of EZH2 associates with a poor prognosis in chronic lymphocytic leukemia. ongoing research 2 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/33606672/ Efficient and flexible Integration of variant characteristics in rare variant association studies using integrated nested Laplace approximation. unassigned - 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/27191993/ The histone methyltransferase EZH2 as a novel prosurvival factor in clinically aggressive chronic lymphocytic leukemia. unassigned - 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/25131810/ Overexpression of EZH2 associates with a poor prognosis in chronic lymphocytic leukemia. unassigned - 2.1.1.355 Leukemia, Lymphocytic, Chronic, B-Cell https://pubmed.ncbi.nlm.nih.gov/28833505/ Aberrant levels of SUV39H1 and SUV39H2 methyltransferase are associated with genomic instability in chronic lymphocytic leukemia. unassigned - 2.1.1.355 Leukemia, Mast-Cell https://pubmed.ncbi.nlm.nih.gov/28663576/ SETD2 and histone H3 lysine 36 methylation deficiency in advanced systemic mastocytosis. unassigned - 2.1.1.355 Leukemia, Myelogenous, Chronic, BCR-ABL Positive https://pubmed.ncbi.nlm.nih.gov/25079219/ Inhibition of euchromatic histone methyltransferase 1 and 2 sensitizes chronic myeloid leukemia cells to interferon treatment. causal interaction 3 2.1.1.355 Leukemia, Myelogenous, Chronic, BCR-ABL Positive https://pubmed.ncbi.nlm.nih.gov/33931742/ Targeting protein lysine methyltransferase G9A impairs self-renewal of chronic myelogenous leukemia stem cells via upregulation of SOX6. causal interaction 3 2.1.1.355 Leukemia, Myelogenous, Chronic, BCR-ABL Positive https://pubmed.ncbi.nlm.nih.gov/25079219/ Inhibition of euchromatic histone methyltransferase 1 and 2 sensitizes chronic myeloid leukemia cells to interferon treatment. therapeutic application 1 2.1.1.355 Leukemia, Myelogenous, Chronic, BCR-ABL Positive https://pubmed.ncbi.nlm.nih.gov/33931742/ Targeting protein lysine methyltransferase G9A impairs self-renewal of chronic myelogenous leukemia stem cells via upregulation of SOX6. therapeutic application 3 2.1.1.355 Leukemia, Myelogenous, Chronic, BCR-ABL Positive https://pubmed.ncbi.nlm.nih.gov/33931742/ Targeting protein lysine methyltransferase G9A impairs self-renewal of chronic myelogenous leukemia stem cells via upregulation of SOX6. ongoing research 2 2.1.1.355 Leukemia, Myelogenous, Chronic, BCR-ABL Positive https://pubmed.ncbi.nlm.nih.gov/25079219/ Inhibition of euchromatic histone methyltransferase 1 and 2 sensitizes chronic myeloid leukemia cells to interferon treatment. unassigned - 2.1.1.355 Leukemia, Myelogenous, Chronic, BCR-ABL Positive https://pubmed.ncbi.nlm.nih.gov/33931742/ Targeting protein lysine methyltransferase G9A impairs self-renewal of chronic myelogenous leukemia stem cells via upregulation of SOX6. unassigned - 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. causal interaction 3 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/24832370/ Euchromatic histone methyltransferase 2 inhibitor, BIX-01294, sensitizes human promyelocytic leukemia HL-60 and NB4 cells to growth inhibition and differentiation. causal interaction 4 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. therapeutic application 1 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/17855633/ A role for the MLL fusion partner ENL in transcriptional elongation and chromatin modification. therapeutic application 1 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/24832370/ Euchromatic histone methyltransferase 2 inhibitor, BIX-01294, sensitizes human promyelocytic leukemia HL-60 and NB4 cells to growth inhibition and differentiation. therapeutic application 4 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/25490442/ DOTting the path to doom: how acceleration of histone methylation leads to leukemia. therapeutic application 1 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. ongoing research 1 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/24832370/ Euchromatic histone methyltransferase 2 inhibitor, BIX-01294, sensitizes human promyelocytic leukemia HL-60 and NB4 cells to growth inhibition and differentiation. ongoing research 2 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/17855633/ A role for the MLL fusion partner ENL in transcriptional elongation and chromatin modification. unassigned - 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/25490442/ DOTting the path to doom: how acceleration of histone methylation leads to leukemia. unassigned - 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. unassigned - 2.1.1.355 Leukemia, Myeloid https://pubmed.ncbi.nlm.nih.gov/24832370/ Euchromatic histone methyltransferase 2 inhibitor, BIX-01294, sensitizes human promyelocytic leukemia HL-60 and NB4 cells to growth inhibition and differentiation. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21205756/ Prognostic importance of histone methyltransferase MLL5 expression in acute myeloid leukemia. causal interaction 2 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/23484697/ [Effect of SUV39H1 siRNA Silence on Apoptosis and Proliferation of Acute Myelogenous Leukemia KG-1 Cell Line]. causal interaction 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/25978433/ The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells. causal interaction 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/27941792/ Loss of the histone methyltransferase EZH2 induces resistance to multiple drugs in acute myeloid leukemia. causal interaction 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/30922329/ Genetic polymorphisms of histone methyltransferase SETD2 predicts prognosis and chemotherapy response in Chinese acute myeloid leukemia patients. causal interaction 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. causal interaction 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/34509612/ Histone methyltransferase EZH2 epigenetically affects CCNA1 expression in acute myeloid leukemia. causal interaction 2 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/17172412/ Histone deacetylase inhibitors deplete enhancer of zeste 2 and associated polycomb repressive complex 2 proteins in human acute leukemia cells. causal interaction 2 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/20176155/ The NIZP1 KRAB and C2HR domains cross-talk for transcriptional regulation. causal interaction 2 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. causal interaction 2 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. causal interaction 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/28887438/ ---Silencing of retrotransposons by SETDB1 inhibits the interferon response in acute myeloid leukemia-. causal interaction 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/31558673/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. causal interaction 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/32293500/ PERK/NRF2 and autophagy form a resistance mechanism against G9a inhibition in leukemia stem cells. causal interaction 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/33054052/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. causal interaction 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21205756/ Prognostic importance of histone methyltransferase MLL5 expression in acute myeloid leukemia. diagnostic usage 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/27941792/ Loss of the histone methyltransferase EZH2 induces resistance to multiple drugs in acute myeloid leukemia. diagnostic usage 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/29343972/ Targeting histone methyltransferase and demethylase in acute myeloid leukemia therapy. diagnostic usage 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/30922329/ Genetic polymorphisms of histone methyltransferase SETD2 predicts prognosis and chemotherapy response in Chinese acute myeloid leukemia patients. diagnostic usage 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. diagnostic usage 2 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/34509612/ Histone methyltransferase EZH2 epigenetically affects CCNA1 expression in acute myeloid leukemia. diagnostic usage 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/17172412/ Histone deacetylase inhibitors deplete enhancer of zeste 2 and associated polycomb repressive complex 2 proteins in human acute leukemia cells. diagnostic usage 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/31558673/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. diagnostic usage 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/32293500/ PERK/NRF2 and autophagy form a resistance mechanism against G9a inhibition in leukemia stem cells. diagnostic usage 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/33054052/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. diagnostic usage 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/23484697/ [Effect of SUV39H1 siRNA Silence on Apoptosis and Proliferation of Acute Myelogenous Leukemia KG-1 Cell Line]. therapeutic application 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/25978433/ The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells. therapeutic application 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/27941792/ Loss of the histone methyltransferase EZH2 induces resistance to multiple drugs in acute myeloid leukemia. therapeutic application 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/29343972/ Targeting histone methyltransferase and demethylase in acute myeloid leukemia therapy. therapeutic application 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/30922329/ Genetic polymorphisms of histone methyltransferase SETD2 predicts prognosis and chemotherapy response in Chinese acute myeloid leukemia patients. therapeutic application 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. therapeutic application 2 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/18566324/ DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication. therapeutic application 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. therapeutic application 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. therapeutic application 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/31558673/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. therapeutic application 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/32293500/ PERK/NRF2 and autophagy form a resistance mechanism against G9a inhibition in leukemia stem cells. therapeutic application 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/33054052/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. therapeutic application 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21205756/ Prognostic importance of histone methyltransferase MLL5 expression in acute myeloid leukemia. ongoing research 1 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21901171/ Critical Role of c-Myc in Acute Myeloid Leukemia Involving Direct Regulation of miR-26a and Histone Methyltransferase EZH2. ongoing research 2 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/23484697/ [Effect of SUV39H1 siRNA Silence on Apoptosis and Proliferation of Acute Myelogenous Leukemia KG-1 Cell Line]. ongoing research 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/17172412/ Histone deacetylase inhibitors deplete enhancer of zeste 2 and associated polycomb repressive complex 2 proteins in human acute leukemia cells. ongoing research 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/28887438/ ---Silencing of retrotransposons by SETDB1 inhibits the interferon response in acute myeloid leukemia-. ongoing research 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/31558673/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. ongoing research 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/33054052/ SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation. ongoing research 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21901171/ Critical Role of c-Myc in Acute Myeloid Leukemia Involving Direct Regulation of miR-26a and Histone Methyltransferase EZH2. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/29343972/ Targeting histone methyltransferase and demethylase in acute myeloid leukemia therapy. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/29774127/ PAF1 complex interactions with SETDB1 mediate promoter H3K9 methylation and transcriptional repression of Hoxa9 and Meis1 in acute myeloid leukemia. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/18566324/ DNA hypermethylation and epigenetic silencing of the tumor suppressor gene, SLC5A8, in acute myeloid leukemia with the MLL partial tandem duplication. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/19881540/ Reexpression of epigenetically silenced AML tumor suppressor genes by SUV39H1 inhibition. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/28447382/ Quantitative proteomic analysis of EZH2 inhibition in acute myeloid leukemia reveals the targets and pathways that precede the induction of cell death. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/32634241/ Specific patterns of H3K79 methylation influence genetic interaction of oncogenes in AML. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/23484697/ [Effect of SUV39H1 siRNA Silence on Apoptosis and Proliferation of Acute Myelogenous Leukemia KG-1 Cell Line]. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/25978433/ The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/20176155/ The NIZP1 KRAB and C2HR domains cross-talk for transcriptional regulation. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/28887438/ ---Silencing of retrotransposons by SETDB1 inhibits the interferon response in acute myeloid leukemia-. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/21205756/ Prognostic importance of histone methyltransferase MLL5 expression in acute myeloid leukemia. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/34509612/ Histone methyltransferase EZH2 epigenetically affects CCNA1 expression in acute myeloid leukemia. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/17172412/ Histone deacetylase inhibitors deplete enhancer of zeste 2 and associated polycomb repressive complex 2 proteins in human acute leukemia cells. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/27941792/ Loss of the histone methyltransferase EZH2 induces resistance to multiple drugs in acute myeloid leukemia. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/30922329/ Genetic polymorphisms of histone methyltransferase SETD2 predicts prognosis and chemotherapy response in Chinese acute myeloid leukemia patients. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. unassigned - 2.1.1.355 Leukemia, Myeloid, Acute https://pubmed.ncbi.nlm.nih.gov/32293500/ PERK/NRF2 and autophagy form a resistance mechanism against G9a inhibition in leukemia stem cells. unassigned - 2.1.1.355 Liver Cirrhosis https://pubmed.ncbi.nlm.nih.gov/28129116/ A Proof-of-Concept for Epigenetic Therapy of Tissue Fibrosis: Inhibition of Liver Fibrosis Progression by 3-Deazaneplanocin A. therapeutic application 4 2.1.1.355 Liver Cirrhosis https://pubmed.ncbi.nlm.nih.gov/31811111/ A twenty gene-based gene set variation score reflects the pathological progression from cirrhosis to hepatocellular carcinoma. ongoing research 3 2.1.1.355 Liver Cirrhosis https://pubmed.ncbi.nlm.nih.gov/28129116/ A Proof-of-Concept for Epigenetic Therapy of Tissue Fibrosis: Inhibition of Liver Fibrosis Progression by 3-Deazaneplanocin A. unassigned - 2.1.1.355 Liver Cirrhosis https://pubmed.ncbi.nlm.nih.gov/31811111/ A twenty gene-based gene set variation score reflects the pathological progression from cirrhosis to hepatocellular carcinoma. unassigned - 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. causal interaction 3 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32964965/ Inactivation of lncRNA HOTAIRM1 caused by histone methyltransferase RIZ1 accelerated the proliferation and invasion of liver cancer. causal interaction 2 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32684241/ Euchromatin histone methyltransferase II (EHMT2) regulates the expression of ras-related GTP binding C (RRAGC) protein. causal interaction 3 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. diagnostic usage 1 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32964965/ Inactivation of lncRNA HOTAIRM1 caused by histone methyltransferase RIZ1 accelerated the proliferation and invasion of liver cancer. diagnostic usage 3 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. therapeutic application 1 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/33468997/ Inhibition of histone methyltransferase G9a attenuates liver cancer initiation by sensitizing DNA-damaged hepatocytes to p53-induced apoptosis. therapeutic application 1 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32030886/ miR24-2 accelerates progression of liver cancer cells by activating Pim1 through tri-methylation of Histone H3 on the ninth lysine. therapeutic application 1 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32684241/ Euchromatin histone methyltransferase II (EHMT2) regulates the expression of ras-related GTP binding C (RRAGC) protein. therapeutic application 1 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. ongoing research 2 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/28532996/ Histone methyltransferase G9a promotes liver cancer development by epigenetic silencing of tumor suppressor gene RARRES3. ongoing research 4 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32964965/ Inactivation of lncRNA HOTAIRM1 caused by histone methyltransferase RIZ1 accelerated the proliferation and invasion of liver cancer. ongoing research 3 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/28532996/ Histone methyltransferase G9a promotes liver cancer development by epigenetic silencing of tumor suppressor gene RARRES3. unassigned - 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/33468997/ Inhibition of histone methyltransferase G9a attenuates liver cancer initiation by sensitizing DNA-damaged hepatocytes to p53-induced apoptosis. unassigned - 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32030886/ miR24-2 accelerates progression of liver cancer cells by activating Pim1 through tri-methylation of Histone H3 on the ninth lysine. unassigned - 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32684241/ Euchromatin histone methyltransferase II (EHMT2) regulates the expression of ras-related GTP binding C (RRAGC) protein. unassigned - 2.1.1.355 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32964965/ Inactivation of lncRNA HOTAIRM1 caused by histone methyltransferase RIZ1 accelerated the proliferation and invasion of liver cancer. unassigned - 2.1.1.355 Lung Injury https://pubmed.ncbi.nlm.nih.gov/34217280/ Inhibition of EZH2 prevents acute respiratory distress syndrome (ARDS)-associated pulmonary fibrosis by regulating the macrophage polarization phenotype. causal interaction 3 2.1.1.355 Lung Injury https://pubmed.ncbi.nlm.nih.gov/34217280/ Inhibition of EZH2 prevents acute respiratory distress syndrome (ARDS)-associated pulmonary fibrosis by regulating the macrophage polarization phenotype. therapeutic application 2 2.1.1.355 Lung Injury https://pubmed.ncbi.nlm.nih.gov/34217280/ Inhibition of EZH2 prevents acute respiratory distress syndrome (ARDS)-associated pulmonary fibrosis by regulating the macrophage polarization phenotype. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/16774942/ Novel polymorphisms in the SUV39H2 histone methyltransferase and the risk of lung cancer. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23933322/ DZNep, inhibitor of S-adenosylhomocysteine hydrolase, down-regulates expression of SETDB1 H3K9me3 HMTase in human lung cancer cells. causal interaction 2 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24932239/ Modulation of microRNA expression in human lung cancer cells by the G9a histone methyltransferase inhibitor BIX01294. causal interaction 2 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. causal interaction 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32095117/ Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34219384/ Histone methyltransferase SETD1A participates in lung cancer progression. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. causal interaction 2 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23955539/ Lung tumor-associated dendritic cell-derived resistin promoted cancer progression by increasing Wolf-Hirschhorn syndrome candidate 1/Twist pathway. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24732359/ S100A4 is frequently overexpressed in lung cancer cells and promotes cell growth and cell motility. causal interaction 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26568301/ Variants of ubiquitin-specific peptidase 24 play a crucial role in lung cancer malignancy. causal interaction 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/27116120/ Combined inhibition of EZH2 and histone deacetylases as a potential epigenetic therapy for non-small-cell lung cancer cells. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/28314309/ Elevated Metabolic Activity on (18)F-FDG PET/CT Is Associated with the Expression of EZH2 in Non-small Cell Lung Cancer. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32243837/ KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33298547/ G9a Promotes Invasion and Metastasis of Non-Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-?B Signaling Pathway. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. causal interaction 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/16774942/ Novel polymorphisms in the SUV39H2 histone methyltransferase and the risk of lung cancer. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. diagnostic usage 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26536195/ Clinicopathological and Survival Analysis of Japanese Patients with Resected Non-Small-Cell Lung Cancer Harboring NKX2-1, SETDB1, MET, HER2, SOX2, FGFR1, or PIK3CA Gene Amplification. diagnostic usage 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. diagnostic usage 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. diagnostic usage 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32095117/ Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death. diagnostic usage 2 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34219384/ Histone methyltransferase SETD1A participates in lung cancer progression. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24732359/ S100A4 is frequently overexpressed in lung cancer cells and promotes cell growth and cell motility. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. diagnostic usage 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/16774942/ Novel polymorphisms in the SUV39H2 histone methyltransferase and the risk of lung cancer. therapeutic application 2 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/22925699/ Epigenetic therapy with 3-deazaneplanocin A, an inhibitor of the histone methyltransferase EZH2, inhibits growth of non-small cell lung cancer cells. therapeutic application 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23933322/ DZNep, inhibitor of S-adenosylhomocysteine hydrolase, down-regulates expression of SETDB1 H3K9me3 HMTase in human lung cancer cells. therapeutic application 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24966940/ Methylation of PRDM2, PRDM5 and PRDM16 genes in lung cancer cells. therapeutic application 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. therapeutic application 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. therapeutic application 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. therapeutic application 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. therapeutic application 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. therapeutic application 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32095117/ Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death. therapeutic application 2 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. therapeutic application 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. therapeutic application 2 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34219384/ Histone methyltransferase SETD1A participates in lung cancer progression. therapeutic application 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. therapeutic application 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. therapeutic application 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24732359/ S100A4 is frequently overexpressed in lung cancer cells and promotes cell growth and cell motility. therapeutic application 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. therapeutic application 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32243837/ KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer. therapeutic application 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23933322/ DZNep, inhibitor of S-adenosylhomocysteine hydrolase, down-regulates expression of SETDB1 H3K9me3 HMTase in human lung cancer cells. ongoing research 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24932239/ Modulation of microRNA expression in human lung cancer cells by the G9a histone methyltransferase inhibitor BIX01294. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26536195/ Clinicopathological and Survival Analysis of Japanese Patients with Resected Non-Small-Cell Lung Cancer Harboring NKX2-1, SETDB1, MET, HER2, SOX2, FGFR1, or PIK3CA Gene Amplification. ongoing research 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/28007623/ Small Cell Lung Cancer Exhibits Frequent Inactivating Mutations in the Histone Methyltransferase KMT2D/MLL2: CALGB 151111 (Alliance). ongoing research 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. ongoing research 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/31398867/ Expression of the Major and Pro-Oncogenic H3K9 Lysine Methyltransferase SETDB1 in Non-Small Cell Lung Cancer. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32095117/ Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death. ongoing research 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. ongoing research 3 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34219384/ Histone methyltransferase SETD1A participates in lung cancer progression. ongoing research 1 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32243837/ KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer. ongoing research 2 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/22925699/ Epigenetic therapy with 3-deazaneplanocin A, an inhibitor of the histone methyltransferase EZH2, inhibits growth of non-small cell lung cancer cells. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24966940/ Methylation of PRDM2, PRDM5 and PRDM16 genes in lung cancer cells. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26536195/ Clinicopathological and Survival Analysis of Japanese Patients with Resected Non-Small-Cell Lung Cancer Harboring NKX2-1, SETDB1, MET, HER2, SOX2, FGFR1, or PIK3CA Gene Amplification. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/28007623/ Small Cell Lung Cancer Exhibits Frequent Inactivating Mutations in the Histone Methyltransferase KMT2D/MLL2: CALGB 151111 (Alliance). unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/30054425/ A regulatory circuitry comprising TP53, miR-29 family, and SETDB1 in non-small cell lung cancer. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25746006/ DNA methylation in small cell lung cancer defines distinct disease subtypes and correlates with high expression of EZH2. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/31042721/ The association and prognostic impact of enhancer of zeste homologue 2 expression and epithelial-mesenchymal transition in resected lung adenocarcinoma. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23933322/ DZNep, inhibitor of S-adenosylhomocysteine hydrolase, down-regulates expression of SETDB1 H3K9me3 HMTase in human lung cancer cells. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24932239/ Modulation of microRNA expression in human lung cancer cells by the G9a histone methyltransferase inhibitor BIX01294. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/23955539/ Lung tumor-associated dendritic cell-derived resistin promoted cancer progression by increasing Wolf-Hirschhorn syndrome candidate 1/Twist pathway. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/26568301/ Variants of ubiquitin-specific peptidase 24 play a crucial role in lung cancer malignancy. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/27116120/ Combined inhibition of EZH2 and histone deacetylases as a potential epigenetic therapy for non-small-cell lung cancer cells. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/28314309/ Elevated Metabolic Activity on (18)F-FDG PET/CT Is Associated with the Expression of EZH2 in Non-small Cell Lung Cancer. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/32243837/ KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33298547/ G9a Promotes Invasion and Metastasis of Non-Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-?B Signaling Pathway. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/16774942/ Novel polymorphisms in the SUV39H2 histone methyltransferase and the risk of lung cancer. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. unassigned - 2.1.1.355 Lung Neoplasms https://pubmed.ncbi.nlm.nih.gov/24732359/ S100A4 is frequently overexpressed in lung cancer cells and promotes cell growth and cell motility. unassigned - 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. causal interaction 4 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. causal interaction 4 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. causal interaction 4 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. causal interaction 3 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. causal interaction 3 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. diagnostic usage 3 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. diagnostic usage 4 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. diagnostic usage 2 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. diagnostic usage 3 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. diagnostic usage 4 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. therapeutic application 2 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. ongoing research 4 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. ongoing research 4 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. ongoing research 2 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/23504335/ High expressions of histone methylation- and phosphorylation-related proteins are associated with prognosis of oral squamous cell carcinoma in male population of Taiwan. unassigned - 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. unassigned - 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. unassigned - 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. unassigned - 2.1.1.355 Lymphatic Metastasis https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/33530253/ Prognostic value of lymphocyte-to-monocyte ratio and histone methyltransferase G9a histone methyltransferase in patients with double expression lymphoma: A retrospective observational study. causal interaction 3 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/21190999/ Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. causal interaction 2 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/23680150/ EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation. causal interaction 2 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25131304/ MLL/KMT2A translocations in diffuse large B-cell lymphomas. causal interaction 4 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25893294/ Development of secondary mutations in wild-type and mutant EZH2 alleles cooperates to confer resistance to EZH2 inhibitors. causal interaction 4 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. causal interaction 3 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/27135738/ An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. causal interaction 3 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/30218753/ Aberrant differential expression of EZH2 and H3K27me3 in extranodal NK/T-cell lymphoma, nasal type is associated with disease progression and prognosis. causal interaction 2 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/30393995/ Common origin of sequential cutaneous CD30+ lymphoproliferations with nodal involvement evidenced by genome-wide clonal evolution. causal interaction 1 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/33530253/ Prognostic value of lymphocyte-to-monocyte ratio and histone methyltransferase G9a histone methyltransferase in patients with double expression lymphoma: A retrospective observational study. diagnostic usage 4 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25131304/ MLL/KMT2A translocations in diffuse large B-cell lymphomas. diagnostic usage 3 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. diagnostic usage 2 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. therapeutic application 1 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/29669287/ ZRANB1 Is an EZH2 Deubiquitinase and a Potential Therapeutic Target in Breast Cancer. therapeutic application 4 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/33530253/ Prognostic value of lymphocyte-to-monocyte ratio and histone methyltransferase G9a histone methyltransferase in patients with double expression lymphoma: A retrospective observational study. ongoing research 2 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/23945590/ Synthetic lethal metabolic targeting of cellular senescence in cancer therapy. ongoing research 3 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25131304/ MLL/KMT2A translocations in diffuse large B-cell lymphomas. ongoing research 2 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. ongoing research 3 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. ongoing research 2 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/21087793/ Absence of mutations of the histone methyltransferase gene EZH2 in splenic b-cell marginal zone lymphoma. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/23529930/ EZH2 overexpression in natural killer /T-cell lymphoma confers growth advantage independently of histone methyltransferase activity. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/23945590/ Synthetic lethal metabolic targeting of cellular senescence in cancer therapy. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/29669287/ ZRANB1 Is an EZH2 Deubiquitinase and a Potential Therapeutic Target in Breast Cancer. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/21190999/ Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/23680150/ EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25893294/ Development of secondary mutations in wild-type and mutant EZH2 alleles cooperates to confer resistance to EZH2 inhibitors. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/27135738/ An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/30218753/ Aberrant differential expression of EZH2 and H3K27me3 in extranodal NK/T-cell lymphoma, nasal type is associated with disease progression and prognosis. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/30393995/ Common origin of sequential cutaneous CD30+ lymphoproliferations with nodal involvement evidenced by genome-wide clonal evolution. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/33530253/ Prognostic value of lymphocyte-to-monocyte ratio and histone methyltransferase G9a histone methyltransferase in patients with double expression lymphoma: A retrospective observational study. unassigned - 2.1.1.355 Lymphoma https://pubmed.ncbi.nlm.nih.gov/25131304/ MLL/KMT2A translocations in diffuse large B-cell lymphomas. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/22323599/ Mutation of A677 in histone methyltransferase EZH2 in human B-cell lymphoma promotes hypertrimethylation of histone H3 on lysine 27 (H3K27). causal interaction 4 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/21190999/ Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. causal interaction 2 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. causal interaction 3 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/27135738/ An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. causal interaction 3 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/28943305/ Targeting the cancer epigenome: synergistic therapy with bromodomain inhibitors. causal interaction 4 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/29473431/ Enhancer of zeste homolog 2 (EZH2) inhibitors. causal interaction 4 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/33104794/ Combined EZH2 and Bcl-2 inhibitors as precision therapy for genetically defined DLBCL subtypes. diagnostic usage 3 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/27739677/ Identification of (R)-N-((4-Methoxy-6-methyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-2-methyl-1-(1-(1-(2,2,2-trifluoroethyl)piperidin-4-yl)ethyl)-1H-indole-3-carboxamide (CPI-1205), a Potent and Selective Inhibitor of Histone Methyltransferase EZH2, Suitable for Phase I Clinical Trials for B-Cell Lymphomas. therapeutic application 4 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/33442400/ EHMT2 inhibitor BIX-01294 induces endoplasmic reticulum stress mediated apoptosis and autophagy in diffuse large B-cell lymphoma cells. therapeutic application 1 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. therapeutic application 1 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/28943305/ Targeting the cancer epigenome: synergistic therapy with bromodomain inhibitors. therapeutic application 4 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/33904892/ Treating lymphoma is now a bit EZ-er. therapeutic application 1 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/34449935/ The EZH2 inhibitor tazemetostat upregulates the expression of CCL17/TARC in B-cell lymphoma and enhances T-cell recruitment. therapeutic application 4 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/17205536/ Lack of A563G (I188V) missense mutation in RIZ/ PRDM2 in human diffuse large B-cell lymphomas. ongoing research 1 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/22323599/ Mutation of A677 in histone methyltransferase EZH2 in human B-cell lymphoma promotes hypertrimethylation of histone H3 on lysine 27 (H3K27). ongoing research 2 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/33442400/ EHMT2 inhibitor BIX-01294 induces endoplasmic reticulum stress mediated apoptosis and autophagy in diffuse large B-cell lymphoma cells. ongoing research 2 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. ongoing research 2 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/17205536/ Lack of A563G (I188V) missense mutation in RIZ/ PRDM2 in human diffuse large B-cell lymphomas. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/27739677/ Identification of (R)-N-((4-Methoxy-6-methyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-2-methyl-1-(1-(1-(2,2,2-trifluoroethyl)piperidin-4-yl)ethyl)-1H-indole-3-carboxamide (CPI-1205), a Potent and Selective Inhibitor of Histone Methyltransferase EZH2, Suitable for Phase I Clinical Trials for B-Cell Lymphomas. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/33442400/ EHMT2 inhibitor BIX-01294 induces endoplasmic reticulum stress mediated apoptosis and autophagy in diffuse large B-cell lymphoma cells. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/20104248/ Deregulation of H3K27 methylation in cancer. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/24802772/ A transgenic mouse model demonstrating the oncogenic role of mutations in the polycomb-group gene EZH2 in lymphomagenesis. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/33104794/ Combined EZH2 and Bcl-2 inhibitors as precision therapy for genetically defined DLBCL subtypes. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/33904892/ Treating lymphoma is now a bit EZ-er. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/34449935/ The EZH2 inhibitor tazemetostat upregulates the expression of CCL17/TARC in B-cell lymphoma and enhances T-cell recruitment. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/22323599/ Mutation of A677 in histone methyltransferase EZH2 in human B-cell lymphoma promotes hypertrimethylation of histone H3 on lysine 27 (H3K27). unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/21190999/ Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/27135738/ An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/28943305/ Targeting the cancer epigenome: synergistic therapy with bromodomain inhibitors. unassigned - 2.1.1.355 Lymphoma, B-Cell https://pubmed.ncbi.nlm.nih.gov/29473431/ Enhancer of zeste homolog 2 (EZH2) inhibitors. unassigned - 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/21190999/ Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. causal interaction 2 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. causal interaction 3 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/28430172/ EZH2 alterations in follicular lymphoma: biological and clinical correlations. causal interaction 3 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/34488340/ Targeting the Nuclear Receptor-Binding SET Domain Family of Histone Lysine Methyltransferases for Cancer Therapy: Recent Progress and Perspectives. causal interaction 1 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. therapeutic application 1 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/34488340/ Targeting the Nuclear Receptor-Binding SET Domain Family of Histone Lysine Methyltransferases for Cancer Therapy: Recent Progress and Perspectives. therapeutic application 4 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. ongoing research 2 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/24802772/ A transgenic mouse model demonstrating the oncogenic role of mutations in the polycomb-group gene EZH2 in lymphomagenesis. unassigned - 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/21190999/ Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. unassigned - 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. unassigned - 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/28430172/ EZH2 alterations in follicular lymphoma: biological and clinical correlations. unassigned - 2.1.1.355 Lymphoma, Follicular https://pubmed.ncbi.nlm.nih.gov/34488340/ Targeting the Nuclear Receptor-Binding SET Domain Family of Histone Lysine Methyltransferases for Cancer Therapy: Recent Progress and Perspectives. unassigned - 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. causal interaction 3 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/33104794/ Combined EZH2 and Bcl-2 inhibitors as precision therapy for genetically defined DLBCL subtypes. diagnostic usage 3 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/33442400/ EHMT2 inhibitor BIX-01294 induces endoplasmic reticulum stress mediated apoptosis and autophagy in diffuse large B-cell lymphoma cells. therapeutic application 1 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. therapeutic application 1 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/33904892/ Treating lymphoma is now a bit EZ-er. therapeutic application 1 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/33442400/ EHMT2 inhibitor BIX-01294 induces endoplasmic reticulum stress mediated apoptosis and autophagy in diffuse large B-cell lymphoma cells. ongoing research 2 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. ongoing research 2 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/33442400/ EHMT2 inhibitor BIX-01294 induces endoplasmic reticulum stress mediated apoptosis and autophagy in diffuse large B-cell lymphoma cells. unassigned - 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/20104248/ Deregulation of H3K27 methylation in cancer. unassigned - 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/24802772/ A transgenic mouse model demonstrating the oncogenic role of mutations in the polycomb-group gene EZH2 in lymphomagenesis. unassigned - 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/33104794/ Combined EZH2 and Bcl-2 inhibitors as precision therapy for genetically defined DLBCL subtypes. unassigned - 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/33904892/ Treating lymphoma is now a bit EZ-er. unassigned - 2.1.1.355 Lymphoma, Large B-Cell, Diffuse https://pubmed.ncbi.nlm.nih.gov/26366710/ The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development. unassigned - 2.1.1.355 Lymphoma, Large-Cell, Anaplastic https://pubmed.ncbi.nlm.nih.gov/30393995/ Common origin of sequential cutaneous CD30+ lymphoproliferations with nodal involvement evidenced by genome-wide clonal evolution. causal interaction 1 2.1.1.355 Lymphoma, Large-Cell, Anaplastic https://pubmed.ncbi.nlm.nih.gov/30393995/ Common origin of sequential cutaneous CD30+ lymphoproliferations with nodal involvement evidenced by genome-wide clonal evolution. unassigned - 2.1.1.355 Lymphoma, Mantle-Cell https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. diagnostic usage 2 2.1.1.355 Lymphoma, Mantle-Cell https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. ongoing research 3 2.1.1.355 Lymphoma, Mantle-Cell https://pubmed.ncbi.nlm.nih.gov/25755704/ JARID1B deletion induced apoptosis in Jeko-1 and HL-60 cell lines. unassigned - 2.1.1.355 Lymphoma, Non-Hodgkin https://pubmed.ncbi.nlm.nih.gov/24563539/ Selective Inhibition of EZH2 by EPZ-6438 Leads to Potent Antitumor Activity in EZH2-Mutant Non-Hodgkin Lymphoma. causal interaction 4 2.1.1.355 Lymphoma, Non-Hodgkin https://pubmed.ncbi.nlm.nih.gov/26463831/ Studies Identify Non-Hodgkin Lymphoma Suppressor. causal interaction 1 2.1.1.355 Lymphoma, Non-Hodgkin https://pubmed.ncbi.nlm.nih.gov/27555605/ Initial testing (stage 1) of tazemetostat (EPZ-6438), a novel EZH2 inhibitor, by the Pediatric Preclinical Testing Program. causal interaction 4 2.1.1.355 Lymphoma, Non-Hodgkin https://pubmed.ncbi.nlm.nih.gov/27555605/ Initial testing (stage 1) of tazemetostat (EPZ-6438), a novel EZH2 inhibitor, by the Pediatric Preclinical Testing Program. therapeutic application 4 2.1.1.355 Lymphoma, Non-Hodgkin https://pubmed.ncbi.nlm.nih.gov/24563539/ Selective Inhibition of EZH2 by EPZ-6438 Leads to Potent Antitumor Activity in EZH2-Mutant Non-Hodgkin Lymphoma. unassigned - 2.1.1.355 Lymphoma, Non-Hodgkin https://pubmed.ncbi.nlm.nih.gov/26463831/ Studies Identify Non-Hodgkin Lymphoma Suppressor. unassigned - 2.1.1.355 Lymphoma, Non-Hodgkin https://pubmed.ncbi.nlm.nih.gov/27555605/ Initial testing (stage 1) of tazemetostat (EPZ-6438), a novel EZH2 inhibitor, by the Pediatric Preclinical Testing Program. unassigned - 2.1.1.355 Lymphoma, T-Cell https://pubmed.ncbi.nlm.nih.gov/16079837/ Oncogene-induced senescence as an initial barrier in lymphoma development. causal interaction 1 2.1.1.355 Lymphoma, T-Cell https://pubmed.ncbi.nlm.nih.gov/29248547/ Dual Role of EZH2 in Cutaneous Anaplastic Large Cell Lymphoma: Promoting Tumor Cell Survival and Regulating Tumor Microenvironment. causal interaction 1 2.1.1.355 Lymphoma, T-Cell https://pubmed.ncbi.nlm.nih.gov/29248547/ Dual Role of EZH2 in Cutaneous Anaplastic Large Cell Lymphoma: Promoting Tumor Cell Survival and Regulating Tumor Microenvironment. therapeutic application 1 2.1.1.355 Lymphoma, T-Cell https://pubmed.ncbi.nlm.nih.gov/16079837/ Oncogene-induced senescence as an initial barrier in lymphoma development. ongoing research 2 2.1.1.355 Lymphoma, T-Cell https://pubmed.ncbi.nlm.nih.gov/29248547/ Dual Role of EZH2 in Cutaneous Anaplastic Large Cell Lymphoma: Promoting Tumor Cell Survival and Regulating Tumor Microenvironment. ongoing research 1 2.1.1.355 Lymphoma, T-Cell https://pubmed.ncbi.nlm.nih.gov/16079837/ Oncogene-induced senescence as an initial barrier in lymphoma development. unassigned - 2.1.1.355 Lymphoma, T-Cell https://pubmed.ncbi.nlm.nih.gov/29248547/ Dual Role of EZH2 in Cutaneous Anaplastic Large Cell Lymphoma: Promoting Tumor Cell Survival and Regulating Tumor Microenvironment. unassigned - 2.1.1.355 Lymphopenia https://pubmed.ncbi.nlm.nih.gov/33236014/ Novel gene-specific translation mechanism of dysregulated, chronic inflammation reveals promising, multifaceted COVID-19 therapeutics. causal interaction 4 2.1.1.355 Lymphopenia https://pubmed.ncbi.nlm.nih.gov/33236014/ Novel gene-specific translation mechanism of dysregulated, chronic inflammation reveals promising, multifaceted COVID-19 therapeutics. unassigned - 2.1.1.355 Malaria https://pubmed.ncbi.nlm.nih.gov/25421480/ Histone Methyltransferase Inhibitors Are Orally Bioavailable, Fast-Acting Molecules with Activity against Different Species Causing Malaria in Humans. causal interaction 3 2.1.1.355 Malaria https://pubmed.ncbi.nlm.nih.gov/25421480/ Histone Methyltransferase Inhibitors Are Orally Bioavailable, Fast-Acting Molecules with Activity against Different Species Causing Malaria in Humans. therapeutic application 4 2.1.1.355 Malaria https://pubmed.ncbi.nlm.nih.gov/32179524/ A histone methyltransferase inhibitor can reverse epigenetically acquired drug resistance in the malaria parasite Plasmodium falciparum. therapeutic application 4 2.1.1.355 Malaria https://pubmed.ncbi.nlm.nih.gov/32179524/ A histone methyltransferase inhibitor can reverse epigenetically acquired drug resistance in the malaria parasite Plasmodium falciparum. unassigned - 2.1.1.355 Malaria https://pubmed.ncbi.nlm.nih.gov/33536326/ The Role of the Histone Methyltransferase PfSET10 in Antigenic Variation by Malaria Parasites: a Cautionary Tale. unassigned - 2.1.1.355 Malaria https://pubmed.ncbi.nlm.nih.gov/25421480/ Histone Methyltransferase Inhibitors Are Orally Bioavailable, Fast-Acting Molecules with Activity against Different Species Causing Malaria in Humans. unassigned - 2.1.1.355 Mastocytosis https://pubmed.ncbi.nlm.nih.gov/32366397/ Histone Methyltransferase Inhibition Has a Cytotoxic Impact on Transformed Mast Cells: Implications for Mastocytosis. therapeutic application 3 2.1.1.355 Mastocytosis https://pubmed.ncbi.nlm.nih.gov/32366397/ Histone Methyltransferase Inhibition Has a Cytotoxic Impact on Transformed Mast Cells: Implications for Mastocytosis. unassigned - 2.1.1.355 Medulloblastoma https://pubmed.ncbi.nlm.nih.gov/28978137/ The histone methyltransferase EZH2 as a druggable target in SHH medulloblastoma cancer stem cells. causal interaction 4 2.1.1.355 Medulloblastoma https://pubmed.ncbi.nlm.nih.gov/22820256/ Medulloblastoma exome sequencing uncovers subtype-specific somatic mutations. causal interaction 1 2.1.1.355 Medulloblastoma https://pubmed.ncbi.nlm.nih.gov/28978137/ The histone methyltransferase EZH2 as a druggable target in SHH medulloblastoma cancer stem cells. therapeutic application 1 2.1.1.355 Medulloblastoma https://pubmed.ncbi.nlm.nih.gov/22820256/ Medulloblastoma exome sequencing uncovers subtype-specific somatic mutations. therapeutic application 1 2.1.1.355 Medulloblastoma https://pubmed.ncbi.nlm.nih.gov/33545678/ Preclinical efficacy of ribavirin in SHH and group 3 medulloblastoma. unassigned - 2.1.1.355 Medulloblastoma https://pubmed.ncbi.nlm.nih.gov/28978137/ The histone methyltransferase EZH2 as a druggable target in SHH medulloblastoma cancer stem cells. unassigned - 2.1.1.355 Medulloblastoma https://pubmed.ncbi.nlm.nih.gov/22820256/ Medulloblastoma exome sequencing uncovers subtype-specific somatic mutations. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/21430779/ The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset. causal interaction 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24673285/ High frequency p16(INK) (4A) promoter methylation is associated with histone methyltransferase SETDB1 expression in sporadic cutaneous melanoma. causal interaction 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/28042025/ Androgen receptor regulation by histone methyltransferase Suppressor of variegation 3-9 homolog 2 and Melanoma antigen-A11. causal interaction 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32637583/ Mithramycin A and Mithralog EC-8042 Inhibit SETDB1 Expression and Its Oncogenic Activity in Malignant Melanoma. causal interaction 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33064882/ Recurrent co-alteration of HDGF and SETDB1 on chromosome 1q drives cutaneous melanoma progression and poor prognosis. causal interaction 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24912396/ EZH2: an emerging role in melanoma biology and strategies for targeted therapy. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/25099074/ Matrix softness regulates plasticity of tumour-repopulating cells via H3K9 demethylation and Sox2 expression. causal interaction 1 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/26813693/ Characterization of the Enzymatic Activity of SETDB1 and Its 1:1 Complex with ATF7IP. causal interaction 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/27105109/ Role of EZH2 histone methyltrasferase in melanoma progression and metastasis. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/27135738/ An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. causal interaction 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/29750576/ SUV39H1/DNMT3A-dependent methylation of the RB1 promoter stimulates PIN1 expression and melanoma development. causal interaction 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/30850015/ Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31524790/ A novel germline variant in the DOT1L gene co-segregating in a Dutch family with a history of melanoma. causal interaction 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32269030/ Gain-of-Function Genetic Alterations of G9a Drive Oncogenesis. causal interaction 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32512705/ G9a Is SETting the Stage for Colorectal Oncogenesis. causal interaction 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32629178/ BRAF inhibition in melanoma is associated with the dysregulation of histone methylation and histone methyltransferases. causal interaction 1 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33086062/ Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33589432/ G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. diagnostic usage 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24673285/ High frequency p16(INK) (4A) promoter methylation is associated with histone methyltransferase SETDB1 expression in sporadic cutaneous melanoma. diagnostic usage 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. diagnostic usage 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32637583/ Mithramycin A and Mithralog EC-8042 Inhibit SETDB1 Expression and Its Oncogenic Activity in Malignant Melanoma. diagnostic usage 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33064882/ Recurrent co-alteration of HDGF and SETDB1 on chromosome 1q drives cutaneous melanoma progression and poor prognosis. diagnostic usage 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/29750576/ SUV39H1/DNMT3A-dependent methylation of the RB1 promoter stimulates PIN1 expression and melanoma development. diagnostic usage 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. therapeutic application 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24673285/ High frequency p16(INK) (4A) promoter methylation is associated with histone methyltransferase SETDB1 expression in sporadic cutaneous melanoma. therapeutic application 1 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. therapeutic application 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32637583/ Mithramycin A and Mithralog EC-8042 Inhibit SETDB1 Expression and Its Oncogenic Activity in Malignant Melanoma. therapeutic application 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33064882/ Recurrent co-alteration of HDGF and SETDB1 on chromosome 1q drives cutaneous melanoma progression and poor prognosis. therapeutic application 1 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/26813693/ Characterization of the Enzymatic Activity of SETDB1 and Its 1:1 Complex with ATF7IP. therapeutic application 1 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/30850015/ Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming. therapeutic application 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32041674/ H3K27me3 and EZH2 expression in melanoma: relevance for melanoma progression and response to immune checkpoint blockade. therapeutic application 1 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33086062/ Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. therapeutic application 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. therapeutic application 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33589432/ G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma. therapeutic application 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. ongoing research 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24673285/ High frequency p16(INK) (4A) promoter methylation is associated with histone methyltransferase SETDB1 expression in sporadic cutaneous melanoma. ongoing research 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. ongoing research 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32637583/ Mithramycin A and Mithralog EC-8042 Inhibit SETDB1 Expression and Its Oncogenic Activity in Malignant Melanoma. ongoing research 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33064882/ Recurrent co-alteration of HDGF and SETDB1 on chromosome 1q drives cutaneous melanoma progression and poor prognosis. ongoing research 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/29750576/ SUV39H1/DNMT3A-dependent methylation of the RB1 promoter stimulates PIN1 expression and melanoma development. ongoing research 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31524790/ A novel germline variant in the DOT1L gene co-segregating in a Dutch family with a history of melanoma. ongoing research 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31693439/ Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments. ongoing research 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33086062/ Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. ongoing research 2 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. ongoing research 3 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33589432/ G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma. ongoing research 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/21983785/ Genome-wide association study identifies a new melanoma susceptibility locus at 1q21.3. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31693439/ Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32041674/ H3K27me3 and EZH2 expression in melanoma: relevance for melanoma progression and response to immune checkpoint blockade. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/21430779/ The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/28042025/ Androgen receptor regulation by histone methyltransferase Suppressor of variegation 3-9 homolog 2 and Melanoma antigen-A11. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/24912396/ EZH2: an emerging role in melanoma biology and strategies for targeted therapy. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/25099074/ Matrix softness regulates plasticity of tumour-repopulating cells via H3K9 demethylation and Sox2 expression. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/26813693/ Characterization of the Enzymatic Activity of SETDB1 and Its 1:1 Complex with ATF7IP. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/27105109/ Role of EZH2 histone methyltrasferase in melanoma progression and metastasis. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/27135738/ An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/30850015/ Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/31524790/ A novel germline variant in the DOT1L gene co-segregating in a Dutch family with a history of melanoma. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32269030/ Gain-of-Function Genetic Alterations of G9a Drive Oncogenesis. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32512705/ G9a Is SETting the Stage for Colorectal Oncogenesis. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/32629178/ BRAF inhibition in melanoma is associated with the dysregulation of histone methylation and histone methyltransferases. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33086062/ Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/33589432/ G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Melanoma https://pubmed.ncbi.nlm.nih.gov/29750576/ SUV39H1/DNMT3A-dependent methylation of the RB1 promoter stimulates PIN1 expression and melanoma development. unassigned - 2.1.1.355 Meningioma https://pubmed.ncbi.nlm.nih.gov/25934289/ The transducible TAT-RIZ1-PR protein exerts histone methyltransferase activity and tumor-suppressive functions in human malignant meningiomas. therapeutic application 1 2.1.1.355 Meningioma https://pubmed.ncbi.nlm.nih.gov/25934289/ The transducible TAT-RIZ1-PR protein exerts histone methyltransferase activity and tumor-suppressive functions in human malignant meningiomas. ongoing research 2 2.1.1.355 Meningioma https://pubmed.ncbi.nlm.nih.gov/25934289/ The transducible TAT-RIZ1-PR protein exerts histone methyltransferase activity and tumor-suppressive functions in human malignant meningiomas. unassigned - 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/26824986/ Whole exome and targeted deep sequencing identify genome-wide allelic loss and frequent SETDB1 mutations in malignant pleural mesotheliomas. causal interaction 2 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. causal interaction 4 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. causal interaction 4 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/34277422/ CDKN2A Determines Mesothelioma Cell Fate to EZH2 Inhibition. causal interaction 3 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. diagnostic usage 3 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/34277422/ CDKN2A Determines Mesothelioma Cell Fate to EZH2 Inhibition. diagnostic usage 3 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. therapeutic application 4 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. therapeutic application 4 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/34277422/ CDKN2A Determines Mesothelioma Cell Fate to EZH2 Inhibition. therapeutic application 1 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/33922336/ Inhibition of the Histone Methyltransferase EZH2 Enhances Protumor Monocyte Recruitment in Human Mesothelioma Spheroids. ongoing research 1 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. ongoing research 3 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/34277422/ CDKN2A Determines Mesothelioma Cell Fate to EZH2 Inhibition. ongoing research 4 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/33922336/ Inhibition of the Histone Methyltransferase EZH2 Enhances Protumor Monocyte Recruitment in Human Mesothelioma Spheroids. unassigned - 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/26824986/ Whole exome and targeted deep sequencing identify genome-wide allelic loss and frequent SETDB1 mutations in malignant pleural mesotheliomas. unassigned - 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. unassigned - 2.1.1.355 Mesothelioma https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. unassigned - 2.1.1.355 Mesothelioma, Malignant https://pubmed.ncbi.nlm.nih.gov/26824986/ Whole exome and targeted deep sequencing identify genome-wide allelic loss and frequent SETDB1 mutations in malignant pleural mesotheliomas. causal interaction 2 2.1.1.355 Mesothelioma, Malignant https://pubmed.ncbi.nlm.nih.gov/26824986/ Whole exome and targeted deep sequencing identify genome-wide allelic loss and frequent SETDB1 mutations in malignant pleural mesotheliomas. unassigned - 2.1.1.355 Microcephaly https://pubmed.ncbi.nlm.nih.gov/28361100/ A novel de novo frameshift deletion in EHMT1 in a patient with Kleefstra Syndrome results in decreased H3K9 dimethylation. causal interaction 1 2.1.1.355 Microcephaly https://pubmed.ncbi.nlm.nih.gov/28361100/ A novel de novo frameshift deletion in EHMT1 in a patient with Kleefstra Syndrome results in decreased H3K9 dimethylation. unassigned - 2.1.1.355 Movement Disorders https://pubmed.ncbi.nlm.nih.gov/21469201/ Variants in estrogen-related genes and risk of Parkinson's disease. causal interaction 3 2.1.1.355 Movement Disorders https://pubmed.ncbi.nlm.nih.gov/21469201/ Variants in estrogen-related genes and risk of Parkinson's disease. diagnostic usage 1 2.1.1.355 Movement Disorders https://pubmed.ncbi.nlm.nih.gov/21469201/ Variants in estrogen-related genes and risk of Parkinson's disease. ongoing research 1 2.1.1.355 Movement Disorders https://pubmed.ncbi.nlm.nih.gov/21469201/ Variants in estrogen-related genes and risk of Parkinson's disease. unassigned - 2.1.1.355 Multiple Endocrine Neoplasia https://pubmed.ncbi.nlm.nih.gov/16651450/ Menin links estrogen receptor activation to histone H3K4 trimethylation. therapeutic application 1 2.1.1.355 Multiple Endocrine Neoplasia https://pubmed.ncbi.nlm.nih.gov/16651450/ Menin links estrogen receptor activation to histone H3K4 trimethylation. unassigned - 2.1.1.355 Multiple Endocrine Neoplasia Type 1 https://pubmed.ncbi.nlm.nih.gov/16651450/ Menin links estrogen receptor activation to histone H3K4 trimethylation. therapeutic application 1 2.1.1.355 Multiple Endocrine Neoplasia Type 1 https://pubmed.ncbi.nlm.nih.gov/16651450/ Menin links estrogen receptor activation to histone H3K4 trimethylation. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/27404348/ Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells. causal interaction 2 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/22751105/ Multiple myeloma-associated chromosomal translocation activates orphan snoRNA ACA11 to suppress oxidative stress. causal interaction 2 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/25188243/ Histone methyltransferase MMSET/NSD2 alters EZH2 binding and reprograms the myeloma epigenome through global and focal changes in H3K36 and H3K27 methylation. causal interaction 1 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/26151044/ Inhibition of Nuclear Receptor Binding SET Domain 2/Multiple Myeloma SET Domain by LEM-06 Implication for Epigenetic Cancer Therapies. causal interaction 4 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/28664185/ The miR-125a and miR-320c are potential tumor suppressor microRNAs epigenetically silenced by the polycomb repressive complex 2 in multiple myeloma. causal interaction 2 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/30013191/ Methylation of Aurora kinase A by MMSET reduces p53 stability and regulates cell proliferation and apoptosis. causal interaction 4 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/27404348/ Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells. therapeutic application 1 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/33661013/ Design and Synthesis of Novel Epigenetic Inhibitors Targeting Histone Deacetylases, DNA Methyltransferase 1, and Lysine Methyltransferase G9a with In Vivo Efficacy in Multiple Myeloma. therapeutic application 4 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/25188243/ Histone methyltransferase MMSET/NSD2 alters EZH2 binding and reprograms the myeloma epigenome through global and focal changes in H3K36 and H3K27 methylation. therapeutic application 1 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/27109101/ MMSET/WHSC1 enhances DNA damage repair leading to an increase in resistance to chemotherapeutic agents. therapeutic application 1 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/28664185/ The miR-125a and miR-320c are potential tumor suppressor microRNAs epigenetically silenced by the polycomb repressive complex 2 in multiple myeloma. therapeutic application 3 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/30013191/ Methylation of Aurora kinase A by MMSET reduces p53 stability and regulates cell proliferation and apoptosis. therapeutic application 4 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/27404348/ Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells. ongoing research 3 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/25188243/ Histone methyltransferase MMSET/NSD2 alters EZH2 binding and reprograms the myeloma epigenome through global and focal changes in H3K36 and H3K27 methylation. ongoing research 1 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/26272979/ Unabridged Analysis of Human Histone H3 by Differential Top-Down Mass Spectrometry Reveals Hypermethylated Proteoforms from MMSET/NSD2 Overexpression. ongoing research 4 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/27109101/ MMSET/WHSC1 enhances DNA damage repair leading to an increase in resistance to chemotherapeutic agents. ongoing research 3 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/32533097/ The BLIMP1-EZH2 nexus in a non-Hodgkin lymphoma. ongoing research 2 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/33661013/ Design and Synthesis of Novel Epigenetic Inhibitors Targeting Histone Deacetylases, DNA Methyltransferase 1, and Lysine Methyltransferase G9a with In Vivo Efficacy in Multiple Myeloma. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/26272979/ Unabridged Analysis of Human Histone H3 by Differential Top-Down Mass Spectrometry Reveals Hypermethylated Proteoforms from MMSET/NSD2 Overexpression. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/26590165/ EZH2 Inhibition Blocks Multiple Myeloma Cell Growth through Upregulation of Epithelial Tumor Suppressor Genes. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/27109101/ MMSET/WHSC1 enhances DNA damage repair leading to an increase in resistance to chemotherapeutic agents. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/31649247/ NSD2 overexpression drives clustered chromatin and transcriptional changes in a subset of insulated domains. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/32014459/ Twist-1 is upregulated by NSD2 and contributes to tumour dissemination and an epithelial-mesenchymal transition-like gene expression signature in t(4;14)-positive multiple myeloma. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/32472076/ H3K36 dimethylation by MMSET promotes classical non-homologous end-joining at unprotected telomeres. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/32533097/ The BLIMP1-EZH2 nexus in a non-Hodgkin lymphoma. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/34147909/ 5-Aminonaphthalene derivatives as selective nonnucleoside nuclear receptor binding SET domain-protein 2 (NSD2) inhibitors for the treatment of multiple myeloma. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/27404348/ Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/22751105/ Multiple myeloma-associated chromosomal translocation activates orphan snoRNA ACA11 to suppress oxidative stress. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/25188243/ Histone methyltransferase MMSET/NSD2 alters EZH2 binding and reprograms the myeloma epigenome through global and focal changes in H3K36 and H3K27 methylation. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/26151044/ Inhibition of Nuclear Receptor Binding SET Domain 2/Multiple Myeloma SET Domain by LEM-06 Implication for Epigenetic Cancer Therapies. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/28664185/ The miR-125a and miR-320c are potential tumor suppressor microRNAs epigenetically silenced by the polycomb repressive complex 2 in multiple myeloma. unassigned - 2.1.1.355 Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/30013191/ Methylation of Aurora kinase A by MMSET reduces p53 stability and regulates cell proliferation and apoptosis. unassigned - 2.1.1.355 Multiple Sclerosis https://pubmed.ncbi.nlm.nih.gov/30367633/ Circulating EZH2-positive T cells are decreased in multiple sclerosis patients. unassigned - 2.1.1.355 Muscle Hypotonia https://pubmed.ncbi.nlm.nih.gov/24362066/ Reduced Euchromatin histone methyltransferase 1 causes developmental delay, hypotonia, and cranial abnormalities associated with increased bone gene expression in Kleefstra syndrome mice. causal interaction 3 2.1.1.355 Muscle Hypotonia https://pubmed.ncbi.nlm.nih.gov/28361100/ A novel de novo frameshift deletion in EHMT1 in a patient with Kleefstra Syndrome results in decreased H3K9 dimethylation. causal interaction 1 2.1.1.355 Muscle Hypotonia https://pubmed.ncbi.nlm.nih.gov/27123477/ Reversible white matter lesions associated with mutant EHMT1 and Kleefstra syndrome. unassigned - 2.1.1.355 Muscle Hypotonia https://pubmed.ncbi.nlm.nih.gov/34010111/ First episode of psychosis in Kleefstra syndrome: a case report. unassigned - 2.1.1.355 Muscle Hypotonia https://pubmed.ncbi.nlm.nih.gov/24362066/ Reduced Euchromatin histone methyltransferase 1 causes developmental delay, hypotonia, and cranial abnormalities associated with increased bone gene expression in Kleefstra syndrome mice. unassigned - 2.1.1.355 Muscle Hypotonia https://pubmed.ncbi.nlm.nih.gov/28361100/ A novel de novo frameshift deletion in EHMT1 in a patient with Kleefstra Syndrome results in decreased H3K9 dimethylation. unassigned - 2.1.1.355 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/23720823/ FSHD muscular dystrophy region gene 1 binds Suv4-20h1 histone methyltransferase and impairs myogenesis. unassigned - 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/20346008/ Decreased expression of PRDM2 (RIZ1) and its correlation with risk stratification in patients with myelodysplastic syndrome. causal interaction 3 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/26575690/ RNA splicing, cell signaling, and response to therapies. causal interaction 1 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/20346008/ Decreased expression of PRDM2 (RIZ1) and its correlation with risk stratification in patients with myelodysplastic syndrome. diagnostic usage 3 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/26575690/ RNA splicing, cell signaling, and response to therapies. diagnostic usage 3 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/25195579/ Epigenomic networking in drug development: from pathogenic mechanisms to pharmacogenomics. therapeutic application 4 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/20601954/ Somatic mutations of the histone methyltransferase gene EZH2 in myelodysplastic syndromes. unassigned - 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/22475286/ The role of histone methyltransferase EZH2 in myelodysplastic syndromes. unassigned - 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/25195579/ Epigenomic networking in drug development: from pathogenic mechanisms to pharmacogenomics. unassigned - 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/30747066/ Anti-cancer effects of curcumin on myelodysplastic syndrome through the inhibition of enhancer of zeste homolog-2 (EZH2). unassigned - 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/20346008/ Decreased expression of PRDM2 (RIZ1) and its correlation with risk stratification in patients with myelodysplastic syndrome. unassigned - 2.1.1.355 Myelodysplastic Syndromes https://pubmed.ncbi.nlm.nih.gov/26575690/ RNA splicing, cell signaling, and response to therapies. unassigned - 2.1.1.355 Myocardial Infarction https://pubmed.ncbi.nlm.nih.gov/32774698/ The combination of G9a histone methyltransferase inhibitors with erythropoietin protects heart against damage from acute myocardial infarction. causal interaction 4 2.1.1.355 Myocardial Infarction https://pubmed.ncbi.nlm.nih.gov/28361889/ The histone H3K9 methyltransferase SUV39H links SIRT1 repression to myocardial infarction. therapeutic application 2 2.1.1.355 Myocardial Infarction https://pubmed.ncbi.nlm.nih.gov/32774698/ The combination of G9a histone methyltransferase inhibitors with erythropoietin protects heart against damage from acute myocardial infarction. therapeutic application 4 2.1.1.355 Myocardial Infarction https://pubmed.ncbi.nlm.nih.gov/32977624/ Role of Muscle-Specific Histone Methyltransferase (Smyd1) in Exercise-Induced Cardioprotection against Pathological Remodeling after Myocardial Infarction. therapeutic application 3 2.1.1.355 Myocardial Infarction https://pubmed.ncbi.nlm.nih.gov/28361889/ The histone H3K9 methyltransferase SUV39H links SIRT1 repression to myocardial infarction. unassigned - 2.1.1.355 Myocardial Infarction https://pubmed.ncbi.nlm.nih.gov/32977624/ Role of Muscle-Specific Histone Methyltransferase (Smyd1) in Exercise-Induced Cardioprotection against Pathological Remodeling after Myocardial Infarction. unassigned - 2.1.1.355 Myocardial Infarction https://pubmed.ncbi.nlm.nih.gov/32774698/ The combination of G9a histone methyltransferase inhibitors with erythropoietin protects heart against damage from acute myocardial infarction. unassigned - 2.1.1.355 Myocardial Ischemia https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. causal interaction 4 2.1.1.355 Myocardial Ischemia https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. therapeutic application 4 2.1.1.355 Myocardial Ischemia https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. unassigned - 2.1.1.355 Nasopharyngeal Carcinoma https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. causal interaction 1 2.1.1.355 Nasopharyngeal Carcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Nasopharyngeal Carcinoma https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. diagnostic usage 3 2.1.1.355 Nasopharyngeal Carcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Nasopharyngeal Carcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Nasopharyngeal Carcinoma https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. ongoing research 4 2.1.1.355 Nasopharyngeal Carcinoma https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Nasopharyngeal Carcinoma https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25373480/ Histone methyltransferase hSETD1A is a Novel Regulator of Metastasis in Breast Cancer. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. causal interaction 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28319045/ AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. causal interaction 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29337058/ EHMT2 is a metastasis regulator in breast cancer. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31720371/ Targeting Histone Methyltransferase DOT1L by a Novel Psammaplin A Analog Inhibits Growth and Metastasis of Triple-Negative Breast Cancer. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33129761/ Su(var)3-9, Enhancer of Zeste, and Trithorax Domain-Containing 5 Facilitates Tumor Growth and Pulmonary Metastasis through Up-Regulation of AKT1 Signaling in Breast Cancer. causal interaction 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/34164392/ Histone Methyltransferase SETD1A Induces Epithelial-Mesenchymal Transition to Promote Invasion and Metastasis Through Epigenetic Reprogramming of Snail in Gastric Cancer. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/15196462/ The functions of E(Z)/EZH2-mediated methylation of lysine 27 in histone H3. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/19008416/ Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/19285253/ Commentary on Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer Varambally S, Cao Q, Mani RS, Shankar S, Wang X, Ateeq B, Laxman B, Cao X, Jing X, Ramnarayanan K, Brenner JC, Yu J, Kim JH, Han B, Tan P, Kumar-Sinha C, Lonigro RJ, Palanisamy N, Maher CA, Chinnaiyan AM, Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/22991213/ Histone lysine methyltransferase, SUV39H1, promotes HCC progression and is negatively regulated by microRNA-125b. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/23807219/ Gossypol and an HMT G9a inhibitor act in synergy to induce cell death in pancreatic cancer cells. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/23981787/ Sox4, EMT programs, and the metastatic progression of breast cancers: mastering the masters of EMT. causal interaction 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25613390/ The H3K9 Methyltransferase G9a Represses E-cadherin and is Associated with Myometrial Invasion in Endometrial Cancer. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25877750/ Overexpression of YB1 and EZH2 are associated with cancer metastasis and poor prognosis in renal cell carcinomas. causal interaction 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26648239/ A crucial epithelial to mesenchymal transition regulator, Sox4/Ezh2 axis is closely related to the clinical outcome in pancreatic cancer patients. causal interaction 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26846621/ Quantitative proteomic study of human prostate cancer cells with different metastatic potentials. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/27105109/ Role of EZH2 histone methyltrasferase in melanoma progression and metastasis. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/27164857/ Dysregulation of the epigenetic regulator SETDB1 in liver carcinogenesis-more than one way to skin a cat. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28977928/ Methyltransferase G9a promotes cervical cancer angiogenesis and decreases patient survival. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29449539/ G9A promotes gastric cancer metastasis by upregulating ITGB3 in a SET domain-independent manner. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30483750/ SETDB1 induces epithelial?mesenchymal transition in breast carcinoma by directly binding with Snail promoter. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31579098/ DZNep inhibits Hif-1? and Wnt signalling molecules to attenuate the proliferation and invasion of BGC-823 gastric cancer cells. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32477831/ Frequent upregulation of G9a promotes RelB-dependent proliferation and survival in multiple myeloma. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33298547/ G9a Promotes Invasion and Metastasis of Non-Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-?B Signaling Pathway. causal interaction 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33387131/ BIX-01294, a G9a inhibitor, suppresses cell proliferation by inhibiting autophagic flux in nasopharyngeal carcinoma cells. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33938943/ G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death. causal interaction 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. diagnostic usage 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25115793/ The H3K9 methyltransferase G9a is a marker of aggressive ovarian cancer that promotes peritoneal metastasis. diagnostic usage 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. diagnostic usage 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. diagnostic usage 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. diagnostic usage 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28319045/ AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. diagnostic usage 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28817916/ Re: AKT-Mediated Stabilization of Histone Methyltransferase WHSC1 Promotes Prostate Cancer Metastasis. diagnostic usage 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/34164392/ Histone Methyltransferase SETD1A Induces Epithelial-Mesenchymal Transition to Promote Invasion and Metastasis Through Epigenetic Reprogramming of Snail in Gastric Cancer. diagnostic usage 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/15196462/ The functions of E(Z)/EZH2-mediated methylation of lysine 27 in histone H3. diagnostic usage 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. diagnostic usage 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. diagnostic usage 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. diagnostic usage 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/27164857/ Dysregulation of the epigenetic regulator SETDB1 in liver carcinogenesis-more than one way to skin a cat. diagnostic usage 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29449539/ G9A promotes gastric cancer metastasis by upregulating ITGB3 in a SET domain-independent manner. diagnostic usage 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. diagnostic usage 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. diagnostic usage 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. diagnostic usage 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. diagnostic usage 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. diagnostic usage 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33938943/ G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death. diagnostic usage 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25115793/ The H3K9 methyltransferase G9a is a marker of aggressive ovarian cancer that promotes peritoneal metastasis. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. therapeutic application 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25998860/ The histone methyltransferase EZH2 promotes mammary stem and luminal progenitor cell expansion, metastasis and inhibits estrogen receptor-positive cellular differentiation in a model of basal breast cancer. therapeutic application 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28319045/ AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. therapeutic application 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28817916/ Re: AKT-Mediated Stabilization of Histone Methyltransferase WHSC1 Promotes Prostate Cancer Metastasis. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29337058/ EHMT2 is a metastasis regulator in breast cancer. therapeutic application 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30545440/ SETDB1 regulates SMAD7 expression for breast cancer metastasis. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31720371/ Targeting Histone Methyltransferase DOT1L by a Novel Psammaplin A Analog Inhibits Growth and Metastasis of Triple-Negative Breast Cancer. therapeutic application 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/34164392/ Histone Methyltransferase SETD1A Induces Epithelial-Mesenchymal Transition to Promote Invasion and Metastasis Through Epigenetic Reprogramming of Snail in Gastric Cancer. therapeutic application 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/15225548/ SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/19008416/ Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/19285253/ Commentary on Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer Varambally S, Cao Q, Mani RS, Shankar S, Wang X, Ateeq B, Laxman B, Cao X, Jing X, Ramnarayanan K, Brenner JC, Yu J, Kim JH, Han B, Tan P, Kumar-Sinha C, Lonigro RJ, Palanisamy N, Maher CA, Chinnaiyan AM, Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/22562246/ Interaction with Suv39H1 is critical for Snail-mediated E-cadherin repression in breast cancer. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/22991213/ Histone lysine methyltransferase, SUV39H1, promotes HCC progression and is negatively regulated by microRNA-125b. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. therapeutic application 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. therapeutic application 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26846621/ Quantitative proteomic study of human prostate cancer cells with different metastatic potentials. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. therapeutic application 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. therapeutic application 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30483750/ SETDB1 induces epithelial?mesenchymal transition in breast carcinoma by directly binding with Snail promoter. therapeutic application 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32041674/ H3K27me3 and EZH2 expression in melanoma: relevance for melanoma progression and response to immune checkpoint blockade. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. therapeutic application 3 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32477831/ Frequent upregulation of G9a promotes RelB-dependent proliferation and survival in multiple myeloma. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33742125/ NSD2 promotes tumor angiogenesis through methylating and activating STAT3 protein. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33938943/ G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death. therapeutic application 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25373480/ Histone methyltransferase hSETD1A is a Novel Regulator of Metastasis in Breast Cancer. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25998860/ The histone methyltransferase EZH2 promotes mammary stem and luminal progenitor cell expansion, metastasis and inhibits estrogen receptor-positive cellular differentiation in a model of basal breast cancer. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28319045/ AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. ongoing research 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. ongoing research 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31720371/ Targeting Histone Methyltransferase DOT1L by a Novel Psammaplin A Analog Inhibits Growth and Metastasis of Triple-Negative Breast Cancer. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. ongoing research 1 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/15225548/ SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/22991213/ Histone lysine methyltransferase, SUV39H1, promotes HCC progression and is negatively regulated by microRNA-125b. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. ongoing research 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25070049/ MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway. ongoing research 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. ongoing research 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. ongoing research 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30483750/ SETDB1 induces epithelial?mesenchymal transition in breast carcinoma by directly binding with Snail promoter. ongoing research 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. ongoing research 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. ongoing research 4 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. ongoing research 2 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25115793/ The H3K9 methyltransferase G9a is a marker of aggressive ovarian cancer that promotes peritoneal metastasis. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25998860/ The histone methyltransferase EZH2 promotes mammary stem and luminal progenitor cell expansion, metastasis and inhibits estrogen receptor-positive cellular differentiation in a model of basal breast cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28817916/ Re: AKT-Mediated Stabilization of Histone Methyltransferase WHSC1 Promotes Prostate Cancer Metastasis. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30545440/ SETDB1 regulates SMAD7 expression for breast cancer metastasis. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/15225548/ SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/22562246/ Interaction with Suv39H1 is critical for Snail-mediated E-cadherin repression in breast cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/23504335/ High expressions of histone methylation- and phosphorylation-related proteins are associated with prognosis of oral squamous cell carcinoma in male population of Taiwan. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25070049/ MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28910750/ Analysis of methylation profiling data of hyperplasia and primary and metastatic endometrial cancers. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31012192/ LncRNA TRERNA1 facilitates hepatocellular carcinoma metastasis by dimethylating H3K9 in the CDH1 promoter region via the recruitment of the EHMT2/SNAI1 complex. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31042721/ The association and prognostic impact of enhancer of zeste homologue 2 expression and epithelial-mesenchymal transition in resected lung adenocarcinoma. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32041674/ H3K27me3 and EZH2 expression in melanoma: relevance for melanoma progression and response to immune checkpoint blockade. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33742125/ NSD2 promotes tumor angiogenesis through methylating and activating STAT3 protein. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25373480/ Histone methyltransferase hSETD1A is a Novel Regulator of Metastasis in Breast Cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29337058/ EHMT2 is a metastasis regulator in breast cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31720371/ Targeting Histone Methyltransferase DOT1L by a Novel Psammaplin A Analog Inhibits Growth and Metastasis of Triple-Negative Breast Cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33129761/ Su(var)3-9, Enhancer of Zeste, and Trithorax Domain-Containing 5 Facilitates Tumor Growth and Pulmonary Metastasis through Up-Regulation of AKT1 Signaling in Breast Cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/19008416/ Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/19285253/ Commentary on Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer Varambally S, Cao Q, Mani RS, Shankar S, Wang X, Ateeq B, Laxman B, Cao X, Jing X, Ramnarayanan K, Brenner JC, Yu J, Kim JH, Han B, Tan P, Kumar-Sinha C, Lonigro RJ, Palanisamy N, Maher CA, Chinnaiyan AM, Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/22991213/ Histone lysine methyltransferase, SUV39H1, promotes HCC progression and is negatively regulated by microRNA-125b. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/23807219/ Gossypol and an HMT G9a inhibitor act in synergy to induce cell death in pancreatic cancer cells. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/23981787/ Sox4, EMT programs, and the metastatic progression of breast cancers: mastering the masters of EMT. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25613390/ The H3K9 Methyltransferase G9a Represses E-cadherin and is Associated with Myometrial Invasion in Endometrial Cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25877750/ Overexpression of YB1 and EZH2 are associated with cancer metastasis and poor prognosis in renal cell carcinomas. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26648239/ A crucial epithelial to mesenchymal transition regulator, Sox4/Ezh2 axis is closely related to the clinical outcome in pancreatic cancer patients. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26846621/ Quantitative proteomic study of human prostate cancer cells with different metastatic potentials. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/27105109/ Role of EZH2 histone methyltrasferase in melanoma progression and metastasis. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/28977928/ Methyltransferase G9a promotes cervical cancer angiogenesis and decreases patient survival. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30483750/ SETDB1 induces epithelial?mesenchymal transition in breast carcinoma by directly binding with Snail promoter. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/31579098/ DZNep inhibits Hif-1? and Wnt signalling molecules to attenuate the proliferation and invasion of BGC-823 gastric cancer cells. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32477831/ Frequent upregulation of G9a promotes RelB-dependent proliferation and survival in multiple myeloma. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33298547/ G9a Promotes Invasion and Metastasis of Non-Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-?B Signaling Pathway. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33387131/ BIX-01294, a G9a inhibitor, suppresses cell proliferation by inhibiting autophagic flux in nasopharyngeal carcinoma cells. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/15196462/ The functions of E(Z)/EZH2-mediated methylation of lysine 27 in histone H3. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/27164857/ Dysregulation of the epigenetic regulator SETDB1 in liver carcinogenesis-more than one way to skin a cat. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29449539/ G9A promotes gastric cancer metastasis by upregulating ITGB3 in a SET domain-independent manner. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/34164392/ Histone Methyltransferase SETD1A Induces Epithelial-Mesenchymal Transition to Promote Invasion and Metastasis Through Epigenetic Reprogramming of Snail in Gastric Cancer. unassigned - 2.1.1.355 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33938943/ G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/14633678/ Inactivation of a histone methyltransferase by mutations in human cancers. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15235609/ SMYD3 encodes a histone methyltransferase involved in the proliferation of cancer cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16799634/ 5-Aza-2'-deoxycytidine-mediated reductions in G9A histone methyltransferase and histone H3 K9 di-methylation levels are linked to tumor suppressor gene reactivation. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18446223/ Downregulation of histone H3 lysine 9 methyltransferase G9a induces centrosome disruption and chromosome instability in cancer cells. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19008416/ Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19285253/ Commentary on Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer Varambally S, Cao Q, Mani RS, Shankar S, Wang X, Ateeq B, Laxman B, Cao X, Jing X, Ramnarayanan K, Brenner JC, Yu J, Kim JH, Han B, Tan P, Kumar-Sinha C, Lonigro RJ, Palanisamy N, Maher CA, Chinnaiyan AM, Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20501857/ Histone methyltransferase gene SETD2 is a novel tumor suppressor gene in clear cell renal cell carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21175789/ Epigenetic regulation of signaling pathways in cancer: role of the histone methyltransferase EZH2. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21383990/ Regulation of the DNA Damage Response and Gene Expression by the Dot1L Histone Methyltransferase and the 53Bp1 Tumour Suppressor. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21385930/ The histone methyltransferase and putative oncoprotein MMSET is overexpressed in a large variety of human tumors. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22645312/ Histone methyltransferase NSD2/MMSET mediates constitutive NF-?B signaling for cancer cell proliferation, survival, and tumor growth via a feed-forward loop. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23159737/ Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23210854/ Histone methyltransferase inhibitors: novel epigenetic agents for cancer treatment. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24292603/ The histone methyltransferase EZH2, an oncogene common to benign and malignant parathyroid tumors. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25168426/ Involvement of EZH2, SUV39H1, G9a and associated molecules in pathogenesis of urethane induced mouse lung tumors: potential targets for cancer control. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25884948/ Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26441991/ Functional Role of G9a Histone Methyltransferase in Cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26609488/ The histone methyltransferase DOT1L: regulatory functions and a cancer therapy target. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26848522/ The transcription factor GATA1 and the histone methyltransferase SET7 interact to promote VEGF-mediated angiogenesis and tumor growth and predict clinical outcome of breast cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27179746/ Role of the EZH2 histone methyltransferase as a therapeutic target in cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28182322/ Somatic cancer mutations in the MLL1 histone methyltransferase modulate its enzymatic activity and dependence on the WDR5/RBBP5/ASH2L complex. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28746871/ The Histone Methyltransferase Ezh2 Controls Mechanisms of Adaptive Resistance to Tumor Immunotherapy. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28978137/ The histone methyltransferase EZH2 as a druggable target in SHH medulloblastoma cancer stem cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32231741/ Histone methyltransferase SETD2: a potential tumor suppressor in solid cancers. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32291851/ Histone methyltransferase SETD1A interacts with HIF1? to enhance glycolysis and promote cancer progression in gastric cancer. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32391195/ The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32859239/ Histone methyltransferase and drug resistance in cancers. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33129761/ Su(var)3-9, Enhancer of Zeste, and Trithorax Domain-Containing 5 Facilitates Tumor Growth and Pulmonary Metastasis through Up-Regulation of AKT1 Signaling in Breast Cancer. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33223508/ Histone methyltransferase SETD2 inhibits tumor growth via suppressing CXCL1-mediated activation of cell cycle in lung adenocarcinoma. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33632299/ Chromatin remodeling by the histone methyltransferase EZH2 drives lung pre-malignancy and is a target for cancer prevention. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33665162/ Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33953401/ Epigenetic silencing by SETDB1 suppresses tumour intrinsic immunogenicity. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34194626/ Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15196462/ The functions of E(Z)/EZH2-mediated methylation of lysine 27 in histone H3. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16007202/ The polycomb group protein enhancer of zeste homolog 2 (EZH 2) is an oncogene that influences myeloma cell growth and the mutant ras phenotype. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16195383/ Menin regulates pancreatic islet growth by promoting histone methylation and expression of genes encoding p27Kip1 and p18INK4c. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16497704/ Histone H3 lysine 9 and H4 lysine 20 trimethylation and the expression of Suv4-20h2 and Suv-39h1 histone methyltransferases in hepatocarcinogenesis induced by methyl deficiency in rats. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16953217/ RIZ1 repression is associated with insulin-like growth factor-1 signaling activation in chronic myeloid leukemia cell lines. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/17245754/ Loss of RB compromises specific heterochromatin modifications and modulates HP1alpha dynamics. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/17453341/ EZH2 regulates the transcription of estrogen-responsive genes through association with REA, an estrogen receptor corepressor. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19128641/ Epigenetic perspective into head and neck cancer through in silico gene expression profiling of histone lysine methyltransferases. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19472189/ Effects of SMYD3 overexpression on transformation, serum dependence, and apoptosis sensitivity in NIH3T3 cells. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19799859/ RNA interference targeting against S100A4 suppresses cell growth and motility and induces apoptosis in human pancreatic cancer cells. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20081860/ Somatic mutations altering EZH2 (Tyr641) in follicular and diffuse large B-cell lymphomas of germinal-center origin. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20601953/ Inactivating mutations of the histone methyltransferase gene EZH2 in myeloid disorders. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20614940/ Protein lysine methyltransferase G9a inhibitors: design, synthesis, and structure activity relationships of 2,4-diamino-7-aminoalkoxy-quinazolines. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20631058/ The role of EZH2 and DNA methylation in the silencing of the tumour suppressor RUNX3 in colorectal cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20861184/ Histone Methyltransferase MLL1 Regulates MDR1 Transcription and Chemoresistance. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20864510/ ANCCA/ATAD2 Overexpression Identifies Breast Cancer Patients with Poor Prognosis, Acting to Drive Proliferation and Survival of Triple-Negative Cells through Control of B-Myb and EZH2. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21493592/ Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21659531/ Cyclin-dependent Kinase 1 (CDK1)-mediated Phosphorylation of Enhancer of Zeste 2 (Ezh2) Regulates Its Stability. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21780790/ Optimization of Cellular Activity of G9a Inhibitors 7-Aminoalkoxy-quinazolines. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22040993/ [An update on epigenetic regulator gene mutations and pathogenesis of myelodysplasic syndromes]. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22330138/ The SRA protein UHRF1 promotes epigenetic crosstalks and is involved in prostate cancer progression. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22505352/ Clinically significant copy number alterations and complex rearrangements of MYB and NFIB in head and neck adenoid cystic carcinoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22505648/ Polycomb protein EZH2 regulates tumor invasion via the transcriptional repression of the metastasis suppressor RKIP in breast and prostate cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22662197/ Enhancer of zeste homolog 2 induces pulmonary artery smooth muscle cell proliferation. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22740705/ Identification of somatic mutations in parathyroid tumors using whole-exome sequencing. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22751105/ Multiple myeloma-associated chromosomal translocation activates orphan snoRNA ACA11 to suppress oxidative stress. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22797064/ The histone methyltransferase MMSET/WHSC1 activates TWIST1 to promote an epithelial-mesenchymal transition and invasive properties of prostate cancer. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22972034/ MMSET stimulates myeloma cell growth through microRNA-mediated modulation of c-MYC. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22991213/ Histone lysine methyltransferase, SUV39H1, promotes HCC progression and is negatively regulated by microRNA-125b. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23110793/ Poorly differentiated synovial sarcoma is associated with high expression of enhancer of zeste homologue 2 (EZH2). causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23400519/ Improved therapeutic effect against leukemia by a combination of the histone methyltransferase inhibitor chaetocin and the histone deacetylase inhibitor trichostatin A. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23421437/ Sorafenib suppresses growth and survival of hepatoma cells by accelerating degradation of enhancer of zeste homolog 2. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23424038/ Role of STAT3 and Vitamin D Receptor in EZH2-mediated invasion of human colorectal cancer. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23509280/ Methylation of SUV39H1 by SET7/9 results in heterochromatin relaxation and genome instability. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23636686/ EZH2, an epigenetic driver of prostate cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23644490/ Multifaceted role of EZH2 in breast and prostate tumorigenesis: epigenetics and beyond. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23705022/ The histone methyltransferase SUV39H1 suppresses embryonal rhabdomyosarcoma formation in zebrafish. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23807219/ Gossypol and an HMT G9a inhibitor act in synergy to induce cell death in pancreatic cancer cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23907130/ Polycomb repressive complex 2 contributes to DNA double-strand break repair. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23943221/ Role of Histone Lysine Methyltransferases SUV39H1 and SETDB1 in Gliomagenesis: Modulation of Cell Proliferation, Migration, and Colony Formation. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23981787/ Sox4, EMT programs, and the metastatic progression of breast cancers: mastering the masters of EMT. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24151879/ The Discovery of Novel Histone Lysine Methyltransferase G9a Inhibitors (Part 1): Molecular Design Based on a Series of Substituted 2,4-Diamino-7-aminoalkoxyquinazoline by Molecular-Docking-Guided 3D Quantitative Structure-Activity Relationship Studies. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24183969/ Identification of EZH2 and EZH1 small molecule inhibitors with selective impact on diffuse large B cell lymphoma cell growth. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24184908/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24212330/ Cancer-associated fibroblasts enhance the migration ability of ovarian cancer cells by increasing EZH2 expression. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24322755/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24391143/ Kinesin Family Deregulation Coordinated by Bromodomain Protein ANCCA and Histone Methyltransferase MLL for Breast Cancer Cell Growth, Survival, and Tamoxifen Resistance. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24691023/ Impact of EZH2 Polymorphisms on Urothelial Cell Carcinoma Susceptibility and Clinicopathologic Features. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24844570/ Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24852755/ 3-Deazaneplanocin A (DZNep), an inhibitor of the histone methyltransferase EZH2, induces apoptosis and reduces cell migration in chondrosarcoma cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24874471/ Identification of druggable cancer driver genes amplified across TCGA datasets. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24912396/ EZH2: an emerging role in melanoma biology and strategies for targeted therapy. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24925220/ Frameshift mutation of a histone methylation-related gene SETD1B and its regional heterogeneity in gastric and colorectal cancers with high microsatellite instability. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24983772/ Histone H3K4 methyltransferase Mll1 regulates protein glycosylation and tunicamycin-induced apoptosis through transcriptional regulation. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25027955/ Inhibition of G9a induces DUSP4-dependent autophagic cell death in head and neck squamous cell carcinoma. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25071150/ The hypoxia-inducible epigenetic regulators Jmjd1a and G9a provide a mechanistic link between angiogenesis and tumor growth. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25131201/ A macrohistone variant links dynamic chromatin compaction to BRCA1-dependent genome maintenance. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25131810/ Overexpression of EZH2 associates with a poor prognosis in chronic lymphocytic leukemia. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25415657/ Analysis of the antiproliferative effects of 3-deazaneoplanocin A in combination with standard anticancer agents in rhabdoid tumor cell lines. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25437343/ NNK-induced DNA methyltransferase 1 in lung tumorigenesis in A/J mice and inhibitory effects of (-)-epigallocatechin-3-gallate. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25472580/ SMYD3 overexpression was a risk factor in the biological behavior and prognosis of gastric carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25505154/ Quantitative Nuclear Proteomics Identifies that miR-137-mediated EZH2 Reduction Regulates Resveratrol-induced Apoptosis of Neuroblastoma Cells. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25535899/ EZH2 inhibition enhances the efficacy of an EGFR inhibitor in suppressing colon cancer cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25549357/ EZH2 regulates cofilin activity and colon cancer cell migration by targeting ITGA2 gene. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25595900/ Down-regulation of G9a triggers DNA damage response and inhibits colorectal cancer cells proliferation. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25602259/ Emerging role of linker histone variant H1x as a biomarker with prognostic value in astrocytic gliomas. A multivariate analysis including trimethylation of H3K9 and H4K20. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25613390/ The H3K9 Methyltransferase G9a Represses E-cadherin and is Associated with Myometrial Invasion in Endometrial Cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25671303/ Epigenetic reprogramming by tumor-derived EZH2 gain-of-function mutations promotes aggressive 3D cell morphologies and enhances melanoma tumor growth. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25710335/ Biochemical Assay Development for Histone Methyltransferases Using a Transcreener-Based Assay for S-Adenosylhomocysteine. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25739318/ The polycomb group protein EZH2 is a novel therapeutic target for cervical cancer. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25877750/ Overexpression of YB1 and EZH2 are associated with cancer metastasis and poor prognosis in renal cell carcinomas. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25893294/ Development of secondary mutations in wild-type and mutant EZH2 alleles cooperates to confer resistance to EZH2 inhibitors. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25978433/ The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26013382/ The Histone Methyltransferase Inhibitor BIX01294 Inhibits HIF-1? Stability and Angiogenesis. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26040698/ A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26147105/ The Histone Methyltransferase Inhibitor A-366 Uncovers a Role for G9a/GLP in the Epigenetics of Leukemia. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26151044/ Inhibition of Nuclear Receptor Binding SET Domain 2/Multiple Myeloma SET Domain by LEM-06 Implication for Epigenetic Cancer Therapies. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26292256/ Two Loops Undergoing Concerted Dynamics Regulate the Activity of the ASH1L Histone Methyltransferase. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26336998/ TERT promoter mutations in primary liver tumors. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26444031/ Inhibition of H3K9 histone methyltransferase G9a attenuates renal fibrosis and retains klotho expression. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26463831/ Studies Identify Non-Hodgkin Lymphoma Suppressor. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26500027/ Targeting Suppressor of Variegation 3-9 Homologue 2 (SUV39H2) in Acute Lymphoblastic Leukemia (ALL). causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26552009/ SWI/SNF-mutant cancers depend on catalytic and non-catalytic activity of EZH2. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26568301/ Variants of ubiquitin-specific peptidase 24 play a crucial role in lung cancer malignancy. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26648239/ A crucial epithelial to mesenchymal transition regulator, Sox4/Ezh2 axis is closely related to the clinical outcome in pancreatic cancer patients. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26697392/ Identification of PRDM2 regulated genes in quiescent C2C12 myoblasts. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26765460/ Association of Histone Methyltransferase G9a and Overall Survival After Liver Resection of Patients With Hepatocellular Carcinoma With a Median Observation of 40 Months. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26771714/ MMSET is dynamically regulated during cell-cycle progression and promotes normal DNA replication. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26883360/ Mutation of cancer driver MLL2 results in transcription stress and genome instability. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27034728/ Global histone modification profiling reveals the epigenomic dynamics during malignant transformation in a four-stage breast cancer model. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27081761/ Depletion of G9a gene induces cell apoptosis in human gastric carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27174920/ Inhibition of EHMT2/G9a epigenetically increases the transcription of Beclin-1 via an increase in ROS and activation of NF-?B. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27223432/ Morphoproteomics and biomedical analytics confirm the mTORC2/Akt pathway as a resistance signature and activated ERK and STAT3 as concomitant prosurvival/antiapoptotic pathways in metastatic renal cell carcinoma (RCC) progressing on rapalogs: Pathogenesis. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27399922/ EZH2 Protein Expression and Tumor Response to Neoadjuvant Chemotherapy in Locally Advanced Breast Cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27468692/ DNA-PK-mediated phosphorylation of EZH2 regulates the DNA damage-induced apoptosis to maintain T-cell genomic integrity. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27555605/ Initial testing (stage 1) of tazemetostat (EPZ-6438), a novel EZH2 inhibitor, by the Pediatric Preclinical Testing Program. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27604143/ NSD2 contributes to oncogenic RAS-driven transcription in lung cancer cells through long-range epigenetic activation. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27605386/ miR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27698795/ Whole-exome sequencing identifies variants in invasive pituitary adenomas. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27843326/ MLL1 promotes cervical carcinoma cell tumorigenesis and metastasis through interaction with ?-catenin. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28278257/ Inhibition of H3K9 methyltransferase G9a ameliorates methylglyoxal-induced peritoneal fibrosis. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28459432/ Metformin inhibits SUV39H1-mediated migration of prostate cancer cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28692054/ Modeling cancer driver events in vitro using barrier bypass-clonal expansion assays and massively parallel sequencing. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28785086/ MUC1-C activates EZH2 expression and function in human cancer cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28795320/ EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28819251/ G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28864533/ First critical repressive H3K27me3 marks in embryonic stem cells identified using designed protein inhibitor. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28887438/ ---Silencing of retrotransposons by SETDB1 inhibits the interferon response in acute myeloid leukemia-. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28913972/ Significance of histone methyltransferase SETDB1 expression in colon adenocarcinoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28943305/ Targeting the cancer epigenome: synergistic therapy with bromodomain inhibitors. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28977928/ Methyltransferase G9a promotes cervical cancer angiogenesis and decreases patient survival. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29113759/ Pharmacological and transcriptional inhibition of the G9a histone methyltransferase suppresses proliferation and modulates redox homeostasis in human microvascular endothelial cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29145444/ Inhibition of the H3K9 methyltransferase G9A attenuates oncogenicity and activates the hypoxia signaling pathway. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29233829/ Smad3-mediated recruitment of the methyltransferase SETDB1/ESET controls causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29302370/ ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29374157/ Targeting EHMT2 reverses EGFR-TKI resistance in NSCLC by epigenetically regulating the PTEN/AKT signaling pathway. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29408993/ Effects of histone methyltransferase inhibition in endometriosis. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29449539/ G9A promotes gastric cancer metastasis by upregulating ITGB3 in a SET domain-independent manner. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29473431/ Enhancer of zeste homolog 2 (EZH2) inhibitors. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29627316/ KMT2D Mutation Is Associated With Poor Prognosis in Non-Small-Cell Lung Cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29724721/ SETD2 Is Recurrently Mutated in Whole-Exome Sequenced Canine Osteosarcoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29739365/ Histone methyltransferase SETDB1 promotes cells proliferation and migration by interacting withTiam1 in hepatocellular carcinoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29742153/ Identification of a peptide inhibitor for the histone methyltransferase WHSC1. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29805595/ Clinicopathological significance of G9A expression in colorectal carcinoma. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29848731/ Prevalence of Enhancer of Zeste Homolog 2 in Patients with Resected Small Cell Lung Cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29864144/ Impact of OGT deregulation on EZH2 target genes FOXA1 and FOXC1 expression in breast cancer cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29872311/ The methylation profiles of PRDM promoters in non-small cell lung cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29897144/ Surveillance of Retroelement Expression and Nucleic-Acid Immunity by Histone Methyltransferase SETDB1. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30013191/ Methylation of Aurora kinase A by MMSET reduces p53 stability and regulates cell proliferation and apoptosis. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30117667/ Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30185548/ Dual Inhibition of DNA and Histone Methyltransferases Increases Viral Mimicry in Ovarian Cancer Cells. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30214616/ Increased EZH2 expression during the adenoma-carcinoma sequence in colorectal cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30218753/ Aberrant differential expression of EZH2 and H3K27me3 in extranodal NK/T-cell lymphoma, nasal type is associated with disease progression and prognosis. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30263847/ SMYD3-associated pathway is involved in the anti-tumor effects of sulforaphane on gastric carcinoma cells. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30305431/ Reduced miR-125a-5p level in non-small-cell lung cancer is associated with tumour progression. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30323973/ Preprogramming therapeutic response of PI3K/mTOR dual inhibitor via the regulation of EHMT2 and p27 in pancreatic cancer. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30393995/ Common origin of sequential cutaneous CD30+ lymphoproliferations with nodal involvement evidenced by genome-wide clonal evolution. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30455465/ H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30555699/ EZH2 as a therapeutic target for multiple myeloma and other haematological malignancies. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30692625/ AKT methylation by SETDB1 promotes AKT kinase activity and oncogenic functions. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30761216/ Targeting EZH2 in Multiple Myeloma-Multifaceted Anti-Tumor Activity. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30833420/ Epigenetic Regulation of the PTEN-AKT-RAC1 Axis by G9a Is Critical for Tumor Growth in Alveolar Rhabdomyosarcoma. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30968962/ BRCA1 and EZH2 cooperate in regulation of prostate cancer stem cell phenotype. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30990809/ Genetic mutational status of genes regulating epigenetics: Role of the histone methyltransferase KMT2D in triple negative breast tumors. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31050579/ Fine-tuning AKT kinase activity through direct lysine methylation. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31090199/ KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31127101/ Selective binding of the PHD6 finger of MLL4 to histone H4K16ac links MLL4 and MOF. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31223458/ Discovery of Irreversible Inhibitors Targeting Histone Methyltransferase, SMYD3. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31232159/ Loss of KMT2D induces prostate cancer ROS-mediated DNA damage by suppressing the enhancer activity and DNA binding of antioxidant transcription factor FOXO3. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31306481/ Histone Methyltransferase SETDB1 Promotes Colorectal Cancer Proliferation through the STAT1-CCND1/CDK6 Axis. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31338003/ In vivo administration of G9a inhibitor A366 decreases osteogenic potential of bone marrow-derived mesenchymal stem cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31417652/ Overexpression of SMYD3 in Ovarian Cancer is Associated with Ovarian Cancer Proliferation and Apoptosis via Methylating H3K4 and H4K20. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31422102/ SETDB1 modulates the differentiation of both the crystal cells and the lamellocytes in Drosophila. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31434093/ Inhibition of Euchromatic Histone Lysine Methyltransferase 2 (EHMT2) Suppresses the Proliferation and Invasion of Cervical Cancer Cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31465303/ Precocious neuronal differentiation and disrupted oxygen responses in Kabuki syndrome. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31521697/ Targeting epigenetic machinery: Emerging novel allosteric inhibitors. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31579098/ DZNep inhibits Hif-1? and Wnt signalling molecules to attenuate the proliferation and invasion of BGC-823 gastric cancer cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31579944/ Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31599405/ EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31654063/ SETD3 is regulated by a couple of microRNAs and plays opposing roles in proliferation and metastasis of hepatocellular carcinoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31768101/ Knockdown of SET Domain, Bifurcated 1 suppresses head and neck cancer cell viability and wound-healing ability in vitro. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31776268/ Human Papillomavirus E7 Oncoprotein Subverts Host Innate Immunity via SUV39H1-Mediated Epigenetic Silencing of Immune Sensor Genes. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31877341/ Combining epigenetic and immune therapy to overcome cancer resistance. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32062438/ Arsenic and benzo[a]pyrene co-exposure acts synergistically in inducing cancer stem cell-like property and tumorigenesis by epigenetically down-regulating SOCS3 expression. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32095117/ Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32103168/ SMURF2 prevents detrimental changes to chromatin, protecting human dermal fibroblasts from chromosomal instability and tumorigenesis. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32174799/ EHMT2/G9a Inhibits Aortic Smooth Muscle Cell Death by Suppressing Autophagy Activation. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32269030/ Gain-of-Function Genetic Alterations of G9a Drive Oncogenesis. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32445185/ The Promise for Histone Methyltransferase Inhibitors for Epigenetic Therapy in Clinical Oncology: A Narrative Review. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32477831/ Frequent upregulation of G9a promotes RelB-dependent proliferation and survival in multiple myeloma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32486217/ SETDB1-Mediated Silencing of Retroelements. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32684241/ Euchromatin histone methyltransferase II (EHMT2) regulates the expression of ras-related GTP binding C (RRAGC) protein. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32723083/ The complex role of EZH2 in the tumor microenvironment: opportunities and challenges for immunotherapy combinations. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32889036/ Epigenetic priming by EHMT1/EHMT2 in acute lymphoblastic leukemia induces TP53 and TP73 overexpression and promotes cell death. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32934721/ The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32972752/ Knockout of SETDB1 gene using the CRISPR/cas-9 system increases migration and transforming activities via complex regulations of E-cadherin, ?-catenin, STAT3, and Akt. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33059737/ SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33086062/ Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33099471/ Deletion of Histone Methyltransferase G9a Suppresses Mutant Kras-driven Pancreatic Carcinogenesis. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33121982/ Whole-proteome analysis of mesonephric-derived cancers describes new potential biomarkers. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33147463/ G9a Promotes Breast Cancer Recurrence through Repression of a Pro-inflammatory Program. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33159839/ KMT2C promoter methylation in plasma-circulating tumor DNA is a prognostic biomarker in non-small cell lung cancer. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33168810/ EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33232890/ Structural basis for PRC2 engagement with chromatin. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33330479/ Deficiency of G9a Inhibits Cell Proliferation and Activates Autophagy via Transcriptionally Regulating c-Myc Expression in Glioblastoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33387131/ BIX-01294, a G9a inhibitor, suppresses cell proliferation by inhibiting autophagic flux in nasopharyngeal carcinoma cells. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33530253/ Prognostic value of lymphocyte-to-monocyte ratio and histone methyltransferase G9a histone methyltransferase in patients with double expression lymphoma: A retrospective observational study. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33589432/ G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33681705/ Targeting FBXO44/SUV39H1 elicits tumor cell-specific DNA replication stress and viral mimicry. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33910928/ Multilevel Regulation of ?-Catenin Activity by SETD2 Suppresses the Transition from Polycystic Kidney Disease to Clear Cell Renal Cell Carcinoma. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33938943/ G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34249932/ Inactivation of the Euchromatic Histone-Lysine N-Methyltransferase 2 Pathway in Pancreatic Epithelial Cells Antagonizes Cancer Initiation and Pancreatitis-Associated Promotion by Altering Growth and Immune Gene Expression Networks. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34294888/ Exosomal miR-101-3p and miR-423-5p inhibit medulloblastoma tumorigenesis through targeting FOXP4 and EZH2. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34326167/ WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. causal interaction 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34357103/ High WHSC1L1 Expression Reduces Survival Rates in Operated Breast Cancer Patients with Decreased CD8+ T Cells: Machine Learning Approach. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34425630/ Histone methyltransferase Ezh2 negatively regulates NK cell terminal maturation and function. causal interaction 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34428935/ Wolf-Hirschhorn syndrome candidate 1 facilitates alveolar macrophage pyroptosis in sepsis-induced acute lung injury through NEK7-mediated NLRP3 inflammasome activation. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34462284/ Targeting the Atf7ip-Setdb1 complex augments antitumor immunity by boosting tumor immunogenicity. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34479190/ Targeting of cyclin-dependent kinases in atypical teratoid rhabdoid tumors with multikinase inhibitor TG02. causal interaction 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34531375/ PRMT5 regulates cell pyroptosis by silencing CASP1 in multiple myeloma. causal interaction 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18723033/ Roles of the EZH2 histone methyltransferase in cancer epigenetics. diagnostic usage 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21385930/ The histone methyltransferase and putative oncoprotein MMSET is overexpressed in a large variety of human tumors. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21539681/ Validation of the histone methyltransferase EZH2 as a therapeutic target for various types of human cancer and as a prognostic marker. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22645312/ Histone methyltransferase NSD2/MMSET mediates constitutive NF-?B signaling for cancer cell proliferation, survival, and tumor growth via a feed-forward loop. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23159737/ Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25179367/ Targeting histone methyltransferase EZH2 as cancer treatment. diagnostic usage 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25884948/ Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26848522/ The transcription factor GATA1 and the histone methyltransferase SET7 interact to promote VEGF-mediated angiogenesis and tumor growth and predict clinical outcome of breast cancer. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30503969/ MicroRNA-621 Acts as a Tumor Radiosensitizer by Directly Targeting SETDB1 in Hepatocellular Carcinoma. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32291851/ Histone methyltransferase SETD1A interacts with HIF1? to enhance glycolysis and promote cancer progression in gastric cancer. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32391195/ The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33665162/ Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15196462/ The functions of E(Z)/EZH2-mediated methylation of lysine 27 in histone H3. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16638127/ Differential expression of selected histone modifier genes in human solid cancers. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16687068/ [Inhibition of SMYD3 gene expression by RNA interference induces apoptosis in human hepatocellular carcinoma cell line HepG2] diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18819746/ Aberrant methylation of candidate tumor suppressor genes in neuroblastoma. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19128641/ Epigenetic perspective into head and neck cancer through in silico gene expression profiling of histone lysine methyltransferases. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21493592/ Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22068036/ EZH2 Mediates epigenetic silencing of neuroblastoma suppressor genes CASZ1, CLU, RUNX3, and NGFR. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22199269/ Histone-modifier gene expression profiles are associated with pathological and clinical outcomes in human breast cancer. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22330138/ The SRA protein UHRF1 promotes epigenetic crosstalks and is involved in prostate cancer progression. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22406368/ High expression of trimethylated histone H3 lysine 4 is associated with poor prognosis in hepatocellular carcinoma. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22505648/ Polycomb protein EZH2 regulates tumor invasion via the transcriptional repression of the metastasis suppressor RKIP in breast and prostate cancer. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23636686/ EZH2, an epigenetic driver of prostate cancer. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23943221/ Role of Histone Lysine Methyltransferases SUV39H1 and SETDB1 in Gliomagenesis: Modulation of Cell Proliferation, Migration, and Colony Formation. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24183969/ Identification of EZH2 and EZH1 small molecule inhibitors with selective impact on diffuse large B cell lymphoma cell growth. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24391143/ Kinesin Family Deregulation Coordinated by Bromodomain Protein ANCCA and Histone Methyltransferase MLL for Breast Cancer Cell Growth, Survival, and Tamoxifen Resistance. diagnostic usage 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24874471/ Identification of druggable cancer driver genes amplified across TCGA datasets. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24925220/ Frameshift mutation of a histone methylation-related gene SETD1B and its regional heterogeneity in gastric and colorectal cancers with high microsatellite instability. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25437343/ NNK-induced DNA methyltransferase 1 in lung tumorigenesis in A/J mice and inhibitory effects of (-)-epigallocatechin-3-gallate. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25472580/ SMYD3 overexpression was a risk factor in the biological behavior and prognosis of gastric carcinoma. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25499219/ The transcriptional repressor ZBTB4 regulates EZH2 through a MicroRNA-ZBTB4-specificity protein signaling axis. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25505154/ Quantitative Nuclear Proteomics Identifies that miR-137-mediated EZH2 Reduction Regulates Resveratrol-induced Apoptosis of Neuroblastoma Cells. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26765460/ Association of Histone Methyltransferase G9a and Overall Survival After Liver Resection of Patients With Hepatocellular Carcinoma With a Median Observation of 40 Months. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27223432/ Morphoproteomics and biomedical analytics confirm the mTORC2/Akt pathway as a resistance signature and activated ERK and STAT3 as concomitant prosurvival/antiapoptotic pathways in metastatic renal cell carcinoma (RCC) progressing on rapalogs: Pathogenesis. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27279906/ Recapitulating the Size and Cargo of Tumor Exosomes in a Tissue-Engineered Model. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27698795/ Whole-exome sequencing identifies variants in invasive pituitary adenomas. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28765327/ The KMT1A-GATA3-STAT3 circuit is a novel self-renewal signaling of human bladder cancer stem cells. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28819251/ G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28913972/ Significance of histone methyltransferase SETDB1 expression in colon adenocarcinoma. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29233829/ Smad3-mediated recruitment of the methyltransferase SETDB1/ESET controls diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29302370/ ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29449539/ G9A promotes gastric cancer metastasis by upregulating ITGB3 in a SET domain-independent manner. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29627316/ KMT2D Mutation Is Associated With Poor Prognosis in Non-Small-Cell Lung Cancer. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. diagnostic usage 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29872311/ The methylation profiles of PRDM promoters in non-small cell lung cancer. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30772380/ A SUV39H1-low chromatin state characterises and promotes migratory properties of cervical cancer cells. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30968962/ BRCA1 and EZH2 cooperate in regulation of prostate cancer stem cell phenotype. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30990809/ Genetic mutational status of genes regulating epigenetics: Role of the histone methyltransferase KMT2D in triple negative breast tumors. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31090199/ KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31232159/ Loss of KMT2D induces prostate cancer ROS-mediated DNA damage by suppressing the enhancer activity and DNA binding of antioxidant transcription factor FOXO3. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31306481/ Histone Methyltransferase SETDB1 Promotes Colorectal Cancer Proliferation through the STAT1-CCND1/CDK6 Axis. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31417652/ Overexpression of SMYD3 in Ovarian Cancer is Associated with Ovarian Cancer Proliferation and Apoptosis via Methylating H3K4 and H4K20. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31434093/ Inhibition of Euchromatic Histone Lysine Methyltransferase 2 (EHMT2) Suppresses the Proliferation and Invasion of Cervical Cancer Cells. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31579944/ Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis. diagnostic usage 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31599405/ EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31654063/ SETD3 is regulated by a couple of microRNAs and plays opposing roles in proliferation and metastasis of hepatocellular carcinoma. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. diagnostic usage 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32095117/ Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death. diagnostic usage 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. diagnostic usage 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32934721/ The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. diagnostic usage 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33056982/ Long non-coding RNA CASC9 promotes gefitinib resistance in NSCLC by epigenetic repression of DUSP1. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33099471/ Deletion of Histone Methyltransferase G9a Suppresses Mutant Kras-driven Pancreatic Carcinogenesis. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33159839/ KMT2C promoter methylation in plasma-circulating tumor DNA is a prognostic biomarker in non-small cell lung cancer. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33530253/ Prognostic value of lymphocyte-to-monocyte ratio and histone methyltransferase G9a histone methyltransferase in patients with double expression lymphoma: A retrospective observational study. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33938943/ G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34326167/ WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. diagnostic usage 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34357103/ High WHSC1L1 Expression Reduces Survival Rates in Operated Breast Cancer Patients with Decreased CD8+ T Cells: Machine Learning Approach. diagnostic usage 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15235609/ SMYD3 encodes a histone methyltransferase involved in the proliferation of cancer cells. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19008416/ Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19285253/ Commentary on Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer Varambally S, Cao Q, Mani RS, Shankar S, Wang X, Ateeq B, Laxman B, Cao X, Jing X, Ramnarayanan K, Brenner JC, Yu J, Kim JH, Han B, Tan P, Kumar-Sinha C, Lonigro RJ, Palanisamy N, Maher CA, Chinnaiyan AM, Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21385930/ The histone methyltransferase and putative oncoprotein MMSET is overexpressed in a large variety of human tumors. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21539681/ Validation of the histone methyltransferase EZH2 as a therapeutic target for various types of human cancer and as a prognostic marker. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22036763/ Hydrogen peroxide induces Sp1 methylation and thereby suppresses cyclin B1 via recruitment of Suv39H1 and HDAC1 in cancer cells. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22645312/ Histone methyltransferase NSD2/MMSET mediates constitutive NF-?B signaling for cancer cell proliferation, survival, and tumor growth via a feed-forward loop. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23159737/ Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23210854/ Histone methyltransferase inhibitors: novel epigenetic agents for cancer treatment. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23868976/ Promoter occupancy of MLL1 histone methyltransferase seems to specify the proliferative and apoptotic functions of E2F1 in a tumour microenvironment. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24833465/ Histone methyltransferase G9a and H3K9 dimethylation inhibit the self-renewal of glioma cancer stem cells. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25168426/ Involvement of EZH2, SUV39H1, G9a and associated molecules in pathogenesis of urethane induced mouse lung tumors: potential targets for cancer control. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25179367/ Targeting histone methyltransferase EZH2 as cancer treatment. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25203626/ S-Adenosyl-L-methionine-competitive inhibitors of the histone methyltransferase EZH2 induce autophagy and enhance drug sensitivity in cancer cells. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25884948/ Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26441991/ Functional Role of G9a Histone Methyltransferase in Cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26609488/ The histone methyltransferase DOT1L: regulatory functions and a cancer therapy target. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26848522/ The transcription factor GATA1 and the histone methyltransferase SET7 interact to promote VEGF-mediated angiogenesis and tumor growth and predict clinical outcome of breast cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27179746/ Role of the EZH2 histone methyltransferase as a therapeutic target in cancer. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27551509/ ?Np63? modulates histone methyl transferase SETDB1 to transcriptionally repress target genes in cancers. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28248941/ Anticancer agents: Allosteric histone methyltransferase modulators block tumour growth. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28746871/ The Histone Methyltransferase Ezh2 Controls Mechanisms of Adaptive Resistance to Tumor Immunotherapy. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28978137/ The histone methyltransferase EZH2 as a druggable target in SHH medulloblastoma cancer stem cells. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29133140/ The histone methyltransferase G9a: a new therapeutic target in biliary tract cancer. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30503969/ MicroRNA-621 Acts as a Tumor Radiosensitizer by Directly Targeting SETDB1 in Hepatocellular Carcinoma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32231741/ Histone methyltransferase SETD2: a potential tumor suppressor in solid cancers. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32291851/ Histone methyltransferase SETD1A interacts with HIF1? to enhance glycolysis and promote cancer progression in gastric cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32391195/ The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32859239/ Histone methyltransferase and drug resistance in cancers. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33632299/ Chromatin remodeling by the histone methyltransferase EZH2 drives lung pre-malignancy and is a target for cancer prevention. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33665162/ Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33953401/ Epigenetic silencing by SETDB1 suppresses tumour intrinsic immunogenicity. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34194626/ Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15225548/ SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16007202/ The polycomb group protein enhancer of zeste homolog 2 (EZH 2) is an oncogene that influences myeloma cell growth and the mutant ras phenotype. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16195383/ Menin regulates pancreatic islet growth by promoting histone methylation and expression of genes encoding p27Kip1 and p18INK4c. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16497704/ Histone H3 lysine 9 and H4 lysine 20 trimethylation and the expression of Suv4-20h2 and Suv-39h1 histone methyltransferases in hepatocarcinogenesis induced by methyl deficiency in rats. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16638127/ Differential expression of selected histone modifier genes in human solid cancers. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16651450/ Menin links estrogen receptor activation to histone H3K4 trimethylation. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16687068/ [Inhibition of SMYD3 gene expression by RNA interference induces apoptosis in human hepatocellular carcinoma cell line HepG2] therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16953217/ RIZ1 repression is associated with insulin-like growth factor-1 signaling activation in chronic myeloid leukemia cell lines. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20601953/ Inactivating mutations of the histone methyltransferase gene EZH2 in myeloid disorders. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20861184/ Histone Methyltransferase MLL1 Regulates MDR1 Transcription and Chemoresistance. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20864510/ ANCCA/ATAD2 Overexpression Identifies Breast Cancer Patients with Poor Prognosis, Acting to Drive Proliferation and Survival of Triple-Negative Cells through Control of B-Myb and EZH2. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22040993/ [An update on epigenetic regulator gene mutations and pathogenesis of myelodysplasic syndromes]. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22199269/ Histone-modifier gene expression profiles are associated with pathological and clinical outcomes in human breast cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22330138/ The SRA protein UHRF1 promotes epigenetic crosstalks and is involved in prostate cancer progression. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22552406/ The expression and significance of the enhancer of zeste homolog 2 in lung adenocarcinoma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22991213/ Histone lysine methyltransferase, SUV39H1, promotes HCC progression and is negatively regulated by microRNA-125b. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23373415/ [The significance of histone modifications in malignant transformation]. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23400519/ Improved therapeutic effect against leukemia by a combination of the histone methyltransferase inhibitor chaetocin and the histone deacetylase inhibitor trichostatin A. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23705022/ The histone methyltransferase SUV39H1 suppresses embryonal rhabdomyosarcoma formation in zebrafish. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23826380/ EZH2-Mediated H3K27me3 Is Involved in Epigenetic Repression of Deleted in Liver Cancer 1 in Human Cancers. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23943221/ Role of Histone Lysine Methyltransferases SUV39H1 and SETDB1 in Gliomagenesis: Modulation of Cell Proliferation, Migration, and Colony Formation. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24184908/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24212330/ Cancer-associated fibroblasts enhance the migration ability of ovarian cancer cells by increasing EZH2 expression. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24322755/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24391143/ Kinesin Family Deregulation Coordinated by Bromodomain Protein ANCCA and Histone Methyltransferase MLL for Breast Cancer Cell Growth, Survival, and Tamoxifen Resistance. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24691023/ Impact of EZH2 Polymorphisms on Urothelial Cell Carcinoma Susceptibility and Clinicopathologic Features. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24844570/ Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24852755/ 3-Deazaneplanocin A (DZNep), an inhibitor of the histone methyltransferase EZH2, induces apoptosis and reduces cell migration in chondrosarcoma cells. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24912918/ Negative regulation of DAB2IP by Akt and SCFFbw7 pathways. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25131201/ A macrohistone variant links dynamic chromatin compaction to BRCA1-dependent genome maintenance. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25195579/ Epigenomic networking in drug development: from pathogenic mechanisms to pharmacogenomics. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25437343/ NNK-induced DNA methyltransferase 1 in lung tumorigenesis in A/J mice and inhibitory effects of (-)-epigallocatechin-3-gallate. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25472580/ SMYD3 overexpression was a risk factor in the biological behavior and prognosis of gastric carcinoma. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25490442/ DOTting the path to doom: how acceleration of histone methylation leads to leukemia. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25535899/ EZH2 inhibition enhances the efficacy of an EGFR inhibitor in suppressing colon cancer cells. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25549357/ EZH2 regulates cofilin activity and colon cancer cell migration by targeting ITGA2 gene. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25602259/ Emerging role of linker histone variant H1x as a biomarker with prognostic value in astrocytic gliomas. A multivariate analysis including trimethylation of H3K9 and H4K20. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25710335/ Biochemical Assay Development for Histone Methyltransferases Using a Transcreener-Based Assay for S-Adenosylhomocysteine. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25739318/ The polycomb group protein EZH2 is a novel therapeutic target for cervical cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25947258/ Genome-wide transcriptional profiling analysis reveals annexin A6 as a novel EZH2 target gene involving gastric cellular proliferation. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25978433/ The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26013382/ The Histone Methyltransferase Inhibitor BIX01294 Inhibits HIF-1? Stability and Angiogenesis. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26147105/ The Histone Methyltransferase Inhibitor A-366 Uncovers a Role for G9a/GLP in the Epigenetics of Leukemia. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26552009/ SWI/SNF-mutant cancers depend on catalytic and non-catalytic activity of EZH2. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26815947/ Structures of Nahuoic Acids B-E Produced in Culture by a Streptomyces sp. Isolated from a Marine Sediment and Evidence for the Inhibition of the Histone Methyl Transferase SETD8 in Human Cancer Cells by Nahuoic Acid A. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26898301/ The novel EZH2 inhibitor, GSK126, suppresses cell migration and angiogenesis via down-regulating VEGF-A. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27109020/ Epidrugs in the immunotherapy of cutaneous and uveal melanoma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27174920/ Inhibition of EHMT2/G9a epigenetically increases the transcription of Beclin-1 via an increase in ROS and activation of NF-?B. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27223432/ Morphoproteomics and biomedical analytics confirm the mTORC2/Akt pathway as a resistance signature and activated ERK and STAT3 as concomitant prosurvival/antiapoptotic pathways in metastatic renal cell carcinoma (RCC) progressing on rapalogs: Pathogenesis. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27371576/ An Achilles' Heel for MLL-Rearranged Leukemias: Writers and Readers of H3 Lysine 36 Dimethylation. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27555605/ Initial testing (stage 1) of tazemetostat (EPZ-6438), a novel EZH2 inhibitor, by the Pediatric Preclinical Testing Program. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27843326/ MLL1 promotes cervical carcinoma cell tumorigenesis and metastasis through interaction with ?-catenin. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28159833/ SETting the Stage for Cancer Development: SETD2 and the Consequences of Lost Methylation. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28278257/ Inhibition of H3K9 methyltransferase G9a ameliorates methylglyoxal-induced peritoneal fibrosis. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28429794/ Bone-in-culture array as a platform to model early-stage bone metastases and discover anti-metastasis therapies. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28444909/ The histone methyltransferase EZH2 is a therapeutic target in small cell carcinoma of the ovary, hypercalcaemic type. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28459432/ Metformin inhibits SUV39H1-mediated migration of prostate cancer cells. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28785086/ MUC1-C activates EZH2 expression and function in human cancer cells. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28819251/ G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28868353/ Dual epigenetic modifiers for cancer therapy. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28913972/ Significance of histone methyltransferase SETDB1 expression in colon adenocarcinoma. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28943305/ Targeting the cancer epigenome: synergistic therapy with bromodomain inhibitors. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29113759/ Pharmacological and transcriptional inhibition of the G9a histone methyltransferase suppresses proliferation and modulates redox homeostasis in human microvascular endothelial cells. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29145444/ Inhibition of the H3K9 methyltransferase G9A attenuates oncogenicity and activates the hypoxia signaling pathway. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29233829/ Smad3-mediated recruitment of the methyltransferase SETDB1/ESET controls therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29374157/ Targeting EHMT2 reverses EGFR-TKI resistance in NSCLC by epigenetically regulating the PTEN/AKT signaling pathway. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29408993/ Effects of histone methyltransferase inhibition in endometriosis. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29531826/ BIX-01294 sensitizes renal cancer Caki cells to TRAIL-induced apoptosis through downregulation of survivin expression and upregulation of DR5 expression. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29627316/ KMT2D Mutation Is Associated With Poor Prognosis in Non-Small-Cell Lung Cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29669287/ ZRANB1 Is an EZH2 Deubiquitinase and a Potential Therapeutic Target in Breast Cancer. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29739365/ Histone methyltransferase SETDB1 promotes cells proliferation and migration by interacting withTiam1 in hepatocellular carcinoma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29742153/ Identification of a peptide inhibitor for the histone methyltransferase WHSC1. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30013191/ Methylation of Aurora kinase A by MMSET reduces p53 stability and regulates cell proliferation and apoptosis. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30117667/ Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30171419/ Identification of protoberberine alkaloids as novel histone methyltransferase G9a inhibitors by structure-based virtual screening. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30305431/ Reduced miR-125a-5p level in non-small-cell lung cancer is associated with tumour progression. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30323973/ Preprogramming therapeutic response of PI3K/mTOR dual inhibitor via the regulation of EHMT2 and p27 in pancreatic cancer. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30455465/ H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30692625/ AKT methylation by SETDB1 promotes AKT kinase activity and oncogenic functions. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30718359/ Genome-wide screening and functional analysis identifies tumor suppressor long non-coding RNAs epigenetically silenced in hepatocellular carcinoma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30761216/ Targeting EZH2 in Multiple Myeloma-Multifaceted Anti-Tumor Activity. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30968962/ BRCA1 and EZH2 cooperate in regulation of prostate cancer stem cell phenotype. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30990809/ Genetic mutational status of genes regulating epigenetics: Role of the histone methyltransferase KMT2D in triple negative breast tumors. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31050579/ Fine-tuning AKT kinase activity through direct lysine methylation. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31090199/ KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31127101/ Selective binding of the PHD6 finger of MLL4 to histone H4K16ac links MLL4 and MOF. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31232159/ Loss of KMT2D induces prostate cancer ROS-mediated DNA damage by suppressing the enhancer activity and DNA binding of antioxidant transcription factor FOXO3. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31338003/ In vivo administration of G9a inhibitor A366 decreases osteogenic potential of bone marrow-derived mesenchymal stem cells. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31417652/ Overexpression of SMYD3 in Ovarian Cancer is Associated with Ovarian Cancer Proliferation and Apoptosis via Methylating H3K4 and H4K20. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31422102/ SETDB1 modulates the differentiation of both the crystal cells and the lamellocytes in Drosophila. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31434093/ Inhibition of Euchromatic Histone Lysine Methyltransferase 2 (EHMT2) Suppresses the Proliferation and Invasion of Cervical Cancer Cells. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31521697/ Targeting epigenetic machinery: Emerging novel allosteric inhibitors. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31579944/ Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31768101/ Knockdown of SET Domain, Bifurcated 1 suppresses head and neck cancer cell viability and wound-healing ability in vitro. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31776268/ Human Papillomavirus E7 Oncoprotein Subverts Host Innate Immunity via SUV39H1-Mediated Epigenetic Silencing of Immune Sensor Genes. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31877341/ Combining epigenetic and immune therapy to overcome cancer resistance. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32095117/ Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32103168/ SMURF2 prevents detrimental changes to chromatin, protecting human dermal fibroblasts from chromosomal instability and tumorigenesis. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32174799/ EHMT2/G9a Inhibits Aortic Smooth Muscle Cell Death by Suppressing Autophagy Activation. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32269620/ SET and MYND domain-containing protein 3 inhibits tumor cell sensitivity to cisplatin. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32445185/ The Promise for Histone Methyltransferase Inhibitors for Epigenetic Therapy in Clinical Oncology: A Narrative Review. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32477831/ Frequent upregulation of G9a promotes RelB-dependent proliferation and survival in multiple myeloma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32508971/ EZH2-inhibitor DZNep enhances apoptosis of renal tubular epithelial cells in presence and absence of cisplatin. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32684241/ Euchromatin histone methyltransferase II (EHMT2) regulates the expression of ras-related GTP binding C (RRAGC) protein. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32934721/ The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32972752/ Knockout of SETDB1 gene using the CRISPR/cas-9 system increases migration and transforming activities via complex regulations of E-cadherin, ?-catenin, STAT3, and Akt. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33056982/ Long non-coding RNA CASC9 promotes gefitinib resistance in NSCLC by epigenetic repression of DUSP1. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33059737/ SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33086062/ Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33147463/ G9a Promotes Breast Cancer Recurrence through Repression of a Pro-inflammatory Program. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33168810/ EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33277444/ The Histone Methyltransferase Gene G9A Is Regulated by Nuclear Receptor 4A1 in Alveolar Rhabdomyosarcoma Cells. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33330479/ Deficiency of G9a Inhibits Cell Proliferation and Activates Autophagy via Transcriptionally Regulating c-Myc Expression in Glioblastoma. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33589432/ G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33681705/ Targeting FBXO44/SUV39H1 elicits tumor cell-specific DNA replication stress and viral mimicry. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33938943/ G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. therapeutic application 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34326167/ WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34357103/ High WHSC1L1 Expression Reduces Survival Rates in Operated Breast Cancer Patients with Decreased CD8+ T Cells: Machine Learning Approach. therapeutic application 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34445452/ Inhibition of WHSC1 Allows for Reprogramming of the Immune Compartment in Prostate Cancer. therapeutic application 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34462284/ Targeting the Atf7ip-Setdb1 complex augments antitumor immunity by boosting tumor immunogenicity. therapeutic application 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15235609/ SMYD3 encodes a histone methyltransferase involved in the proliferation of cancer cells. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16682412/ The histone methyltransferase SETDB1 and the DNA methyltransferase DNMT3A interact directly and localize to promoters silenced in cancer cells. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18446223/ Downregulation of histone H3 lysine 9 methyltransferase G9a induces centrosome disruption and chromosome instability in cancer cells. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18980972/ Regulation of pancreatic tumor cell proliferation and chemoresistance by the histone methyltransferase enhancer of zeste homologue 2. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21383990/ Regulation of the DNA Damage Response and Gene Expression by the Dot1L Histone Methyltransferase and the 53Bp1 Tumour Suppressor. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21385930/ The histone methyltransferase and putative oncoprotein MMSET is overexpressed in a large variety of human tumors. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21847359/ Enhanced Expression of EHMT2 Is Involved in the Proliferation of Cancer Cells through Negative Regulation of SIAH1. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21892211/ Silencing of Kruppel-like factor 2 by the histone methyltransferase EZH2 in human cancer. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23159737/ Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23868976/ Promoter occupancy of MLL1 histone methyltransferase seems to specify the proliferative and apoptotic functions of E2F1 in a tumour microenvironment. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24726141/ The Histone Methyltransferase SMYD2 Methylates PARP1 and Promotes Poly(ADP-ribosyl)ation Activity in Cancer Cells. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25168426/ Involvement of EZH2, SUV39H1, G9a and associated molecules in pathogenesis of urethane induced mouse lung tumors: potential targets for cancer control. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26441991/ Functional Role of G9a Histone Methyltransferase in Cancer. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26848522/ The transcription factor GATA1 and the histone methyltransferase SET7 interact to promote VEGF-mediated angiogenesis and tumor growth and predict clinical outcome of breast cancer. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28532996/ Histone methyltransferase G9a promotes liver cancer development by epigenetic silencing of tumor suppressor gene RARRES3. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28746871/ The Histone Methyltransferase Ezh2 Controls Mechanisms of Adaptive Resistance to Tumor Immunotherapy. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29066607/ Cancer cells, on your histone marks, get SETDB1, silence retrotransposons, and go! ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30610059/ SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32291851/ Histone methyltransferase SETD1A interacts with HIF1? to enhance glycolysis and promote cancer progression in gastric cancer. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32391195/ The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34194626/ Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34336110/ Histone Methyltransferase G9a Promotes the Development of Renal Cancer through Epigenetic Silencing of Tumor Suppressor Gene SPINK5. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15225548/ SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16638127/ Differential expression of selected histone modifier genes in human solid cancers. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16687068/ [Inhibition of SMYD3 gene expression by RNA interference induces apoptosis in human hepatocellular carcinoma cell line HepG2] ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18819746/ Aberrant methylation of candidate tumor suppressor genes in neuroblastoma. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18977321/ Reconstructing the disease model and epigenetic networks for MLL-AF4 leukemia. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19128641/ Epigenetic perspective into head and neck cancer through in silico gene expression profiling of histone lysine methyltransferases. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19472189/ Effects of SMYD3 overexpression on transformation, serum dependence, and apoptosis sensitivity in NIH3T3 cells. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21493592/ Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21726809/ SHP2 tyrosine phosphatase converts parafibromin/Cdc73 from a tumor suppressor to an oncogenic driver. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22199269/ Histone-modifier gene expression profiles are associated with pathological and clinical outcomes in human breast cancer. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22406368/ High expression of trimethylated histone H3 lysine 4 is associated with poor prognosis in hepatocellular carcinoma. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22797064/ The histone methyltransferase MMSET/WHSC1 activates TWIST1 to promote an epithelial-mesenchymal transition and invasive properties of prostate cancer. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22991213/ Histone lysine methyltransferase, SUV39H1, promotes HCC progression and is negatively regulated by microRNA-125b. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23421437/ Sorafenib suppresses growth and survival of hepatoma cells by accelerating degradation of enhancer of zeste homolog 2. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23424038/ Role of STAT3 and Vitamin D Receptor in EZH2-mediated invasion of human colorectal cancer. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23644490/ Multifaceted role of EZH2 in breast and prostate tumorigenesis: epigenetics and beyond. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23770855/ Gene amplification of the histone methyltransferase SETDB1 contributes to human lung tumorigenesis. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23934277/ Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23943221/ Role of Histone Lysine Methyltransferases SUV39H1 and SETDB1 in Gliomagenesis: Modulation of Cell Proliferation, Migration, and Colony Formation. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24391143/ Kinesin Family Deregulation Coordinated by Bromodomain Protein ANCCA and Histone Methyltransferase MLL for Breast Cancer Cell Growth, Survival, and Tamoxifen Resistance. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24658378/ Immunohistochemistry for histone h3 lysine 9 methyltransferase and demethylase proteins in human melanomas. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24844570/ Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24852755/ 3-Deazaneplanocin A (DZNep), an inhibitor of the histone methyltransferase EZH2, induces apoptosis and reduces cell migration in chondrosarcoma cells. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24925220/ Frameshift mutation of a histone methylation-related gene SETD1B and its regional heterogeneity in gastric and colorectal cancers with high microsatellite instability. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25071150/ The hypoxia-inducible epigenetic regulators Jmjd1a and G9a provide a mechanistic link between angiogenesis and tumor growth. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25131810/ Overexpression of EZH2 associates with a poor prognosis in chronic lymphocytic leukemia. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25172130/ Using S-adenosyl-L-homocysteine capture compounds to characterize S-adenosyl-L-methionine and S-adenosyl-L-homocysteine binding proteins. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25404354/ SETDB1 accelerates tumourigenesis by regulating the WNT signalling pathway. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25437343/ NNK-induced DNA methyltransferase 1 in lung tumorigenesis in A/J mice and inhibitory effects of (-)-epigallocatechin-3-gallate. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25472580/ SMYD3 overexpression was a risk factor in the biological behavior and prognosis of gastric carcinoma. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25637186/ Functional regulation of hypoxia inducible factor-1? by SET9 lysine methyltransferase. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26040698/ A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26350217/ Cooperation between SMYD3 and PC4 drives a distinct transcriptional program in cancer cells. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26471002/ Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26542178/ Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26697392/ Identification of PRDM2 regulated genes in quiescent C2C12 myoblasts. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26765460/ Association of Histone Methyltransferase G9a and Overall Survival After Liver Resection of Patients With Hepatocellular Carcinoma With a Median Observation of 40 Months. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26815947/ Structures of Nahuoic Acids B-E Produced in Culture by a Streptomyces sp. Isolated from a Marine Sediment and Evidence for the Inhibition of the Histone Methyl Transferase SETD8 in Human Cancer Cells by Nahuoic Acid A. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26898301/ The novel EZH2 inhibitor, GSK126, suppresses cell migration and angiogenesis via down-regulating VEGF-A. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27843326/ MLL1 promotes cervical carcinoma cell tumorigenesis and metastasis through interaction with ?-catenin. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28692054/ Modeling cancer driver events in vitro using barrier bypass-clonal expansion assays and massively parallel sequencing. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28765327/ The KMT1A-GATA3-STAT3 circuit is a novel self-renewal signaling of human bladder cancer stem cells. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28819251/ G9a regulates breast cancer growth by modulating iron homeostasis through the repression of ferroxidase hephaestin. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28864533/ First critical repressive H3K27me3 marks in embryonic stem cells identified using designed protein inhibitor. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28868353/ Dual epigenetic modifiers for cancer therapy. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28887438/ ---Silencing of retrotransposons by SETDB1 inhibits the interferon response in acute myeloid leukemia-. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28913972/ Significance of histone methyltransferase SETDB1 expression in colon adenocarcinoma. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29113759/ Pharmacological and transcriptional inhibition of the G9a histone methyltransferase suppresses proliferation and modulates redox homeostasis in human microvascular endothelial cells. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29233829/ Smad3-mediated recruitment of the methyltransferase SETDB1/ESET controls ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29302370/ ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29374157/ Targeting EHMT2 reverses EGFR-TKI resistance in NSCLC by epigenetically regulating the PTEN/AKT signaling pathway. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29408993/ Effects of histone methyltransferase inhibition in endometriosis. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29531826/ BIX-01294 sensitizes renal cancer Caki cells to TRAIL-induced apoptosis through downregulation of survivin expression and upregulation of DR5 expression. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29627316/ KMT2D Mutation Is Associated With Poor Prognosis in Non-Small-Cell Lung Cancer. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29872311/ The methylation profiles of PRDM promoters in non-small cell lung cancer. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29897144/ Surveillance of Retroelement Expression and Nucleic-Acid Immunity by Histone Methyltransferase SETDB1. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30309377/ Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30772380/ A SUV39H1-low chromatin state characterises and promotes migratory properties of cervical cancer cells. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30897760/ A Systematic Pan-Cancer Analysis of Genetic Heterogeneity Reveals Associations with Epigenetic Modifiers. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30968962/ BRCA1 and EZH2 cooperate in regulation of prostate cancer stem cell phenotype. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31090199/ KMT2A histone methyltransferase contributes to colorectal cancer development by promoting cathepsin Z transcriptional activation. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31131878/ Histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31263101/ An ErbB2/c-Src axis links bioenergetics with PRC2 translation to drive epigenetic reprogramming and mammary tumorigenesis. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31417652/ Overexpression of SMYD3 in Ovarian Cancer is Associated with Ovarian Cancer Proliferation and Apoptosis via Methylating H3K4 and H4K20. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31422102/ SETDB1 modulates the differentiation of both the crystal cells and the lamellocytes in Drosophila. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31434093/ Inhibition of Euchromatic Histone Lysine Methyltransferase 2 (EHMT2) Suppresses the Proliferation and Invasion of Cervical Cancer Cells. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31599405/ EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31693439/ Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31811272/ A TGF-?-MTA1-SOX4-EZH2 signaling axis drives epithelial-mesenchymal transition in tumor metastasis. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32095117/ Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32103168/ SMURF2 prevents detrimental changes to chromatin, protecting human dermal fibroblasts from chromosomal instability and tumorigenesis. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32269620/ SET and MYND domain-containing protein 3 inhibits tumor cell sensitivity to cisplatin. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32360551/ SETDB1 Inhibits p53-Mediated Apoptosis and Is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32393761/ SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32473242/ Blocking histone methyltransferase SETDB1 inhibits tumorigenesis and enhances cetuximab sensitivity in colorectal cancer. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32934721/ The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33059737/ SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33086062/ Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33147463/ G9a Promotes Breast Cancer Recurrence through Repression of a Pro-inflammatory Program. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33159839/ KMT2C promoter methylation in plasma-circulating tumor DNA is a prognostic biomarker in non-small cell lung cancer. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33277444/ The Histone Methyltransferase Gene G9A Is Regulated by Nuclear Receptor 4A1 in Alveolar Rhabdomyosarcoma Cells. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33370431/ LINC00476 Suppresses the Progression of Non-Small Cell Lung Cancer by Inducing the Ubiquitination of SETDB1. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33530253/ Prognostic value of lymphocyte-to-monocyte ratio and histone methyltransferase G9a histone methyltransferase in patients with double expression lymphoma: A retrospective observational study. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33589432/ G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34214254/ EHMT1 knockdown induces apoptosis and cell cycle arrest in lung cancer cells by increasing CDKN1A expression. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34249932/ Inactivation of the Euchromatic Histone-Lysine N-Methyltransferase 2 Pathway in Pancreatic Epithelial Cells Antagonizes Cancer Initiation and Pancreatitis-Associated Promotion by Altering Growth and Immune Gene Expression Networks. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34326167/ WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34357103/ High WHSC1L1 Expression Reduces Survival Rates in Operated Breast Cancer Patients with Decreased CD8+ T Cells: Machine Learning Approach. ongoing research 4 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34425630/ Histone methyltransferase Ezh2 negatively regulates NK cell terminal maturation and function. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34428935/ Wolf-Hirschhorn syndrome candidate 1 facilitates alveolar macrophage pyroptosis in sepsis-induced acute lung injury through NEK7-mediated NLRP3 inflammasome activation. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34445452/ Inhibition of WHSC1 Allows for Reprogramming of the Immune Compartment in Prostate Cancer. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34455155/ Transcription analysis of a histones modifiers panel coupled with critical tumor suppressor genes displayed frequent changes in patients with AML.: mRNA levels of histones modifiers and TSGs in AML. ongoing research 3 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34462284/ Targeting the Atf7ip-Setdb1 complex augments antitumor immunity by boosting tumor immunogenicity. ongoing research 2 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34531375/ PRMT5 regulates cell pyroptosis by silencing CASP1 in multiple myeloma. ongoing research 1 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16682412/ The histone methyltransferase SETDB1 and the DNA methyltransferase DNMT3A interact directly and localize to promoters silenced in cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18723033/ Roles of the EZH2 histone methyltransferase in cancer epigenetics. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18980972/ Regulation of pancreatic tumor cell proliferation and chemoresistance by the histone methyltransferase enhancer of zeste homologue 2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19734945/ Impaired recruitment of the histone methyltransferase DOT1L contributes to the incomplete reactivation of tumor suppressor genes upon DNA demethylation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19881540/ Reexpression of epigenetically silenced AML tumor suppressor genes by SUV39H1 inhibition. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21539681/ Validation of the histone methyltransferase EZH2 as a therapeutic target for various types of human cancer and as a prognostic marker. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21892211/ Silencing of Kruppel-like factor 2 by the histone methyltransferase EZH2 in human cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21932133/ Carcinogenesis of Intraductal Papillary Mucinous Neoplasm of the Pancreas: Loss of MicroRNA-101 Promotes Overexpression of Histone Methyltransferase EZH2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22036763/ Hydrogen peroxide induces Sp1 methylation and thereby suppresses cyclin B1 via recruitment of Suv39H1 and HDAC1 in cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23684884/ Canonical and non-canonical roles of the histone methyltransferase EZH2 in mammary development and cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23868976/ Promoter occupancy of MLL1 histone methyltransferase seems to specify the proliferative and apoptotic functions of E2F1 in a tumour microenvironment. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24726141/ The Histone Methyltransferase SMYD2 Methylates PARP1 and Promotes Poly(ADP-ribosyl)ation Activity in Cancer Cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24833465/ Histone methyltransferase G9a and H3K9 dimethylation inhibit the self-renewal of glioma cancer stem cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25179367/ Targeting histone methyltransferase EZH2 as cancer treatment. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25203626/ S-Adenosyl-L-methionine-competitive inhibitors of the histone methyltransferase EZH2 induce autophagy and enhance drug sensitivity in cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25583990/ The Histone Methyltransferase Smyd2 Is a Negative Regulator of Macrophage Activation by Suppressing Interleukin 6 (IL-6) and Tumor Necrosis Factor ? (TNF-?) Production. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27551509/ ?Np63? modulates histone methyl transferase SETDB1 to transcriptionally repress target genes in cancers. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28248941/ Anticancer agents: Allosteric histone methyltransferase modulators block tumour growth. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28532996/ Histone methyltransferase G9a promotes liver cancer development by epigenetic silencing of tumor suppressor gene RARRES3. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28701475/ HIF activation causes synthetic lethality between the VHL tumor suppressor and the EZH1 histone methyltransferase. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29066607/ Cancer cells, on your histone marks, get SETDB1, silence retrotransposons, and go! unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29133140/ The histone methyltransferase G9a: a new therapeutic target in biliary tract cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30503969/ MicroRNA-621 Acts as a Tumor Radiosensitizer by Directly Targeting SETDB1 in Hepatocellular Carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32448308/ Symphony of epigenetic and metabolic regulation-interaction between the histone methyltransferase EZH2 and metabolism of tumor. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34336110/ Histone Methyltransferase G9a Promotes the Development of Renal Cancer through Epigenetic Silencing of Tumor Suppressor Gene SPINK5. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/10343109/ Assignment of a novel bifurcated SET domain gene, SETDB1, to human chromosome band 1q21 by in situ hybridization and radiation hybrids. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15199122/ Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15225548/ SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16638127/ Differential expression of selected histone modifier genes in human solid cancers. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16651450/ Menin links estrogen receptor activation to histone H3K4 trimethylation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16687068/ [Inhibition of SMYD3 gene expression by RNA interference induces apoptosis in human hepatocellular carcinoma cell line HepG2] unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18819746/ Aberrant methylation of candidate tumor suppressor genes in neuroblastoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18977321/ Reconstructing the disease model and epigenetic networks for MLL-AF4 leukemia. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20227040/ Tumor stroma-derived TGF-beta limits myc-driven lymphomagenesis via Suv39h1-dependent senescence. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20818171/ Myc, Cdk2 and cellular senescence: Old players, new game. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21546904/ Polycomb protein EZH2 regulates cancer cell fate decision in response to DNA damage. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21726809/ SHP2 tyrosine phosphatase converts parafibromin/Cdc73 from a tumor suppressor to an oncogenic driver. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22028469/ Proteomic and functional genomic landscape of receptor tyrosine kinase and ras to extracellular signal-regulated kinase signaling. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22068036/ EZH2 Mediates epigenetic silencing of neuroblastoma suppressor genes CASZ1, CLU, RUNX3, and NGFR. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22108826/ Curcumin analogue CDF inhibits pancreatic tumor growth by switching on suppressor microRNAs and attenuating EZH2 expression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22199269/ Histone-modifier gene expression profiles are associated with pathological and clinical outcomes in human breast cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22406368/ High expression of trimethylated histone H3 lysine 4 is associated with poor prognosis in hepatocellular carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22552406/ The expression and significance of the enhancer of zeste homolog 2 in lung adenocarcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23145205/ EZH2: a pivotal regulator in controlling cell differentiation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23355073/ Metallothionein 1h Tumor Suppressor Activity in Prostate Cancer Is Mediated By Euchromatin Methyltransferase 1. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23373415/ [The significance of histone modifications in malignant transformation]. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23826380/ EZH2-Mediated H3K27me3 Is Involved in Epigenetic Repression of Deleted in Liver Cancer 1 in Human Cancers. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24077223/ Promiscuous RNA binding by Polycomb repressive complex 2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24912918/ Negative regulation of DAB2IP by Akt and SCFFbw7 pathways. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24992961/ A dimeric state for PRC2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25149548/ Diffuse large B-cell lymphoma with histone H3 trimethylation at lysine 27: another poor prognostic phenotype independent of c-Myc/Bcl2 coexpression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25172130/ Using S-adenosyl-L-homocysteine capture compounds to characterize S-adenosyl-L-methionine and S-adenosyl-L-homocysteine binding proteins. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25195579/ Epigenomic networking in drug development: from pathogenic mechanisms to pharmacogenomics. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25490442/ DOTting the path to doom: how acceleration of histone methylation leads to leukemia. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25499219/ The transcriptional repressor ZBTB4 regulates EZH2 through a MicroRNA-ZBTB4-specificity protein signaling axis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25601759/ Toward a Consensus on the Binding Specificity and Promiscuity of PRC2 for RNA. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25637186/ Functional regulation of hypoxia inducible factor-1? by SET9 lysine methyltransferase. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25640033/ Structural and Functional Characterization of the Acidic Region from the RIZ Tumor Suppressor. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25718650/ The Role of G9a in Tumorigenesis in Head and Neck Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25947258/ Genome-wide transcriptional profiling analysis reveals annexin A6 as a novel EZH2 target gene involving gastric cellular proliferation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26350217/ Cooperation between SMYD3 and PC4 drives a distinct transcriptional program in cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26501191/ Ductal pancreatic cancer modeling and drug screening using human pluripotent stem cell- and patient-derived tumor organoids. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26574518/ The recruitment of chromatin modifiers by long noncoding RNAs: lessons from PRC2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26663801/ NUT Midline Carcinoma: Morphoproteomic Characterization with Genomic and Therapeutic Correlates. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26694085/ Weaver Syndrome-Associated EZH2 Protein Variants Show Impaired Histone Methyltransferase Function In Vitro. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26815947/ Structures of Nahuoic Acids B-E Produced in Culture by a Streptomyces sp. Isolated from a Marine Sediment and Evidence for the Inhibition of the Histone Methyl Transferase SETD8 in Human Cancer Cells by Nahuoic Acid A. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26898301/ The novel EZH2 inhibitor, GSK126, suppresses cell migration and angiogenesis via down-regulating VEGF-A. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27109020/ Epidrugs in the immunotherapy of cutaneous and uveal melanoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27279906/ Recapitulating the Size and Cargo of Tumor Exosomes in a Tissue-Engineered Model. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27371576/ An Achilles' Heel for MLL-Rearranged Leukemias: Writers and Readers of H3 Lysine 36 Dimethylation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28129645/ Epigenetic alterations of gastrokine 1 gene expression in gastric cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28131418/ The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28159833/ SETting the Stage for Cancer Development: SETD2 and the Consequences of Lost Methylation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28167662/ Impaired IRE1 expression and XBP1 activation is a hallmark of GCB-DLBCL and contributes to tumor growth. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28373363/ Re-engineering the Pancreas Tumor Microenvironment: A "Regenerative Program" Hacked. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28429794/ Bone-in-culture array as a platform to model early-stage bone metastases and discover anti-metastasis therapies. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28444909/ The histone methyltransferase EZH2 is a therapeutic target in small cell carcinoma of the ovary, hypercalcaemic type. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28765327/ The KMT1A-GATA3-STAT3 circuit is a novel self-renewal signaling of human bladder cancer stem cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28868353/ Dual epigenetic modifiers for cancer therapy. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28892075/ Analysis of somatic microsatellite indels identifies driver events in human tumors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28928088/ 20(S)-Ginsenoside Rh2 suppresses proliferation and migration of hepatocellular carcinoma cells by targeting EZH2 to regulate CDKN2A-2B gene cluster transcription. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29307797/ Alcoholic hepatitis versus non-alcoholic steatohepatitis: Levels of expression of some proteins involved in tumorigenesis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29467226/ E4BP4/NFIL3 modulates the epigenetically repressed Ras effector RASSF8 function through histone methyl transferases. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29531826/ BIX-01294 sensitizes renal cancer Caki cells to TRAIL-induced apoptosis through downregulation of survivin expression and upregulation of DR5 expression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29669287/ ZRANB1 Is an EZH2 Deubiquitinase and a Potential Therapeutic Target in Breast Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29928350/ Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30171419/ Identification of protoberberine alkaloids as novel histone methyltransferase G9a inhibitors by structure-based virtual screening. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30718359/ Genome-wide screening and functional analysis identifies tumor suppressor long non-coding RNAs epigenetically silenced in hepatocellular carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30772380/ A SUV39H1-low chromatin state characterises and promotes migratory properties of cervical cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30881512/ Association of an miR-502-binding site polymorphism in the 3'-untranslated region of SET8 with colorectal cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30897760/ A Systematic Pan-Cancer Analysis of Genetic Heterogeneity Reveals Associations with Epigenetic Modifiers. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31263101/ An ErbB2/c-Src axis links bioenergetics with PRC2 translation to drive epigenetic reprogramming and mammary tumorigenesis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31405032/ SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31550663/ A drug repurposing screening reveals a novel epigenetic activity of hydroxychloroquine. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31693439/ Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31811272/ A TGF-?-MTA1-SOX4-EZH2 signaling axis drives epithelial-mesenchymal transition in tumor metastasis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32269620/ SET and MYND domain-containing protein 3 inhibits tumor cell sensitivity to cisplatin. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32508971/ EZH2-inhibitor DZNep enhances apoptosis of renal tubular epithelial cells in presence and absence of cisplatin. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32826865/ LncRNA CRNDE facilitates epigenetic suppression of CELF2 and LATS2 to promote proliferation, migration and chemoresistance in hepatocellular carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32967925/ NSD3-induced methylation of H3K36 activates NOTCH signaling to drive breast tumor initiation and metastatic progression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33056982/ Long non-coding RNA CASC9 promotes gefitinib resistance in NSCLC by epigenetic repression of DUSP1. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33277444/ The Histone Methyltransferase Gene G9A Is Regulated by Nuclear Receptor 4A1 in Alveolar Rhabdomyosarcoma Cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33472665/ Reduction of miR-744 delivered by NSCLC cell-derived extracellular vesicles upregulates SUV39H1 to promote NSCLC progression via activation of the Smad9/BMP9 axis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33545678/ Preclinical efficacy of ribavirin in SHH and group 3 medulloblastoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34235289/ The SMYD family proteins in immunology: An update of their obvious and non-obvious relations with the immune system. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34445452/ Inhibition of WHSC1 Allows for Reprogramming of the Immune Compartment in Prostate Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34455155/ Transcription analysis of a histones modifiers panel coupled with critical tumor suppressor genes displayed frequent changes in patients with AML.: mRNA levels of histones modifiers and TSGs in AML. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34464854/ CRISPR/Cas9 mediated generation of a iPSC line EHTJUi005-A-1 with homozygous knockout of the SUV39H1 gene. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34510321/ Novel insights into SMYD2 and SMYD3 inhibitors: from potential anti-tumoural therapy to a variety of new applications. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/14633678/ Inactivation of a histone methyltransferase by mutations in human cancers. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15235609/ SMYD3 encodes a histone methyltransferase involved in the proliferation of cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16799634/ 5-Aza-2'-deoxycytidine-mediated reductions in G9A histone methyltransferase and histone H3 K9 di-methylation levels are linked to tumor suppressor gene reactivation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/18446223/ Downregulation of histone H3 lysine 9 methyltransferase G9a induces centrosome disruption and chromosome instability in cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19008416/ Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19285253/ Commentary on Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer Varambally S, Cao Q, Mani RS, Shankar S, Wang X, Ateeq B, Laxman B, Cao X, Jing X, Ramnarayanan K, Brenner JC, Yu J, Kim JH, Han B, Tan P, Kumar-Sinha C, Lonigro RJ, Palanisamy N, Maher CA, Chinnaiyan AM, Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20501857/ Histone methyltransferase gene SETD2 is a novel tumor suppressor gene in clear cell renal cell carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21175789/ Epigenetic regulation of signaling pathways in cancer: role of the histone methyltransferase EZH2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21383990/ Regulation of the DNA Damage Response and Gene Expression by the Dot1L Histone Methyltransferase and the 53Bp1 Tumour Suppressor. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23210854/ Histone methyltransferase inhibitors: novel epigenetic agents for cancer treatment. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24292603/ The histone methyltransferase EZH2, an oncogene common to benign and malignant parathyroid tumors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25168426/ Involvement of EZH2, SUV39H1, G9a and associated molecules in pathogenesis of urethane induced mouse lung tumors: potential targets for cancer control. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26441991/ Functional Role of G9a Histone Methyltransferase in Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26609488/ The histone methyltransferase DOT1L: regulatory functions and a cancer therapy target. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27179746/ Role of the EZH2 histone methyltransferase as a therapeutic target in cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28182322/ Somatic cancer mutations in the MLL1 histone methyltransferase modulate its enzymatic activity and dependence on the WDR5/RBBP5/ASH2L complex. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28746871/ The Histone Methyltransferase Ezh2 Controls Mechanisms of Adaptive Resistance to Tumor Immunotherapy. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28978137/ The histone methyltransferase EZH2 as a druggable target in SHH medulloblastoma cancer stem cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32231741/ Histone methyltransferase SETD2: a potential tumor suppressor in solid cancers. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32859239/ Histone methyltransferase and drug resistance in cancers. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33129761/ Su(var)3-9, Enhancer of Zeste, and Trithorax Domain-Containing 5 Facilitates Tumor Growth and Pulmonary Metastasis through Up-Regulation of AKT1 Signaling in Breast Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33223508/ Histone methyltransferase SETD2 inhibits tumor growth via suppressing CXCL1-mediated activation of cell cycle in lung adenocarcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33632299/ Chromatin remodeling by the histone methyltransferase EZH2 drives lung pre-malignancy and is a target for cancer prevention. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33953401/ Epigenetic silencing by SETDB1 suppresses tumour intrinsic immunogenicity. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34194626/ Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16007202/ The polycomb group protein enhancer of zeste homolog 2 (EZH 2) is an oncogene that influences myeloma cell growth and the mutant ras phenotype. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16195383/ Menin regulates pancreatic islet growth by promoting histone methylation and expression of genes encoding p27Kip1 and p18INK4c. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16497704/ Histone H3 lysine 9 and H4 lysine 20 trimethylation and the expression of Suv4-20h2 and Suv-39h1 histone methyltransferases in hepatocarcinogenesis induced by methyl deficiency in rats. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16953217/ RIZ1 repression is associated with insulin-like growth factor-1 signaling activation in chronic myeloid leukemia cell lines. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/17245754/ Loss of RB compromises specific heterochromatin modifications and modulates HP1alpha dynamics. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/17453341/ EZH2 regulates the transcription of estrogen-responsive genes through association with REA, an estrogen receptor corepressor. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19472189/ Effects of SMYD3 overexpression on transformation, serum dependence, and apoptosis sensitivity in NIH3T3 cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19799859/ RNA interference targeting against S100A4 suppresses cell growth and motility and induces apoptosis in human pancreatic cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20081860/ Somatic mutations altering EZH2 (Tyr641) in follicular and diffuse large B-cell lymphomas of germinal-center origin. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20601953/ Inactivating mutations of the histone methyltransferase gene EZH2 in myeloid disorders. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20614940/ Protein lysine methyltransferase G9a inhibitors: design, synthesis, and structure activity relationships of 2,4-diamino-7-aminoalkoxy-quinazolines. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20631058/ The role of EZH2 and DNA methylation in the silencing of the tumour suppressor RUNX3 in colorectal cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20861184/ Histone Methyltransferase MLL1 Regulates MDR1 Transcription and Chemoresistance. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20864510/ ANCCA/ATAD2 Overexpression Identifies Breast Cancer Patients with Poor Prognosis, Acting to Drive Proliferation and Survival of Triple-Negative Cells through Control of B-Myb and EZH2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21659531/ Cyclin-dependent Kinase 1 (CDK1)-mediated Phosphorylation of Enhancer of Zeste 2 (Ezh2) Regulates Its Stability. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21734239/ The histone methyltransferase inhibitor DZNep upregulates TXNIP, increases ROS production, and targets leukemia cells in AML. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21780790/ Optimization of Cellular Activity of G9a Inhibitors 7-Aminoalkoxy-quinazolines. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22040993/ [An update on epigenetic regulator gene mutations and pathogenesis of myelodysplasic syndromes]. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22505352/ Clinically significant copy number alterations and complex rearrangements of MYB and NFIB in head and neck adenoid cystic carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22662197/ Enhancer of zeste homolog 2 induces pulmonary artery smooth muscle cell proliferation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22740705/ Identification of somatic mutations in parathyroid tumors using whole-exome sequencing. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22751105/ Multiple myeloma-associated chromosomal translocation activates orphan snoRNA ACA11 to suppress oxidative stress. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22797064/ The histone methyltransferase MMSET/WHSC1 activates TWIST1 to promote an epithelial-mesenchymal transition and invasive properties of prostate cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22972034/ MMSET stimulates myeloma cell growth through microRNA-mediated modulation of c-MYC. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22991213/ Histone lysine methyltransferase, SUV39H1, promotes HCC progression and is negatively regulated by microRNA-125b. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23110793/ Poorly differentiated synovial sarcoma is associated with high expression of enhancer of zeste homologue 2 (EZH2). unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23400519/ Improved therapeutic effect against leukemia by a combination of the histone methyltransferase inhibitor chaetocin and the histone deacetylase inhibitor trichostatin A. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23421437/ Sorafenib suppresses growth and survival of hepatoma cells by accelerating degradation of enhancer of zeste homolog 2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23424038/ Role of STAT3 and Vitamin D Receptor in EZH2-mediated invasion of human colorectal cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23509280/ Methylation of SUV39H1 by SET7/9 results in heterochromatin relaxation and genome instability. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23644490/ Multifaceted role of EZH2 in breast and prostate tumorigenesis: epigenetics and beyond. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23705022/ The histone methyltransferase SUV39H1 suppresses embryonal rhabdomyosarcoma formation in zebrafish. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23803053/ 3-Deazaneplanocin A is a Promising Therapeutic Agent for Ovarian Cancer Cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23807219/ Gossypol and an HMT G9a inhibitor act in synergy to induce cell death in pancreatic cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23907130/ Polycomb repressive complex 2 contributes to DNA double-strand break repair. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23981787/ Sox4, EMT programs, and the metastatic progression of breast cancers: mastering the masters of EMT. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24151879/ The Discovery of Novel Histone Lysine Methyltransferase G9a Inhibitors (Part 1): Molecular Design Based on a Series of Substituted 2,4-Diamino-7-aminoalkoxyquinazoline by Molecular-Docking-Guided 3D Quantitative Structure-Activity Relationship Studies. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24184908/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24212330/ Cancer-associated fibroblasts enhance the migration ability of ovarian cancer cells by increasing EZH2 expression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24322755/ BIX-01294 induces autophagy-associated cell death via EHMT2/G9a dysfunction and intracellular reactive oxygen species production. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24691023/ Impact of EZH2 Polymorphisms on Urothelial Cell Carcinoma Susceptibility and Clinicopathologic Features. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24844570/ Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24852755/ 3-Deazaneplanocin A (DZNep), an inhibitor of the histone methyltransferase EZH2, induces apoptosis and reduces cell migration in chondrosarcoma cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24912396/ EZH2: an emerging role in melanoma biology and strategies for targeted therapy. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24983772/ Histone H3K4 methyltransferase Mll1 regulates protein glycosylation and tunicamycin-induced apoptosis through transcriptional regulation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25027955/ Inhibition of G9a induces DUSP4-dependent autophagic cell death in head and neck squamous cell carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25071150/ The hypoxia-inducible epigenetic regulators Jmjd1a and G9a provide a mechanistic link between angiogenesis and tumor growth. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25131201/ A macrohistone variant links dynamic chromatin compaction to BRCA1-dependent genome maintenance. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25131810/ Overexpression of EZH2 associates with a poor prognosis in chronic lymphocytic leukemia. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25415657/ Analysis of the antiproliferative effects of 3-deazaneoplanocin A in combination with standard anticancer agents in rhabdoid tumor cell lines. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25535899/ EZH2 inhibition enhances the efficacy of an EGFR inhibitor in suppressing colon cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25549357/ EZH2 regulates cofilin activity and colon cancer cell migration by targeting ITGA2 gene. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25595900/ Down-regulation of G9a triggers DNA damage response and inhibits colorectal cancer cells proliferation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25602259/ Emerging role of linker histone variant H1x as a biomarker with prognostic value in astrocytic gliomas. A multivariate analysis including trimethylation of H3K9 and H4K20. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25613390/ The H3K9 Methyltransferase G9a Represses E-cadherin and is Associated with Myometrial Invasion in Endometrial Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25671303/ Epigenetic reprogramming by tumor-derived EZH2 gain-of-function mutations promotes aggressive 3D cell morphologies and enhances melanoma tumor growth. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25710335/ Biochemical Assay Development for Histone Methyltransferases Using a Transcreener-Based Assay for S-Adenosylhomocysteine. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25739318/ The polycomb group protein EZH2 is a novel therapeutic target for cervical cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25877750/ Overexpression of YB1 and EZH2 are associated with cancer metastasis and poor prognosis in renal cell carcinomas. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25893294/ Development of secondary mutations in wild-type and mutant EZH2 alleles cooperates to confer resistance to EZH2 inhibitors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25978433/ The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26013382/ The Histone Methyltransferase Inhibitor BIX01294 Inhibits HIF-1? Stability and Angiogenesis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26040698/ A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26147105/ The Histone Methyltransferase Inhibitor A-366 Uncovers a Role for G9a/GLP in the Epigenetics of Leukemia. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26151044/ Inhibition of Nuclear Receptor Binding SET Domain 2/Multiple Myeloma SET Domain by LEM-06 Implication for Epigenetic Cancer Therapies. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26292256/ Two Loops Undergoing Concerted Dynamics Regulate the Activity of the ASH1L Histone Methyltransferase. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26336998/ TERT promoter mutations in primary liver tumors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26444031/ Inhibition of H3K9 histone methyltransferase G9a attenuates renal fibrosis and retains klotho expression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26463831/ Studies Identify Non-Hodgkin Lymphoma Suppressor. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26500027/ Targeting Suppressor of Variegation 3-9 Homologue 2 (SUV39H2) in Acute Lymphoblastic Leukemia (ALL). unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26552009/ SWI/SNF-mutant cancers depend on catalytic and non-catalytic activity of EZH2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26568301/ Variants of ubiquitin-specific peptidase 24 play a crucial role in lung cancer malignancy. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26648239/ A crucial epithelial to mesenchymal transition regulator, Sox4/Ezh2 axis is closely related to the clinical outcome in pancreatic cancer patients. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26697392/ Identification of PRDM2 regulated genes in quiescent C2C12 myoblasts. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26771714/ MMSET is dynamically regulated during cell-cycle progression and promotes normal DNA replication. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26883360/ Mutation of cancer driver MLL2 results in transcription stress and genome instability. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27034728/ Global histone modification profiling reveals the epigenomic dynamics during malignant transformation in a four-stage breast cancer model. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27081761/ Depletion of G9a gene induces cell apoptosis in human gastric carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27174920/ Inhibition of EHMT2/G9a epigenetically increases the transcription of Beclin-1 via an increase in ROS and activation of NF-?B. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27399922/ EZH2 Protein Expression and Tumor Response to Neoadjuvant Chemotherapy in Locally Advanced Breast Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27468692/ DNA-PK-mediated phosphorylation of EZH2 regulates the DNA damage-induced apoptosis to maintain T-cell genomic integrity. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27555605/ Initial testing (stage 1) of tazemetostat (EPZ-6438), a novel EZH2 inhibitor, by the Pediatric Preclinical Testing Program. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27604143/ NSD2 contributes to oncogenic RAS-driven transcription in lung cancer cells through long-range epigenetic activation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27605386/ miR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27843326/ MLL1 promotes cervical carcinoma cell tumorigenesis and metastasis through interaction with ?-catenin. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28076698/ Emerging role of SETDB1 as a therapeutic target. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28278257/ Inhibition of H3K9 methyltransferase G9a ameliorates methylglyoxal-induced peritoneal fibrosis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28459432/ Metformin inhibits SUV39H1-mediated migration of prostate cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28692054/ Modeling cancer driver events in vitro using barrier bypass-clonal expansion assays and massively parallel sequencing. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28785086/ MUC1-C activates EZH2 expression and function in human cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28795320/ EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28864533/ First critical repressive H3K27me3 marks in embryonic stem cells identified using designed protein inhibitor. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28887438/ ---Silencing of retrotransposons by SETDB1 inhibits the interferon response in acute myeloid leukemia-. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28943305/ Targeting the cancer epigenome: synergistic therapy with bromodomain inhibitors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28977928/ Methyltransferase G9a promotes cervical cancer angiogenesis and decreases patient survival. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29113759/ Pharmacological and transcriptional inhibition of the G9a histone methyltransferase suppresses proliferation and modulates redox homeostasis in human microvascular endothelial cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29145444/ Inhibition of the H3K9 methyltransferase G9A attenuates oncogenicity and activates the hypoxia signaling pathway. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29269867/ Histone methyltransferase KMT2D sustains prostate carcinogenesis and metastasis via epigenetically activating LIFR and KLF4. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29374157/ Targeting EHMT2 reverses EGFR-TKI resistance in NSCLC by epigenetically regulating the PTEN/AKT signaling pathway. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29408993/ Effects of histone methyltransferase inhibition in endometriosis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29473431/ Enhancer of zeste homolog 2 (EZH2) inhibitors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29724721/ SETD2 Is Recurrently Mutated in Whole-Exome Sequenced Canine Osteosarcoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29739365/ Histone methyltransferase SETDB1 promotes cells proliferation and migration by interacting withTiam1 in hepatocellular carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29742153/ Identification of a peptide inhibitor for the histone methyltransferase WHSC1. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29805595/ Clinicopathological significance of G9A expression in colorectal carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29848731/ Prevalence of Enhancer of Zeste Homolog 2 in Patients with Resected Small Cell Lung Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29864144/ Impact of OGT deregulation on EZH2 target genes FOXA1 and FOXC1 expression in breast cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29897144/ Surveillance of Retroelement Expression and Nucleic-Acid Immunity by Histone Methyltransferase SETDB1. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30013191/ Methylation of Aurora kinase A by MMSET reduces p53 stability and regulates cell proliferation and apoptosis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30117667/ Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30185548/ Dual Inhibition of DNA and Histone Methyltransferases Increases Viral Mimicry in Ovarian Cancer Cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30214616/ Increased EZH2 expression during the adenoma-carcinoma sequence in colorectal cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30218753/ Aberrant differential expression of EZH2 and H3K27me3 in extranodal NK/T-cell lymphoma, nasal type is associated with disease progression and prognosis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30263847/ SMYD3-associated pathway is involved in the anti-tumor effects of sulforaphane on gastric carcinoma cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30305431/ Reduced miR-125a-5p level in non-small-cell lung cancer is associated with tumour progression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30323973/ Preprogramming therapeutic response of PI3K/mTOR dual inhibitor via the regulation of EHMT2 and p27 in pancreatic cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30348169/ Targeting histone methyltransferase G9a inhibits growth and Wnt signaling pathway by epigenetically regulating HP1? and APC2 gene expression in non-small cell lung cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30393995/ Common origin of sequential cutaneous CD30+ lymphoproliferations with nodal involvement evidenced by genome-wide clonal evolution. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30455465/ H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30555699/ EZH2 as a therapeutic target for multiple myeloma and other haematological malignancies. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30692625/ AKT methylation by SETDB1 promotes AKT kinase activity and oncogenic functions. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30761216/ Targeting EZH2 in Multiple Myeloma-Multifaceted Anti-Tumor Activity. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30833420/ Epigenetic Regulation of the PTEN-AKT-RAC1 Axis by G9a Is Critical for Tumor Growth in Alveolar Rhabdomyosarcoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31050579/ Fine-tuning AKT kinase activity through direct lysine methylation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31127101/ Selective binding of the PHD6 finger of MLL4 to histone H4K16ac links MLL4 and MOF. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31223458/ Discovery of Irreversible Inhibitors Targeting Histone Methyltransferase, SMYD3. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31338003/ In vivo administration of G9a inhibitor A366 decreases osteogenic potential of bone marrow-derived mesenchymal stem cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31422102/ SETDB1 modulates the differentiation of both the crystal cells and the lamellocytes in Drosophila. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31465303/ Precocious neuronal differentiation and disrupted oxygen responses in Kabuki syndrome. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31521697/ Targeting epigenetic machinery: Emerging novel allosteric inhibitors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31579098/ DZNep inhibits Hif-1? and Wnt signalling molecules to attenuate the proliferation and invasion of BGC-823 gastric cancer cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31768101/ Knockdown of SET Domain, Bifurcated 1 suppresses head and neck cancer cell viability and wound-healing ability in vitro. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31776268/ Human Papillomavirus E7 Oncoprotein Subverts Host Innate Immunity via SUV39H1-Mediated Epigenetic Silencing of Immune Sensor Genes. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31877341/ Combining epigenetic and immune therapy to overcome cancer resistance. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32062438/ Arsenic and benzo[a]pyrene co-exposure acts synergistically in inducing cancer stem cell-like property and tumorigenesis by epigenetically down-regulating SOCS3 expression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32103168/ SMURF2 prevents detrimental changes to chromatin, protecting human dermal fibroblasts from chromosomal instability and tumorigenesis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32174799/ EHMT2/G9a Inhibits Aortic Smooth Muscle Cell Death by Suppressing Autophagy Activation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32269030/ Gain-of-Function Genetic Alterations of G9a Drive Oncogenesis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32312833/ The EZH2-PHACTR2-AS1-Ribosome Axis induces Genomic Instability and Promotes Growth and Metastasis in Breast Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32344701/ Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32445185/ The Promise for Histone Methyltransferase Inhibitors for Epigenetic Therapy in Clinical Oncology: A Narrative Review. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32477831/ Frequent upregulation of G9a promotes RelB-dependent proliferation and survival in multiple myeloma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32486217/ SETDB1-Mediated Silencing of Retroelements. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32684241/ Euchromatin histone methyltransferase II (EHMT2) regulates the expression of ras-related GTP binding C (RRAGC) protein. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32723083/ The complex role of EZH2 in the tumor microenvironment: opportunities and challenges for immunotherapy combinations. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32889036/ Epigenetic priming by EHMT1/EHMT2 in acute lymphoblastic leukemia induces TP53 and TP73 overexpression and promotes cell death. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32972752/ Knockout of SETDB1 gene using the CRISPR/cas-9 system increases migration and transforming activities via complex regulations of E-cadherin, ?-catenin, STAT3, and Akt. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33044755/ SETDB1 promotes gastric carcinogenesis and metastasis via upregulation of CCND1 and MMP9 expression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33059737/ SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33086062/ Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33121982/ Whole-proteome analysis of mesonephric-derived cancers describes new potential biomarkers. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33147463/ G9a Promotes Breast Cancer Recurrence through Repression of a Pro-inflammatory Program. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33168810/ EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33232890/ Structural basis for PRC2 engagement with chromatin. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33330479/ Deficiency of G9a Inhibits Cell Proliferation and Activates Autophagy via Transcriptionally Regulating c-Myc Expression in Glioblastoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33387131/ BIX-01294, a G9a inhibitor, suppresses cell proliferation by inhibiting autophagic flux in nasopharyngeal carcinoma cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33589432/ G9a Inhibition Enhances Checkpoint Inhibitor Blockade Response in Melanoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33681705/ Targeting FBXO44/SUV39H1 elicits tumor cell-specific DNA replication stress and viral mimicry. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33910928/ Multilevel Regulation of ?-Catenin Activity by SETD2 Suppresses the Transition from Polycystic Kidney Disease to Clear Cell Renal Cell Carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34249932/ Inactivation of the Euchromatic Histone-Lysine N-Methyltransferase 2 Pathway in Pancreatic Epithelial Cells Antagonizes Cancer Initiation and Pancreatitis-Associated Promotion by Altering Growth and Immune Gene Expression Networks. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34294888/ Exosomal miR-101-3p and miR-423-5p inhibit medulloblastoma tumorigenesis through targeting FOXP4 and EZH2. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34425630/ Histone methyltransferase Ezh2 negatively regulates NK cell terminal maturation and function. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34428935/ Wolf-Hirschhorn syndrome candidate 1 facilitates alveolar macrophage pyroptosis in sepsis-induced acute lung injury through NEK7-mediated NLRP3 inflammasome activation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34440561/ Structure, Activity and Function of the SETDB1 Protein Methyltransferase. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34462284/ Targeting the Atf7ip-Setdb1 complex augments antitumor immunity by boosting tumor immunogenicity. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34479190/ Targeting of cyclin-dependent kinases in atypical teratoid rhabdoid tumors with multikinase inhibitor TG02. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34531375/ PRMT5 regulates cell pyroptosis by silencing CASP1 in multiple myeloma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26481868/ Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27008202/ Correction: Up-regulation of histone methyltransferase SETDB1 by multiple mechanisms in hepatocellular carcinoma promotes cancer metastasis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32061753/ SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15196462/ The functions of E(Z)/EZH2-mediated methylation of lysine 27 in histone H3. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19128641/ Epigenetic perspective into head and neck cancer through in silico gene expression profiling of histone lysine methyltransferases. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20940408/ H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21493592/ Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22505648/ Polycomb protein EZH2 regulates tumor invasion via the transcriptional repression of the metastasis suppressor RKIP in breast and prostate cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23636686/ EZH2, an epigenetic driver of prostate cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24183969/ Identification of EZH2 and EZH1 small molecule inhibitors with selective impact on diffuse large B cell lymphoma cell growth. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24874471/ Identification of druggable cancer driver genes amplified across TCGA datasets. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24925220/ Frameshift mutation of a histone methylation-related gene SETD1B and its regional heterogeneity in gastric and colorectal cancers with high microsatellite instability. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25505154/ Quantitative Nuclear Proteomics Identifies that miR-137-mediated EZH2 Reduction Regulates Resveratrol-induced Apoptosis of Neuroblastoma Cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26765460/ Association of Histone Methyltransferase G9a and Overall Survival After Liver Resection of Patients With Hepatocellular Carcinoma With a Median Observation of 40 Months. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27698795/ Whole-exome sequencing identifies variants in invasive pituitary adenomas. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29158805/ Histone Methyltransferase SETDB1 Promotes the Progression of Colorectal Cancer by Inhibiting the Expression of TP53. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29302370/ ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29449539/ G9A promotes gastric cancer metastasis by upregulating ITGB3 in a SET domain-independent manner. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29572888/ PRDM8 Exhibits Anti-Tumor Activities Toward Hepatocellular Carcinoma by Targeting NAP1L1. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29844834/ Euchromatic histone lysine methyltransferase 1 regulates cancer development in human gastric cancer by regulating E-cadherin. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29872311/ The methylation profiles of PRDM promoters in non-small cell lung cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/29901162/ Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31306481/ Histone Methyltransferase SETDB1 Promotes Colorectal Cancer Proliferation through the STAT1-CCND1/CDK6 Axis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31599405/ EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31654063/ SETD3 is regulated by a couple of microRNAs and plays opposing roles in proliferation and metastasis of hepatocellular carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32305991/ High SET Domain Bifurcated 1 (SETDB1) Expression Predicts Poor Prognosis in Breast Carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33099471/ Deletion of Histone Methyltransferase G9a Suppresses Mutant Kras-driven Pancreatic Carcinogenesis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33159839/ KMT2C promoter methylation in plasma-circulating tumor DNA is a prognostic biomarker in non-small cell lung cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343623/ SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33530253/ Prognostic value of lymphocyte-to-monocyte ratio and histone methyltransferase G9a histone methyltransferase in patients with double expression lymphoma: A retrospective observational study. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34344448/ EHMT2 promotes the pathogenesis of hepatocellular carcinoma by epigenetically silencing APC expression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22645312/ Histone methyltransferase NSD2/MMSET mediates constitutive NF-?B signaling for cancer cell proliferation, survival, and tumor growth via a feed-forward loop. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25884948/ Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33665162/ Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22330138/ The SRA protein UHRF1 promotes epigenetic crosstalks and is involved in prostate cancer progression. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25477335/ H3K9 histone methyltransferase, KMT1E/SETDB1, cooperates with the SMAD2/3 pathway to suppress lung cancer metastasis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27223432/ Morphoproteomics and biomedical analytics confirm the mTORC2/Akt pathway as a resistance signature and activated ERK and STAT3 as concomitant prosurvival/antiapoptotic pathways in metastatic renal cell carcinoma (RCC) progressing on rapalogs: Pathogenesis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27713173/ Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30990809/ Genetic mutational status of genes regulating epigenetics: Role of the histone methyltransferase KMT2D in triple negative breast tumors. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31232159/ Loss of KMT2D induces prostate cancer ROS-mediated DNA damage by suppressing the enhancer activity and DNA binding of antioxidant transcription factor FOXO3. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31579944/ Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33037410/ SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33938943/ G9a/GLP targeting in MM promotes autophagy-associated apoptosis and boosts proteasome inhibitor-mediated cell death. unassigned - 2.1.1.355 Neoplasms https://pubmed.ncbi.nlm.nih.gov/34299035/ The Updating of Biological Functions of Methyltransferase SETDB1 and Its Relevance in Lung Cancer and Mesothelioma. unassigned - 2.1.1.355 Neoplasms, Germ Cell and Embryonal https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. causal interaction 3 2.1.1.355 Neoplasms, Germ Cell and Embryonal https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. diagnostic usage 3 2.1.1.355 Neoplasms, Germ Cell and Embryonal https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. ongoing research 4 2.1.1.355 Neoplasms, Germ Cell and Embryonal https://pubmed.ncbi.nlm.nih.gov/27983647/ Critical Function of PRDM2 in the Neoplastic Growth of Testicular Germ Cell Tumors. unassigned - 2.1.1.355 Neoplasms, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. causal interaction 4 2.1.1.355 Neoplasms, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. diagnostic usage 3 2.1.1.355 Neoplasms, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/24649311/ Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer. unassigned - 2.1.1.355 Nervous System Diseases https://pubmed.ncbi.nlm.nih.gov/33010785/ Structural and functional annotation of PR/SET Domain (PRDM) protein family: In-silico study elaborating role of PRDM12 mutation in congenital insensitivity to pain. ongoing research 2 2.1.1.355 Nervous System Diseases https://pubmed.ncbi.nlm.nih.gov/33010785/ Structural and functional annotation of PR/SET Domain (PRDM) protein family: In-silico study elaborating role of PRDM12 mutation in congenital insensitivity to pain. unassigned - 2.1.1.355 Neuralgia https://pubmed.ncbi.nlm.nih.gov/34383386/ Downregulation of a Dorsal Root Ganglion-Specifically Enriched Long Noncoding RNA is Required for Neuropathic Pain by Negatively Regulating RALY-Triggered Ehmt2 Expression. causal interaction 2 2.1.1.355 Neuralgia https://pubmed.ncbi.nlm.nih.gov/32670741/ N6-Methyladenosine Demethylase FTO Contributes to Neuropathic Pain by Stabilizing G9a Expression in Primary Sensory Neurons. causal interaction 1 2.1.1.355 Neuralgia https://pubmed.ncbi.nlm.nih.gov/32024693/ Histone methyltransferase G9a diminishes expression of cannabinoid CB1 receptors in primary sensory neurons in neuropathic pain. unassigned - 2.1.1.355 Neuralgia https://pubmed.ncbi.nlm.nih.gov/34383386/ Downregulation of a Dorsal Root Ganglion-Specifically Enriched Long Noncoding RNA is Required for Neuropathic Pain by Negatively Regulating RALY-Triggered Ehmt2 Expression. unassigned - 2.1.1.355 Neuralgia https://pubmed.ncbi.nlm.nih.gov/32670741/ N6-Methyladenosine Demethylase FTO Contributes to Neuropathic Pain by Stabilizing G9a Expression in Primary Sensory Neurons. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/23466651/ Histone-lysine methyltransferase EHMT2 is involved in proliferation, apoptosis, cell invasion, and DNA methylation of human neuroblastoma cells. causal interaction 1 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/25198515/ Inhibition of H3K9 methyltransferase G9a repressed cell proliferation and induced autophagy in neuroblastoma cells. causal interaction 1 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/28209620/ The histone methyltransferase DOT1L promotes neuroblastoma by regulating gene transcription. causal interaction 3 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/30807601/ Correction: Inhibition of H3K9 Methyltransferase G9a Repressed Cell Proliferation and Induced Autophagy in Neuroblastoma Cells. causal interaction 1 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/25505154/ Quantitative Nuclear Proteomics Identifies that miR-137-mediated EZH2 Reduction Regulates Resveratrol-induced Apoptosis of Neuroblastoma Cells. causal interaction 3 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. causal interaction 4 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/28209620/ The histone methyltransferase DOT1L promotes neuroblastoma by regulating gene transcription. diagnostic usage 2 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/18819746/ Aberrant methylation of candidate tumor suppressor genes in neuroblastoma. diagnostic usage 3 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/25505154/ Quantitative Nuclear Proteomics Identifies that miR-137-mediated EZH2 Reduction Regulates Resveratrol-induced Apoptosis of Neuroblastoma Cells. diagnostic usage 3 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. diagnostic usage 1 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/28209620/ The histone methyltransferase DOT1L promotes neuroblastoma by regulating gene transcription. therapeutic application 4 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/28214660/ Enhancer of zeste homologue 2 plays an important role in neuroblastoma cell survival independent of its histone methyltransferase activity. therapeutic application 4 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/30807601/ Correction: Inhibition of H3K9 Methyltransferase G9a Repressed Cell Proliferation and Induced Autophagy in Neuroblastoma Cells. therapeutic application 1 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/32537432/ Increased Efficacy of Histone Methyltransferase G9a Inhibitors Against MYCN-Amplified Neuroblastoma. therapeutic application 2 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. therapeutic application 1 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/20018718/ Epigenetic inactivation of the Sotos overgrowth syndrome gene histone methyltransferase NSD1 in human neuroblastoma and glioma. ongoing research 2 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/23466651/ Histone-lysine methyltransferase EHMT2 is involved in proliferation, apoptosis, cell invasion, and DNA methylation of human neuroblastoma cells. ongoing research 1 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/25198515/ Inhibition of H3K9 methyltransferase G9a repressed cell proliferation and induced autophagy in neuroblastoma cells. ongoing research 3 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/28209620/ The histone methyltransferase DOT1L promotes neuroblastoma by regulating gene transcription. ongoing research 1 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/30807601/ Correction: Inhibition of H3K9 Methyltransferase G9a Repressed Cell Proliferation and Induced Autophagy in Neuroblastoma Cells. ongoing research 3 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/18819746/ Aberrant methylation of candidate tumor suppressor genes in neuroblastoma. ongoing research 2 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. ongoing research 4 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/33361537/ Oxidative stress-induced aberrant G9a activation disturbs RE-1-containing neuron-specific genes expression, leading to degeneration in human SH-SY5Y neuroblastoma cells. ongoing research 4 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/20018718/ Epigenetic inactivation of the Sotos overgrowth syndrome gene histone methyltransferase NSD1 in human neuroblastoma and glioma. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/28214660/ Enhancer of zeste homologue 2 plays an important role in neuroblastoma cell survival independent of its histone methyltransferase activity. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/32537432/ Increased Efficacy of Histone Methyltransferase G9a Inhibitors Against MYCN-Amplified Neuroblastoma. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/18819746/ Aberrant methylation of candidate tumor suppressor genes in neuroblastoma. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/33361537/ Oxidative stress-induced aberrant G9a activation disturbs RE-1-containing neuron-specific genes expression, leading to degeneration in human SH-SY5Y neuroblastoma cells. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/23466651/ Histone-lysine methyltransferase EHMT2 is involved in proliferation, apoptosis, cell invasion, and DNA methylation of human neuroblastoma cells. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/25198515/ Inhibition of H3K9 methyltransferase G9a repressed cell proliferation and induced autophagy in neuroblastoma cells. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/30807601/ Correction: Inhibition of H3K9 Methyltransferase G9a Repressed Cell Proliferation and Induced Autophagy in Neuroblastoma Cells. unassigned - 2.1.1.355 Neuroblastoma https://pubmed.ncbi.nlm.nih.gov/25505154/ Quantitative Nuclear Proteomics Identifies that miR-137-mediated EZH2 Reduction Regulates Resveratrol-induced Apoptosis of Neuroblastoma Cells. unassigned - 2.1.1.355 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/25195579/ Epigenomic networking in drug development: from pathogenic mechanisms to pharmacogenomics. therapeutic application 4 2.1.1.355 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/25195579/ Epigenomic networking in drug development: from pathogenic mechanisms to pharmacogenomics. unassigned - 2.1.1.355 Non-alcoholic Fatty Liver Disease https://pubmed.ncbi.nlm.nih.gov/28244120/ The histone methyltransferase Suv39h2 contributes to nonalcoholic steatohepatitis in mice. unassigned - 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/28663191/ The Histone Methyltransferase MLL1 Directs Macrophage-Mediated Inflammation in Wound Healing and Is Altered in a Murine Model of Obesity and Type 2 Diabetes. causal interaction 3 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/29077881/ Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. causal interaction 1 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/29535452/ ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. causal interaction 3 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. causal interaction 4 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/29535452/ ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. diagnostic usage 2 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. diagnostic usage 4 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/28663191/ The Histone Methyltransferase MLL1 Directs Macrophage-Mediated Inflammation in Wound Healing and Is Altered in a Murine Model of Obesity and Type 2 Diabetes. therapeutic application 1 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/29077881/ Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. therapeutic application 1 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/29535452/ ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. therapeutic application 3 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/31776436/ Correction to: ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. therapeutic application 1 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. therapeutic application 1 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/29077881/ Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. ongoing research 4 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/29535452/ ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. ongoing research 4 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. ongoing research 4 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/31776436/ Correction to: ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1? deacetylation. unassigned - 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/24196706/ EHMT1 controls brown adipose cell fate and thermogenesis through the PRDM16 complex. unassigned - 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/28663191/ The Histone Methyltransferase MLL1 Directs Macrophage-Mediated Inflammation in Wound Healing and Is Altered in a Murine Model of Obesity and Type 2 Diabetes. unassigned - 2.1.1.355 Obesity https://pubmed.ncbi.nlm.nih.gov/29077881/ Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. unassigned - 2.1.1.355 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/33177650/ EZH2 inhibition reduces cartilage loss and functional impairment related to osteoarthritis. causal interaction 3 2.1.1.355 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/27539752/ The inhibition of EZH2 ameliorates osteoarthritis development through the Wnt/?-catenin pathway. therapeutic application 1 2.1.1.355 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/21515604/ Expression and function of EZH2 in synovial fibroblasts: epigenetic repression of the Wnt inhibitor SFRP1 in rheumatoid arthritis. ongoing research 3 2.1.1.355 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/27539752/ The inhibition of EZH2 ameliorates osteoarthritis development through the Wnt/?-catenin pathway. ongoing research 1 2.1.1.355 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/21515604/ Expression and function of EZH2 in synovial fibroblasts: epigenetic repression of the Wnt inhibitor SFRP1 in rheumatoid arthritis. unassigned - 2.1.1.355 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/27539752/ The inhibition of EZH2 ameliorates osteoarthritis development through the Wnt/?-catenin pathway. unassigned - 2.1.1.355 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/33177650/ EZH2 inhibition reduces cartilage loss and functional impairment related to osteoarthritis. unassigned - 2.1.1.355 Osteoporosis https://pubmed.ncbi.nlm.nih.gov/29348610/ The histone methyltransferase DOT1L inhibits osteoclastogenesis and protects against osteoporosis. causal interaction 2 2.1.1.355 Osteoporosis https://pubmed.ncbi.nlm.nih.gov/29348610/ The histone methyltransferase DOT1L inhibits osteoclastogenesis and protects against osteoporosis. therapeutic application 1 2.1.1.355 Osteoporosis https://pubmed.ncbi.nlm.nih.gov/29348610/ The histone methyltransferase DOT1L inhibits osteoclastogenesis and protects against osteoporosis. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/31341965/ Canine osteosarcoma genome sequencing identifies recurrent mutations in DMD and the histone methyltransferase gene SETD2. causal interaction 1 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/29724721/ SETD2 Is Recurrently Mutated in Whole-Exome Sequenced Canine Osteosarcoma. causal interaction 3 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. causal interaction 4 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/28901481/ Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis. therapeutic application 2 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/30683853/ Histone methyltransferase NSD2 regulates apoptosis and chemosensitivity in osteosarcoma. therapeutic application 1 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/14985713/ PRDI-BF1 recruits the histone H3 methyltransferase G9a in transcriptional silencing. therapeutic application 1 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. therapeutic application 4 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/28901481/ Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis. ongoing research 3 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/30683853/ Histone methyltransferase NSD2 regulates apoptosis and chemosensitivity in osteosarcoma. ongoing research 3 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/33397384/ Histone methyltransferase SUV39H2 regulates LSD1-dependent CDH1 expression and promotes epithelial mesenchymal transition of osteosarcoma. ongoing research 1 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/14985713/ PRDI-BF1 recruits the histone H3 methyltransferase G9a in transcriptional silencing. ongoing research 3 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. ongoing research 3 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/28901481/ Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/29842882/ Histone methyltransferase SETD2 regulates osteosarcoma cell growth and chemosensitivity by suppressing Wnt/?-catenin signaling. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/30542727/ Histone methyltransferase SUV39H2 serves oncogenic roles in osteosarcoma. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/30683853/ Histone methyltransferase NSD2 regulates apoptosis and chemosensitivity in osteosarcoma. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/33397384/ Histone methyltransferase SUV39H2 regulates LSD1-dependent CDH1 expression and promotes epithelial mesenchymal transition of osteosarcoma. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/14985713/ PRDI-BF1 recruits the histone H3 methyltransferase G9a in transcriptional silencing. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/31341965/ Canine osteosarcoma genome sequencing identifies recurrent mutations in DMD and the histone methyltransferase gene SETD2. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/29724721/ SETD2 Is Recurrently Mutated in Whole-Exome Sequenced Canine Osteosarcoma. unassigned - 2.1.1.355 Osteosarcoma https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. causal interaction 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/29434212/ CARM1-expressing ovarian cancer depends on the histone methyltransferase EZH2 activity. causal interaction 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. causal interaction 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/21216927/ Ovarian cancer stem cell-like side populations are enriched following chemotherapy and overexpress EZH2. causal interaction 3 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/24335192/ EZH2 participates in malignant biological behavior of epithelial ovarian cancer through regulating the expression of BRCA1. causal interaction 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/30185548/ Dual Inhibition of DNA and Histone Methyltransferases Increases Viral Mimicry in Ovarian Cancer Cells. causal interaction 3 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. causal interaction 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/25115793/ The H3K9 methyltransferase G9a is a marker of aggressive ovarian cancer that promotes peritoneal metastasis. diagnostic usage 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. diagnostic usage 3 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/29726819/ Histone Methyltransferase EZH2: A Therapeutic Target for Ovarian Cancer. diagnostic usage 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. diagnostic usage 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. diagnostic usage 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/25115793/ The H3K9 methyltransferase G9a is a marker of aggressive ovarian cancer that promotes peritoneal metastasis. therapeutic application 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. therapeutic application 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/29726819/ Histone Methyltransferase EZH2: A Therapeutic Target for Ovarian Cancer. therapeutic application 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. therapeutic application 2 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/27114721/ Differential Effects of Estradiol and Bisphenol A on SET8 and SIRT1 Expression in Ovarian Cancer Cells. therapeutic application 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/29669287/ ZRANB1 Is an EZH2 Deubiquitinase and a Potential Therapeutic Target in Breast Cancer. therapeutic application 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. therapeutic application 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/33763107/ Ketamine Inhibits Ovarian Cancer Cell Growth by Regulating the lncRNA-PVT1/EZH2/p57 Axis. therapeutic application 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/28706445/ Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. ongoing research 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/29434212/ CARM1-expressing ovarian cancer depends on the histone methyltransferase EZH2 activity. ongoing research 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/31689915/ The Histone Methyltransferase DOT1L Is a Functional Component of Estrogen Receptor Alpha Signaling in Ovarian Cancer Cells. ongoing research 1 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/21216927/ Ovarian cancer stem cell-like side populations are enriched following chemotherapy and overexpress EZH2. ongoing research 2 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/24335192/ EZH2 participates in malignant biological behavior of epithelial ovarian cancer through regulating the expression of BRCA1. ongoing research 3 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/27114721/ Differential Effects of Estradiol and Bisphenol A on SET8 and SIRT1 Expression in Ovarian Cancer Cells. ongoing research 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/32028644/ EHMT2 Inhibition Induces Cell Death in Human Non-Small Cell Lung Cancer by Altering the Cholesterol Biosynthesis Pathway. ongoing research 4 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/25115793/ The H3K9 methyltransferase G9a is a marker of aggressive ovarian cancer that promotes peritoneal metastasis. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/29726819/ Histone Methyltransferase EZH2: A Therapeutic Target for Ovarian Cancer. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/27114721/ Differential Effects of Estradiol and Bisphenol A on SET8 and SIRT1 Expression in Ovarian Cancer Cells. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/29669287/ ZRANB1 Is an EZH2 Deubiquitinase and a Potential Therapeutic Target in Breast Cancer. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/32506298/ Selective sensitivity of EZH2 inhibitors based on synthetic lethality in ARID1A-deficient gastric cancer. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/33763107/ Ketamine Inhibits Ovarian Cancer Cell Growth by Regulating the lncRNA-PVT1/EZH2/p57 Axis. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/29434212/ CARM1-expressing ovarian cancer depends on the histone methyltransferase EZH2 activity. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/21216927/ Ovarian cancer stem cell-like side populations are enriched following chemotherapy and overexpress EZH2. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/24335192/ EZH2 participates in malignant biological behavior of epithelial ovarian cancer through regulating the expression of BRCA1. unassigned - 2.1.1.355 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/30185548/ Dual Inhibition of DNA and Histone Methyltransferases Increases Viral Mimicry in Ovarian Cancer Cells. unassigned - 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30323973/ Preprogramming therapeutic response of PI3K/mTOR dual inhibitor via the regulation of EHMT2 and p27 in pancreatic cancer. causal interaction 4 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24732359/ S100A4 is frequently overexpressed in lung cancer cells and promotes cell growth and cell motility. causal interaction 1 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/29229751/ SUV420H2 is an epigenetic regulator of epithelial/mesenchymal states in pancreatic cancer. causal interaction 3 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24732359/ S100A4 is frequently overexpressed in lung cancer cells and promotes cell growth and cell motility. diagnostic usage 3 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/29229751/ SUV420H2 is an epigenetic regulator of epithelial/mesenchymal states in pancreatic cancer. diagnostic usage 3 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27531902/ The histone methyltransferase G9a as a therapeutic target to override gemcitabine resistance in pancreatic cancer. therapeutic application 3 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30323973/ Preprogramming therapeutic response of PI3K/mTOR dual inhibitor via the regulation of EHMT2 and p27 in pancreatic cancer. therapeutic application 4 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24732359/ S100A4 is frequently overexpressed in lung cancer cells and promotes cell growth and cell motility. therapeutic application 1 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27531902/ The histone methyltransferase G9a as a therapeutic target to override gemcitabine resistance in pancreatic cancer. unassigned - 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30323973/ Preprogramming therapeutic response of PI3K/mTOR dual inhibitor via the regulation of EHMT2 and p27 in pancreatic cancer. unassigned - 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/29229751/ SUV420H2 is an epigenetic regulator of epithelial/mesenchymal states in pancreatic cancer. unassigned - 2.1.1.355 Pancreatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24732359/ S100A4 is frequently overexpressed in lung cancer cells and promotes cell growth and cell motility. unassigned - 2.1.1.355 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/21469201/ Variants in estrogen-related genes and risk of Parkinson's disease. causal interaction 3 2.1.1.355 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/21469201/ Variants in estrogen-related genes and risk of Parkinson's disease. diagnostic usage 1 2.1.1.355 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/21469201/ Variants in estrogen-related genes and risk of Parkinson's disease. ongoing research 1 2.1.1.355 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/21469201/ Variants in estrogen-related genes and risk of Parkinson's disease. unassigned - 2.1.1.355 Peritoneal Fibrosis https://pubmed.ncbi.nlm.nih.gov/28278257/ Inhibition of H3K9 methyltransferase G9a ameliorates methylglyoxal-induced peritoneal fibrosis. causal interaction 3 2.1.1.355 Peritoneal Fibrosis https://pubmed.ncbi.nlm.nih.gov/28278257/ Inhibition of H3K9 methyltransferase G9a ameliorates methylglyoxal-induced peritoneal fibrosis. therapeutic application 3 2.1.1.355 Peritoneal Fibrosis https://pubmed.ncbi.nlm.nih.gov/28278257/ Inhibition of H3K9 methyltransferase G9a ameliorates methylglyoxal-induced peritoneal fibrosis. unassigned - 2.1.1.355 Persistent Infection https://pubmed.ncbi.nlm.nih.gov/32001678/ Targeting p53 and histone methyltransferases restores exhausted CD8+ T cells in HCV infection. causal interaction 4 2.1.1.355 Persistent Infection https://pubmed.ncbi.nlm.nih.gov/32001678/ Targeting p53 and histone methyltransferases restores exhausted CD8+ T cells in HCV infection. therapeutic application 1 2.1.1.355 Persistent Infection https://pubmed.ncbi.nlm.nih.gov/32001678/ Targeting p53 and histone methyltransferases restores exhausted CD8+ T cells in HCV infection. unassigned - 2.1.1.355 Pituitary Neoplasms https://pubmed.ncbi.nlm.nih.gov/31280474/ Identification of Potential Biomarkers with Diagnostic Value in Pituitary Adenomas Using Prediction Analysis for Microarrays Method. causal interaction 1 2.1.1.355 Pituitary Neoplasms https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. causal interaction 4 2.1.1.355 Pituitary Neoplasms https://pubmed.ncbi.nlm.nih.gov/31280474/ Identification of Potential Biomarkers with Diagnostic Value in Pituitary Adenomas Using Prediction Analysis for Microarrays Method. diagnostic usage 3 2.1.1.355 Pituitary Neoplasms https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. diagnostic usage 4 2.1.1.355 Pituitary Neoplasms https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. therapeutic application 1 2.1.1.355 Pituitary Neoplasms https://pubmed.ncbi.nlm.nih.gov/32044406/ The absence of PRDM2 involved the tumorigenesis of somatotroph adenomas through regulating c-Myc. ongoing research 4 2.1.1.355 Pituitary Neoplasms https://pubmed.ncbi.nlm.nih.gov/31280474/ Identification of Potential Biomarkers with Diagnostic Value in Pituitary Adenomas Using Prediction Analysis for Microarrays Method. unassigned - 2.1.1.355 Prader-Willi Syndrome https://pubmed.ncbi.nlm.nih.gov/33279625/ Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases. therapeutic application 4 2.1.1.355 Prader-Willi Syndrome https://pubmed.ncbi.nlm.nih.gov/28024084/ Targeting the histone methyltransferase G9a activates imprinted genes and improves survival of a mouse model of Prader-Willi syndrome. ongoing research 1 2.1.1.355 Prader-Willi Syndrome https://pubmed.ncbi.nlm.nih.gov/12586828/ Role of histone methyltransferase G9a in CpG methylation of the Prader-Willi syndrome imprinting center. unassigned - 2.1.1.355 Prader-Willi Syndrome https://pubmed.ncbi.nlm.nih.gov/24760766/ Reactivation of maternal SNORD116 cluster via SETDB1 knockdown in Prader-Willi syndrome iPSCs. unassigned - 2.1.1.355 Prader-Willi Syndrome https://pubmed.ncbi.nlm.nih.gov/28024084/ Targeting the histone methyltransferase G9a activates imprinted genes and improves survival of a mouse model of Prader-Willi syndrome. unassigned - 2.1.1.355 Prader-Willi Syndrome https://pubmed.ncbi.nlm.nih.gov/33279625/ Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases. unassigned - 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/30171259/ An activating mutation of the NSD2 histone methyltransferase drives oncogenic reprogramming in acute lymphocytic leukemia. causal interaction 3 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/25421677/ Epigenetic approaches in glioblastoma multiforme and their implication in screening and diagnosis. causal interaction 1 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/20581860/ Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells. diagnostic usage 1 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/23994619/ Symplekin, a polyadenylation factor, prevents MOZ and MLL activity on HOXA9 in hematopoietic cells. diagnostic usage 1 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/30171259/ An activating mutation of the NSD2 histone methyltransferase drives oncogenic reprogramming in acute lymphocytic leukemia. therapeutic application 1 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/20581860/ Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells. therapeutic application 1 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/23994619/ Symplekin, a polyadenylation factor, prevents MOZ and MLL activity on HOXA9 in hematopoietic cells. therapeutic application 1 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/20581860/ Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells. unassigned - 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/23994619/ Symplekin, a polyadenylation factor, prevents MOZ and MLL activity on HOXA9 in hematopoietic cells. unassigned - 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/30171259/ An activating mutation of the NSD2 histone methyltransferase drives oncogenic reprogramming in acute lymphocytic leukemia. unassigned - 2.1.1.355 Precursor Cell Lymphoblastic Leukemia-Lymphoma https://pubmed.ncbi.nlm.nih.gov/25421677/ Epigenetic approaches in glioblastoma multiforme and their implication in screening and diagnosis. unassigned - 2.1.1.355 Progeria https://pubmed.ncbi.nlm.nih.gov/23695662/ Depleting the methyltransferase Suv39h1 improves DNA repair and extends lifespan in a progeria mouse model. therapeutic application 1 2.1.1.355 Progeria https://pubmed.ncbi.nlm.nih.gov/23695662/ Depleting the methyltransferase Suv39h1 improves DNA repair and extends lifespan in a progeria mouse model. ongoing research 2 2.1.1.355 Progeria https://pubmed.ncbi.nlm.nih.gov/23695662/ Depleting the methyltransferase Suv39h1 improves DNA repair and extends lifespan in a progeria mouse model. unassigned - 2.1.1.355 Prolactinoma https://pubmed.ncbi.nlm.nih.gov/25884948/ Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas. causal interaction 4 2.1.1.355 Prolactinoma https://pubmed.ncbi.nlm.nih.gov/25884948/ Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas. diagnostic usage 4 2.1.1.355 Prolactinoma https://pubmed.ncbi.nlm.nih.gov/25884948/ Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas. therapeutic application 1 2.1.1.355 Prolactinoma https://pubmed.ncbi.nlm.nih.gov/34282593/ Treatment Strategies for Dopamine Agonist-Resistant and Aggressive Prolactinomas: A Comprehensive Analysis of the Literature. unassigned - 2.1.1.355 Prolactinoma https://pubmed.ncbi.nlm.nih.gov/25884948/ Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas. unassigned - 2.1.1.355 Prostatic Hyperplasia https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. causal interaction 3 2.1.1.355 Prostatic Hyperplasia https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. diagnostic usage 4 2.1.1.355 Prostatic Hyperplasia https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. therapeutic application 3 2.1.1.355 Prostatic Hyperplasia https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. ongoing research 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22797064/ The histone methyltransferase MMSET/WHSC1 activates TWIST1 to promote an epithelial-mesenchymal transition and invasive properties of prostate cancer. causal interaction 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24289559/ Triptolide inhibits histone methyltransferase EZH2 and modulates the expression of its target genes in prostate cancer cells. causal interaction 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. causal interaction 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27323813/ Histone methyltransferase PRMT6 plays an oncogenic role of in prostate cancer. causal interaction 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27404348/ Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells. causal interaction 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28319045/ AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. causal interaction 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/31599405/ EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway. causal interaction 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/32814769/ Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer. causal interaction 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33066102/ Identification of Differentially Methylated Regions Associated with a Knockout of SUV39H1 in Prostate Cancer Cells. causal interaction 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/17453341/ EZH2 regulates the transcription of estrogen-responsive genes through association with REA, an estrogen receptor corepressor. causal interaction 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22505648/ Polycomb protein EZH2 regulates tumor invasion via the transcriptional repression of the metastasis suppressor RKIP in breast and prostate cancer. causal interaction 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22645312/ Histone methyltransferase NSD2/MMSET mediates constitutive NF-?B signaling for cancer cell proliferation, survival, and tumor growth via a feed-forward loop. causal interaction 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23636686/ EZH2, an epigenetic driver of prostate cancer. causal interaction 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25017995/ Autoregulatory feedback loop of EZH2/miR-200c/E2F3 as a driving force for prostate cancer development. causal interaction 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25486523/ SUV39H1/H3K9me3 attenuates sulforaphane-induced apoptotic signaling in PC3 prostate cancer cells. causal interaction 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27339988/ Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation. causal interaction 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28795320/ EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma. causal interaction 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30385408/ MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity. causal interaction 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. causal interaction 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. causal interaction 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24289559/ Triptolide inhibits histone methyltransferase EZH2 and modulates the expression of its target genes in prostate cancer cells. diagnostic usage 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. diagnostic usage 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/26871869/ The JMJD3 Histone Demethylase and the EZH2 Histone Methyltransferase in Prostate Cancer. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28319045/ AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. diagnostic usage 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28817916/ Re: AKT-Mediated Stabilization of Histone Methyltransferase WHSC1 Promotes Prostate Cancer Metastasis. diagnostic usage 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/29161520/ EZH2 Histone Methyltransferase and JMJD3 Histone Demethylase Implications in Prostate Cancer. diagnostic usage 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30396921/ Transcriptomic Analysis of Histone Methyltransferase Setd7 Knockdown and Phenethyl Isothiocyanate in Human Prostate Cancer Cells. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/31599405/ EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway. diagnostic usage 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/32814769/ Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33066102/ Identification of Differentially Methylated Regions Associated with a Knockout of SUV39H1 in Prostate Cancer Cells. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33976366/ Tandem histone methyltransferase upregulation defines a unique aggressive prostate cancer phenotype. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22505648/ Polycomb protein EZH2 regulates tumor invasion via the transcriptional repression of the metastasis suppressor RKIP in breast and prostate cancer. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22645312/ Histone methyltransferase NSD2/MMSET mediates constitutive NF-?B signaling for cancer cell proliferation, survival, and tumor growth via a feed-forward loop. diagnostic usage 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23636686/ EZH2, an epigenetic driver of prostate cancer. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25486523/ SUV39H1/H3K9me3 attenuates sulforaphane-induced apoptotic signaling in PC3 prostate cancer cells. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30385408/ MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity. diagnostic usage 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. diagnostic usage 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24289559/ Triptolide inhibits histone methyltransferase EZH2 and modulates the expression of its target genes in prostate cancer cells. therapeutic application 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. therapeutic application 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27404348/ Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells. therapeutic application 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28319045/ AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. therapeutic application 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28817916/ Re: AKT-Mediated Stabilization of Histone Methyltransferase WHSC1 Promotes Prostate Cancer Metastasis. therapeutic application 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/32814769/ Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer. therapeutic application 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33066102/ Identification of Differentially Methylated Regions Associated with a Knockout of SUV39H1 in Prostate Cancer Cells. therapeutic application 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22389001/ Recruitment of coregulator G9a by Runx2 for selective enhancement or suppression of transcription. therapeutic application 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22645312/ Histone methyltransferase NSD2/MMSET mediates constitutive NF-?B signaling for cancer cell proliferation, survival, and tumor growth via a feed-forward loop. therapeutic application 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25486523/ SUV39H1/H3K9me3 attenuates sulforaphane-induced apoptotic signaling in PC3 prostate cancer cells. therapeutic application 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. therapeutic application 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30385408/ MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity. therapeutic application 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. therapeutic application 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. therapeutic application 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22797064/ The histone methyltransferase MMSET/WHSC1 activates TWIST1 to promote an epithelial-mesenchymal transition and invasive properties of prostate cancer. ongoing research 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24556744/ Histone methyltransferase SETDB1 is required for prostate cancer cell proliferation, migration and invasion. ongoing research 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27323813/ Histone methyltransferase PRMT6 plays an oncogenic role of in prostate cancer. ongoing research 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27404348/ Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells. ongoing research 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28319045/ AKT-mediated stabilization of histone methyltransferase WHSC1 promotes prostate cancer metastasis. ongoing research 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/29383876/ Histone Methyltransferase Setd7 Regulates Nrf2 Signaling Pathway by Phenethyl Isothiocyanate and Ursolic Acid in Human Prostate Cancer Cells. ongoing research 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30396921/ Transcriptomic Analysis of Histone Methyltransferase Setd7 Knockdown and Phenethyl Isothiocyanate in Human Prostate Cancer Cells. ongoing research 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/31599405/ EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway. ongoing research 2 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33976366/ Tandem histone methyltransferase upregulation defines a unique aggressive prostate cancer phenotype. ongoing research 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25486523/ SUV39H1/H3K9me3 attenuates sulforaphane-induced apoptotic signaling in PC3 prostate cancer cells. ongoing research 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27268279/ KAT8 Regulates Androgen Signaling in Prostate Cancer Cells. ongoing research 1 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30385408/ MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity. ongoing research 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. ongoing research 3 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/34094655/ SETDB1 in cancer: overexpression and its therapeutic implications. ongoing research 4 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/26871869/ The JMJD3 Histone Demethylase and the EZH2 Histone Methyltransferase in Prostate Cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28817916/ Re: AKT-Mediated Stabilization of Histone Methyltransferase WHSC1 Promotes Prostate Cancer Metastasis. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/29161520/ EZH2 Histone Methyltransferase and JMJD3 Histone Demethylase Implications in Prostate Cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/29383876/ Histone Methyltransferase Setd7 Regulates Nrf2 Signaling Pathway by Phenethyl Isothiocyanate and Ursolic Acid in Human Prostate Cancer Cells. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/30396921/ Transcriptomic Analysis of Histone Methyltransferase Setd7 Knockdown and Phenethyl Isothiocyanate in Human Prostate Cancer Cells. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/31895624/ The Inhibition of the Histone Methyltransferase EZH2 by DZNEP or SiRNA Demonstrates Its Involvement in MGMT, TRA2A, RPS6KA2, and U2AF1 Gene Regulation in Prostate Cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33976366/ Tandem histone methyltransferase upregulation defines a unique aggressive prostate cancer phenotype. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22389001/ Recruitment of coregulator G9a by Runx2 for selective enhancement or suppression of transcription. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27268279/ KAT8 Regulates Androgen Signaling in Prostate Cancer Cells. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22797064/ The histone methyltransferase MMSET/WHSC1 activates TWIST1 to promote an epithelial-mesenchymal transition and invasive properties of prostate cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27323813/ Histone methyltransferase PRMT6 plays an oncogenic role of in prostate cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27404348/ Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/17453341/ EZH2 regulates the transcription of estrogen-responsive genes through association with REA, an estrogen receptor corepressor. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/25017995/ Autoregulatory feedback loop of EZH2/miR-200c/E2F3 as a driving force for prostate cancer development. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27339988/ Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/28795320/ EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33115801/ Histone Methyltransferase SETDB1: A Common Denominator of Tumorigenesis with Therapeutic Potential. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/31599405/ EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22505648/ Polycomb protein EZH2 regulates tumor invasion via the transcriptional repression of the metastasis suppressor RKIP in breast and prostate cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/23636686/ EZH2, an epigenetic driver of prostate cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/24289559/ Triptolide inhibits histone methyltransferase EZH2 and modulates the expression of its target genes in prostate cancer cells. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/32814769/ Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/33066102/ Identification of Differentially Methylated Regions Associated with a Knockout of SUV39H1 in Prostate Cancer Cells. unassigned - 2.1.1.355 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22645312/ Histone methyltransferase NSD2/MMSET mediates constitutive NF-?B signaling for cancer cell proliferation, survival, and tumor growth via a feed-forward loop. unassigned - 2.1.1.355 Pseudorabies https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. causal interaction 4 2.1.1.355 Pseudorabies https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. therapeutic application 1 2.1.1.355 Pseudorabies https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. ongoing research 2 2.1.1.355 Pseudorabies https://pubmed.ncbi.nlm.nih.gov/22531939/ Association of multi-pathogenic infections with BAT2, CXCL12, Mx1 and EHMT2 variations in pigs. unassigned - 2.1.1.355 Psoriasis https://pubmed.ncbi.nlm.nih.gov/21715244/ Abnormal histone modifications in PBMCs from patients with psoriasis vulgaris. diagnostic usage 2 2.1.1.355 Psoriasis https://pubmed.ncbi.nlm.nih.gov/21715244/ Abnormal histone modifications in PBMCs from patients with psoriasis vulgaris. unassigned - 2.1.1.355 Pulmonary Disease, Chronic Obstructive https://pubmed.ncbi.nlm.nih.gov/28425504/ SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD. causal interaction 4 2.1.1.355 Pulmonary Disease, Chronic Obstructive https://pubmed.ncbi.nlm.nih.gov/29271410/ Corrigendum: SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD. causal interaction 4 2.1.1.355 Pulmonary Disease, Chronic Obstructive https://pubmed.ncbi.nlm.nih.gov/28425504/ SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD. diagnostic usage 4 2.1.1.355 Pulmonary Disease, Chronic Obstructive https://pubmed.ncbi.nlm.nih.gov/28425504/ SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD. therapeutic application 4 2.1.1.355 Pulmonary Disease, Chronic Obstructive https://pubmed.ncbi.nlm.nih.gov/32540493/ An efficient hybrid feature selection method to identify potential biomarkers in common chronic lung inflammatory diseases. therapeutic application 1 2.1.1.355 Pulmonary Disease, Chronic Obstructive https://pubmed.ncbi.nlm.nih.gov/28425504/ SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD. ongoing research 2 2.1.1.355 Pulmonary Disease, Chronic Obstructive https://pubmed.ncbi.nlm.nih.gov/32540493/ An efficient hybrid feature selection method to identify potential biomarkers in common chronic lung inflammatory diseases. unassigned - 2.1.1.355 Pulmonary Disease, Chronic Obstructive https://pubmed.ncbi.nlm.nih.gov/29271410/ Corrigendum: SUV39H1 Reduction Is Implicated in Abnormal Inflammation in COPD. unassigned - 2.1.1.355 Reperfusion Injury https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. causal interaction 4 2.1.1.355 Reperfusion Injury https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. therapeutic application 4 2.1.1.355 Reperfusion Injury https://pubmed.ncbi.nlm.nih.gov/24752040/ Suv39h1 protects from myocardial ischemia-reperfusion injury in diabetic rats. unassigned - 2.1.1.355 Reperfusion Injury https://pubmed.ncbi.nlm.nih.gov/34102281/ The H3K9 histone methyltransferase G9a modulates renal ischemia reperfusion injury by targeting Sirt1. unassigned - 2.1.1.355 Reperfusion Injury https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. unassigned - 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/17245754/ Loss of RB compromises specific heterochromatin modifications and modulates HP1alpha dynamics. causal interaction 1 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/11533237/ Transcriptional repression by the retinoblastoma protein through the recruitment of a histone methyltransferase. therapeutic application 1 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/11484059/ Rb targets histone H3 methylation and HP1 to promoters. therapeutic application 1 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/21503890/ Identification of a functional estrogen-responsive enhancer element in the promoter 2 of PRDM2 gene in breast cancer cell lines. therapeutic application 1 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/28229975/ Diverse roles of WDR5-RbBP5-ASH2L-DPY30 (WRAD) complex in the functions of the SET1 histone methyltransferase family. therapeutic application 1 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/21503890/ Identification of a functional estrogen-responsive enhancer element in the promoter 2 of PRDM2 gene in breast cancer cell lines. ongoing research 4 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/11533237/ Transcriptional repression by the retinoblastoma protein through the recruitment of a histone methyltransferase. unassigned - 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/11484059/ Rb targets histone H3 methylation and HP1 to promoters. unassigned - 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/21503890/ Identification of a functional estrogen-responsive enhancer element in the promoter 2 of PRDM2 gene in breast cancer cell lines. unassigned - 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/28229975/ Diverse roles of WDR5-RbBP5-ASH2L-DPY30 (WRAD) complex in the functions of the SET1 histone methyltransferase family. unassigned - 2.1.1.355 Retinoblastoma https://pubmed.ncbi.nlm.nih.gov/17245754/ Loss of RB compromises specific heterochromatin modifications and modulates HP1alpha dynamics. unassigned - 2.1.1.355 Rhabdoid Tumor https://pubmed.ncbi.nlm.nih.gov/28292935/ Selective Killing of SMARCA2- and SMARCA4-deficient Small Cell Carcinoma of the Ovary, Hypercalcemic Type Cells by Inhibition of EZH2: causal interaction 3 2.1.1.355 Rhabdoid Tumor https://pubmed.ncbi.nlm.nih.gov/28292935/ Selective Killing of SMARCA2- and SMARCA4-deficient Small Cell Carcinoma of the Ovary, Hypercalcemic Type Cells by Inhibition of EZH2: unassigned - 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/21493592/ Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. causal interaction 3 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/21493592/ Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. diagnostic usage 3 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/33277444/ The Histone Methyltransferase Gene G9A Is Regulated by Nuclear Receptor 4A1 in Alveolar Rhabdomyosarcoma Cells. therapeutic application 1 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/21493592/ Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. ongoing research 1 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/33277444/ The Histone Methyltransferase Gene G9A Is Regulated by Nuclear Receptor 4A1 in Alveolar Rhabdomyosarcoma Cells. ongoing research 2 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/21941084/ Stuck in a balancing act: histone methyltransferase activity of KMT1A traps alveolar rhabdomyosarcomas in an undifferentiated state. unassigned - 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/29899822/ Camptothecin exhibits topoisomerase1-independent KMT1A suppression and myogenic differentiation in alveolar rhabdomyosarcoma cells. unassigned - 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/33277444/ The Histone Methyltransferase Gene G9A Is Regulated by Nuclear Receptor 4A1 in Alveolar Rhabdomyosarcoma Cells. unassigned - 2.1.1.355 Rhabdomyosarcoma, Alveolar https://pubmed.ncbi.nlm.nih.gov/21493592/ Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. unassigned - 2.1.1.355 Rhabdomyosarcoma, Embryonal https://pubmed.ncbi.nlm.nih.gov/23705022/ The histone methyltransferase SUV39H1 suppresses embryonal rhabdomyosarcoma formation in zebrafish. causal interaction 3 2.1.1.355 Rhabdomyosarcoma, Embryonal https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. causal interaction 4 2.1.1.355 Rhabdomyosarcoma, Embryonal https://pubmed.ncbi.nlm.nih.gov/23705022/ The histone methyltransferase SUV39H1 suppresses embryonal rhabdomyosarcoma formation in zebrafish. therapeutic application 3 2.1.1.355 Rhabdomyosarcoma, Embryonal https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. therapeutic application 2 2.1.1.355 Rhabdomyosarcoma, Embryonal https://pubmed.ncbi.nlm.nih.gov/23705022/ The histone methyltransferase SUV39H1 suppresses embryonal rhabdomyosarcoma formation in zebrafish. unassigned - 2.1.1.355 Rhabdomyosarcoma, Embryonal https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. unassigned - 2.1.1.355 Rheumatic Diseases https://pubmed.ncbi.nlm.nih.gov/33177650/ EZH2 inhibition reduces cartilage loss and functional impairment related to osteoarthritis. causal interaction 3 2.1.1.355 Rheumatic Diseases https://pubmed.ncbi.nlm.nih.gov/33177650/ EZH2 inhibition reduces cartilage loss and functional impairment related to osteoarthritis. unassigned - 2.1.1.355 Sarcoma https://pubmed.ncbi.nlm.nih.gov/34488340/ Targeting the Nuclear Receptor-Binding SET Domain Family of Histone Lysine Methyltransferases for Cancer Therapy: Recent Progress and Perspectives. causal interaction 1 2.1.1.355 Sarcoma https://pubmed.ncbi.nlm.nih.gov/33311453/ Inhibition of EZH2 enhances the therapeutic effect of 5-FU via PUMA upregulation in colorectal cancer. therapeutic application 4 2.1.1.355 Sarcoma https://pubmed.ncbi.nlm.nih.gov/34488340/ Targeting the Nuclear Receptor-Binding SET Domain Family of Histone Lysine Methyltransferases for Cancer Therapy: Recent Progress and Perspectives. therapeutic application 4 2.1.1.355 Sarcoma https://pubmed.ncbi.nlm.nih.gov/33311453/ Inhibition of EZH2 enhances the therapeutic effect of 5-FU via PUMA upregulation in colorectal cancer. unassigned - 2.1.1.355 Sarcoma https://pubmed.ncbi.nlm.nih.gov/34488340/ Targeting the Nuclear Receptor-Binding SET Domain Family of Histone Lysine Methyltransferases for Cancer Therapy: Recent Progress and Perspectives. unassigned - 2.1.1.355 Sarcoma, Ewing https://pubmed.ncbi.nlm.nih.gov/30410352/ Identification of driver genes associated with chemotherapy resistance of Ewing's sarcoma. therapeutic application 1 2.1.1.355 Sarcoma, Ewing https://pubmed.ncbi.nlm.nih.gov/30410352/ Identification of driver genes associated with chemotherapy resistance of Ewing's sarcoma. unassigned - 2.1.1.355 Scleroderma, Systemic https://pubmed.ncbi.nlm.nih.gov/28861129/ Genome-wide DNA methylation analysis in blood cells from patients with Werner syndrome. causal interaction 4 2.1.1.355 Scleroderma, Systemic https://pubmed.ncbi.nlm.nih.gov/28861129/ Genome-wide DNA methylation analysis in blood cells from patients with Werner syndrome. unassigned - 2.1.1.355 Scoliosis https://pubmed.ncbi.nlm.nih.gov/31337422/ Suv39h1 promotes facet joint chondrocyte proliferation by targeting miR-15a/Bcl2 in idiopathic scoliosis patients. unassigned - 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/33068867/ Lymphocyte expression of EZH2 is associated with mortality and secondary infectious complications in sepsis. causal interaction 1 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/34217280/ Inhibition of EZH2 prevents acute respiratory distress syndrome (ARDS)-associated pulmonary fibrosis by regulating the macrophage polarization phenotype. causal interaction 3 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/19901031/ Dynamic and selective nucleosome repositioning during endotoxin tolerance. diagnostic usage 3 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/31518916/ Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis. therapeutic application 1 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/34217280/ Inhibition of EZH2 prevents acute respiratory distress syndrome (ARDS)-associated pulmonary fibrosis by regulating the macrophage polarization phenotype. therapeutic application 2 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/19901031/ Dynamic and selective nucleosome repositioning during endotoxin tolerance. ongoing research 3 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/19901031/ Dynamic and selective nucleosome repositioning during endotoxin tolerance. unassigned - 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/31518916/ Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis. unassigned - 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/33068867/ Lymphocyte expression of EZH2 is associated with mortality and secondary infectious complications in sepsis. unassigned - 2.1.1.355 Sepsis https://pubmed.ncbi.nlm.nih.gov/34217280/ Inhibition of EZH2 prevents acute respiratory distress syndrome (ARDS)-associated pulmonary fibrosis by regulating the macrophage polarization phenotype. unassigned - 2.1.1.355 Severe Acute Respiratory Syndrome https://pubmed.ncbi.nlm.nih.gov/34479991/ Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2. causal interaction 1 2.1.1.355 Severe Acute Respiratory Syndrome https://pubmed.ncbi.nlm.nih.gov/34479991/ Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2. therapeutic application 1 2.1.1.355 Severe Acute Respiratory Syndrome https://pubmed.ncbi.nlm.nih.gov/34479991/ Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2. ongoing research 2 2.1.1.355 Severe Acute Respiratory Syndrome https://pubmed.ncbi.nlm.nih.gov/34479991/ Coronavirus induces diabetic macrophage-mediated inflammation via SETDB2. unassigned - 2.1.1.355 Skin Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. therapeutic application 4 2.1.1.355 Skin Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. ongoing research 3 2.1.1.355 Skin Neoplasms https://pubmed.ncbi.nlm.nih.gov/33283949/ Targeting H3K9 methyltransferase G9a and its related molecule GLP as a potential therapeutic strategy for cancer. unassigned - 2.1.1.355 Small Cell Lung Carcinoma https://pubmed.ncbi.nlm.nih.gov/28007623/ Small Cell Lung Cancer Exhibits Frequent Inactivating Mutations in the Histone Methyltransferase KMT2D/MLL2: CALGB 151111 (Alliance). ongoing research 1 2.1.1.355 Small Cell Lung Carcinoma https://pubmed.ncbi.nlm.nih.gov/28007623/ Small Cell Lung Cancer Exhibits Frequent Inactivating Mutations in the Histone Methyltransferase KMT2D/MLL2: CALGB 151111 (Alliance). unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/16969376/ Sotos syndrome. causal interaction 3 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/25887879/ Hypoparathyroidism in a 3-year-old Korean boy with Sotos syndrome and a novel mutation in NSD1. causal interaction 3 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/29802153/ Co-occurrence of a maternally inherited DNMT3A duplication and a paternally inherited pathogenic variant in EZH2 in a child with growth retardation and severe short stature: atypical Weaver syndrome or evidence of a DNMT3A dosage effect? causal interaction 1 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/30601169/ Disrupted epigenetics in the Sotos syndrome neurobehavioral phenotype. causal interaction 4 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/31160375/ Growth disrupting mutations in epigenetic regulatory molecules are associated with abnormalities of epigenetic aging. causal interaction 4 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/31409373/ Screening for genes that accelerate the epigenetic aging clock in humans reveals a role for the H3K36 methyltransferase NSD1. causal interaction 3 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/21196496/ The Structure of NSD1 Reveals an Autoregulatory Mechanism Underlying Histone H3K36 Methylation. therapeutic application 1 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/21204797/ 19p13.2 microduplication causes a Sotos syndrome-like phenotype and alters gene expression. therapeutic application 2 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/31909872/ Investigating cortical features of Sotos syndrome using mice heterozygous for Nsd1. therapeutic application 1 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/27834868/ Steric Clash in the SET Domain of Histone Methyltransferase NSD1 as a Cause of Sotos Syndrome and Its Genetic Heterogeneity in a Brazilian Cohort. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/17437319/ Decreased serum dependence in the growth of NIH3T3 cells from the overexpression of human nuclear receptor-binding SET-domain-containing protein 1 (NSD1) or fission yeast su(var)3-9, enhancer-of-zeste, trithorax 2 (SET2). unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/21196496/ The Structure of NSD1 Reveals an Autoregulatory Mechanism Underlying Histone H3K36 Methylation. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/21204797/ 19p13.2 microduplication causes a Sotos syndrome-like phenotype and alters gene expression. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/26690673/ NSD1 mutations generate a genome-wide DNA methylation signature. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/31909872/ Investigating cortical features of Sotos syndrome using mice heterozygous for Nsd1. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/16969376/ Sotos syndrome. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/25887879/ Hypoparathyroidism in a 3-year-old Korean boy with Sotos syndrome and a novel mutation in NSD1. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/29802153/ Co-occurrence of a maternally inherited DNMT3A duplication and a paternally inherited pathogenic variant in EZH2 in a child with growth retardation and severe short stature: atypical Weaver syndrome or evidence of a DNMT3A dosage effect? unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/30601169/ Disrupted epigenetics in the Sotos syndrome neurobehavioral phenotype. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/31160375/ Growth disrupting mutations in epigenetic regulatory molecules are associated with abnormalities of epigenetic aging. unassigned - 2.1.1.355 Sotos Syndrome https://pubmed.ncbi.nlm.nih.gov/31409373/ Screening for genes that accelerate the epigenetic aging clock in humans reveals a role for the H3K36 methyltransferase NSD1. unassigned - 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/25634693/ Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma. causal interaction 2 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. causal interaction 4 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. causal interaction 3 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. causal interaction 3 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/33626351/ Chromatin dysregulation associated with NSD1 mutation in head and neck squamous cell carcinoma. causal interaction 3 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. diagnostic usage 3 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. diagnostic usage 1 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/25634693/ Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma. therapeutic application 4 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. therapeutic application 2 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. therapeutic application 1 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. therapeutic application 1 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. ongoing research 4 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/25634693/ Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma. ongoing research 3 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. ongoing research 3 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/28265008/ Histone methyltransferase G9a drives chemotherapy resistance by regulating the glutamate-cysteine ligase catalytic subunit in head and neck squamous cell carcinoma. ongoing research 3 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/29636367/ Disruption of NSD1 in Head and Neck Cancer Promotes Favorable Chemotherapeutic Responses Linked to Hypomethylation. ongoing research 1 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/23730406/ The Histone Methyltransferase EZH2 Mediates Tumor Progression on the Chick Chorioallantoic Membrane Assay, a Novel Model of Head and Neck Squamous Cell Carcinoma. unassigned - 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/29636367/ Disruption of NSD1 in Head and Neck Cancer Promotes Favorable Chemotherapeutic Responses Linked to Hypomethylation. unassigned - 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/25634693/ Inhibition of H3K9 methyltransferase G9a induces autophagy and apoptosis in oral squamous cell carcinoma. unassigned - 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/27002147/ Upregulation of histone methyltransferase, DOT1L by matrix hyaluronan promotes MicroRNA-10 expression leading to tumor cell invasion and chemoresistance in cancer stem cells from head and neck squamous cell carcinoma. unassigned - 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/29213088/ NSD1 inactivation defines an immune cold, DNA hypomethylated subtype in squamous cell carcinoma. unassigned - 2.1.1.355 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/33626351/ Chromatin dysregulation associated with NSD1 mutation in head and neck squamous cell carcinoma. unassigned - 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/24493644/ lncRNA recruits RNAi and the exosome to dynamically regulate pho1 expression in response to phosphate levels in fission yeast. causal interaction 2 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/28007739/ Ischemic Preconditioning Confers Epigenetic Repression of Mtor and Induction of Autophagy Through G9a-Dependent H3K9 Dimethylation. causal interaction 4 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/28779125/ Epigenetic regulation of starvation-induced autophagy in Drosophila by histone methyltransferase G9a. causal interaction 1 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/28228757/ Regulation of Epigenetic Modifiers, Including KDM6B, by Interferon-? and Interleukin-4 in Human Macrophages. diagnostic usage 1 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/18485866/ A metabolic throttle regulates the epigenetic state of rDNA. therapeutic application 1 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/24493644/ lncRNA recruits RNAi and the exosome to dynamically regulate pho1 expression in response to phosphate levels in fission yeast. therapeutic application 1 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/28228757/ Regulation of Epigenetic Modifiers, Including KDM6B, by Interferon-? and Interleukin-4 in Human Macrophages. ongoing research 1 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/18485866/ A metabolic throttle regulates the epigenetic state of rDNA. unassigned - 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/28228757/ Regulation of Epigenetic Modifiers, Including KDM6B, by Interferon-? and Interleukin-4 in Human Macrophages. unassigned - 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/24493644/ lncRNA recruits RNAi and the exosome to dynamically regulate pho1 expression in response to phosphate levels in fission yeast. unassigned - 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/28007739/ Ischemic Preconditioning Confers Epigenetic Repression of Mtor and Induction of Autophagy Through G9a-Dependent H3K9 Dimethylation. unassigned - 2.1.1.355 Starvation https://pubmed.ncbi.nlm.nih.gov/28779125/ Epigenetic regulation of starvation-induced autophagy in Drosophila by histone methyltransferase G9a. unassigned - 2.1.1.355 Stomach Diseases https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. causal interaction 4 2.1.1.355 Stomach Diseases https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. diagnostic usage 2 2.1.1.355 Stomach Diseases https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. therapeutic application 4 2.1.1.355 Stomach Diseases https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. ongoing research 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/30117667/ Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. causal interaction 1 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32291851/ Histone methyltransferase SETD1A interacts with HIF1? to enhance glycolysis and promote cancer progression in gastric cancer. causal interaction 1 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. causal interaction 3 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/33639051/ Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2. causal interaction 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/34164392/ Histone Methyltransferase SETD1A Induces Epithelial-Mesenchymal Transition to Promote Invasion and Metastasis Through Epigenetic Reprogramming of Snail in Gastric Cancer. causal interaction 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/20631058/ The role of EZH2 and DNA methylation in the silencing of the tumour suppressor RUNX3 in colorectal cancer. causal interaction 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. causal interaction 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/26676636/ Upregulated SMYD3 promotes bladder cancer progression by targeting BCLAF1 and activating autophagy. causal interaction 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/29302370/ ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells. causal interaction 3 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/27572307/ Oncogenic roles of the SETDB2 histone methyltransferase in gastric cancer. diagnostic usage 1 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32291851/ Histone methyltransferase SETD1A interacts with HIF1? to enhance glycolysis and promote cancer progression in gastric cancer. diagnostic usage 1 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. diagnostic usage 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/33639051/ Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2. diagnostic usage 1 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/34164392/ Histone Methyltransferase SETD1A Induces Epithelial-Mesenchymal Transition to Promote Invasion and Metastasis Through Epigenetic Reprogramming of Snail in Gastric Cancer. diagnostic usage 3 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. diagnostic usage 2 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/26676636/ Upregulated SMYD3 promotes bladder cancer progression by targeting BCLAF1 and activating autophagy. diagnostic usage 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/29302370/ ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells. diagnostic usage 3 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32549764/ SETDB2 promoted breast cancer stem cell maintenance by interaction with and stabilization of ?Np63? protein. diagnostic usage 2 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/30117667/ Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. therapeutic application 3 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32291851/ Histone methyltransferase SETD1A interacts with HIF1? to enhance glycolysis and promote cancer progression in gastric cancer. therapeutic application 1 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/33586364/ Retraction: Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. therapeutic application 2 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/34164392/ Histone Methyltransferase SETD1A Induces Epithelial-Mesenchymal Transition to Promote Invasion and Metastasis Through Epigenetic Reprogramming of Snail in Gastric Cancer. therapeutic application 2 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. therapeutic application 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/26676636/ Upregulated SMYD3 promotes bladder cancer progression by targeting BCLAF1 and activating autophagy. therapeutic application 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/27147598/ LncRNA GClnc1 Promotes Gastric Carcinogenesis and May Act as a Modular Scaffold of WDR5 and KAT2A Complexes to Specify the Histone Modification Pattern. therapeutic application 1 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32291851/ Histone methyltransferase SETD1A interacts with HIF1? to enhance glycolysis and promote cancer progression in gastric cancer. ongoing research 3 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. ongoing research 2 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/33639051/ Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2. ongoing research 3 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/24737085/ Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. ongoing research 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/29302370/ ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells. ongoing research 4 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/27572307/ Oncogenic roles of the SETDB2 histone methyltransferase in gastric cancer. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/33586364/ Retraction: Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/27147598/ LncRNA GClnc1 Promotes Gastric Carcinogenesis and May Act as a Modular Scaffold of WDR5 and KAT2A Complexes to Specify the Histone Modification Pattern. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/28129645/ Epigenetic alterations of gastrokine 1 gene expression in gastric cancer. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32549764/ SETDB2 promoted breast cancer stem cell maintenance by interaction with and stabilization of ?Np63? protein. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/30117667/ Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/20631058/ The role of EZH2 and DNA methylation in the silencing of the tumour suppressor RUNX3 in colorectal cancer. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/32724416/ Increased expression of EHMT2 associated with H3K9me2 level contributes to the poor prognosis of gastric cancer. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/33639051/ Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/29302370/ ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/34164392/ Histone Methyltransferase SETD1A Induces Epithelial-Mesenchymal Transition to Promote Invasion and Metastasis Through Epigenetic Reprogramming of Snail in Gastric Cancer. unassigned - 2.1.1.355 Stomach Neoplasms https://pubmed.ncbi.nlm.nih.gov/26676636/ Upregulated SMYD3 promotes bladder cancer progression by targeting BCLAF1 and activating autophagy. unassigned - 2.1.1.355 Thyroid Cancer, Papillary https://pubmed.ncbi.nlm.nih.gov/29512765/ Histone methyltransferase KMT5A gene modulates oncogenesis and lipid metabolism of papillary thyroid cancer in vitro. causal interaction 4 2.1.1.355 Thyroid Cancer, Papillary https://pubmed.ncbi.nlm.nih.gov/29512765/ Histone methyltransferase KMT5A gene modulates oncogenesis and lipid metabolism of papillary thyroid cancer in vitro. diagnostic usage 3 2.1.1.355 Thyroid Cancer, Papillary https://pubmed.ncbi.nlm.nih.gov/29512765/ Histone methyltransferase KMT5A gene modulates oncogenesis and lipid metabolism of papillary thyroid cancer in vitro. ongoing research 2 2.1.1.355 Thyroid Cancer, Papillary https://pubmed.ncbi.nlm.nih.gov/29512765/ Histone methyltransferase KMT5A gene modulates oncogenesis and lipid metabolism of papillary thyroid cancer in vitro. unassigned - 2.1.1.355 Thyroid Carcinoma, Anaplastic https://pubmed.ncbi.nlm.nih.gov/32398261/ Novel role of ASH1L histone methyltransferase in anaplastic thyroid carcinoma. causal interaction 3 2.1.1.355 Thyroid Carcinoma, Anaplastic https://pubmed.ncbi.nlm.nih.gov/32398261/ Novel role of ASH1L histone methyltransferase in anaplastic thyroid carcinoma. ongoing research 2 2.1.1.355 Thyroid Carcinoma, Anaplastic https://pubmed.ncbi.nlm.nih.gov/32398261/ Novel role of ASH1L histone methyltransferase in anaplastic thyroid carcinoma. unassigned - 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26546619/ mTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer. causal interaction 3 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30670815/ Histone methyltransferase NSD2 mediates the survival and invasion of triple-negative breast cancer cells via stimulating ADAM9-EGFR-AKT signaling. causal interaction 3 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31720371/ Targeting Histone Methyltransferase DOT1L by a Novel Psammaplin A Analog Inhibits Growth and Metastasis of Triple-Negative Breast Cancer. causal interaction 3 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/33665162/ Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. causal interaction 3 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27227949/ Association Between Histone Methyltransferase hSETD1A and Prognosis in Patients With Triple-Negative Breast Cancer After Surgery: A Retrospective Study in the Chinese Female Population. diagnostic usage 3 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/33665162/ Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. diagnostic usage 3 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26546619/ mTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer. therapeutic application 4 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30670815/ Histone methyltransferase NSD2 mediates the survival and invasion of triple-negative breast cancer cells via stimulating ADAM9-EGFR-AKT signaling. therapeutic application 4 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31720371/ Targeting Histone Methyltransferase DOT1L by a Novel Psammaplin A Analog Inhibits Growth and Metastasis of Triple-Negative Breast Cancer. therapeutic application 4 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/33665162/ Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. therapeutic application 1 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27227949/ Association Between Histone Methyltransferase hSETD1A and Prognosis in Patients With Triple-Negative Breast Cancer After Surgery: A Retrospective Study in the Chinese Female Population. ongoing research 4 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31720371/ Targeting Histone Methyltransferase DOT1L by a Novel Psammaplin A Analog Inhibits Growth and Metastasis of Triple-Negative Breast Cancer. ongoing research 2 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/27227949/ Association Between Histone Methyltransferase hSETD1A and Prognosis in Patients With Triple-Negative Breast Cancer After Surgery: A Retrospective Study in the Chinese Female Population. unassigned - 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/26546619/ mTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer. unassigned - 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/30670815/ Histone methyltransferase NSD2 mediates the survival and invasion of triple-negative breast cancer cells via stimulating ADAM9-EGFR-AKT signaling. unassigned - 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/31720371/ Targeting Histone Methyltransferase DOT1L by a Novel Psammaplin A Analog Inhibits Growth and Metastasis of Triple-Negative Breast Cancer. unassigned - 2.1.1.355 Triple Negative Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/33665162/ Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. unassigned - 2.1.1.355 ulp1 peptidase deficiency https://pubmed.ncbi.nlm.nih.gov/29272473/ Senp2 Regulates Adipose Lipid Storage by De-SUMOylation of Setdb1. causal interaction 3 2.1.1.355 ulp1 peptidase deficiency https://pubmed.ncbi.nlm.nih.gov/29272473/ Senp2 Regulates Adipose Lipid Storage by De-SUMOylation of Setdb1. ongoing research 4 2.1.1.355 ulp1 peptidase deficiency https://pubmed.ncbi.nlm.nih.gov/29272473/ Senp2 Regulates Adipose Lipid Storage by De-SUMOylation of Setdb1. unassigned - 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/32626701/ Chaetocin Abrogates the Self-Renewal of Bladder Cancer Stem Cells via the Suppression of the KMT1A-GATA3-STAT3 Circuit. causal interaction 1 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/28765327/ The KMT1A-GATA3-STAT3 circuit is a novel self-renewal signaling of human bladder cancer stem cells. diagnostic usage 1 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/32626701/ Chaetocin Abrogates the Self-Renewal of Bladder Cancer Stem Cells via the Suppression of the KMT1A-GATA3-STAT3 Circuit. diagnostic usage 3 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/25685062/ EHMT2 inhibitor BIX-01294 induces apoptosis through PMAIP1-USP9X-MCL1 axis in human bladder cancer cells. therapeutic application 2 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/23485510/ Methylation of a Novel Panel of Tumor Suppressor Genes in Urine Moves Forward Non-Invasive Diagnosis and Prognosis in Bladder Cancer: A Two Center Prospective Study. therapeutic application 1 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/25685062/ EHMT2 inhibitor BIX-01294 induces apoptosis through PMAIP1-USP9X-MCL1 axis in human bladder cancer cells. ongoing research 1 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/28765327/ The KMT1A-GATA3-STAT3 circuit is a novel self-renewal signaling of human bladder cancer stem cells. ongoing research 3 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/32626701/ Chaetocin Abrogates the Self-Renewal of Bladder Cancer Stem Cells via the Suppression of the KMT1A-GATA3-STAT3 Circuit. ongoing research 4 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/25685062/ EHMT2 inhibitor BIX-01294 induces apoptosis through PMAIP1-USP9X-MCL1 axis in human bladder cancer cells. unassigned - 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/23485510/ Methylation of a Novel Panel of Tumor Suppressor Genes in Urine Moves Forward Non-Invasive Diagnosis and Prognosis in Bladder Cancer: A Two Center Prospective Study. unassigned - 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/24577895/ Methylation of tumor suppressor genes in a novel panel predicts clinical outcome in paraffin-embedded bladder tumors. unassigned - 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/28765327/ The KMT1A-GATA3-STAT3 circuit is a novel self-renewal signaling of human bladder cancer stem cells. unassigned - 2.1.1.355 Urinary Bladder Neoplasms https://pubmed.ncbi.nlm.nih.gov/32626701/ Chaetocin Abrogates the Self-Renewal of Bladder Cancer Stem Cells via the Suppression of the KMT1A-GATA3-STAT3 Circuit. unassigned - 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/25739318/ The polycomb group protein EZH2 is a novel therapeutic target for cervical cancer. causal interaction 2 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/31434093/ Inhibition of Euchromatic Histone Lysine Methyltransferase 2 (EHMT2) Suppresses the Proliferation and Invasion of Cervical Cancer Cells. causal interaction 4 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. diagnostic usage 4 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/30772380/ A SUV39H1-low chromatin state characterises and promotes migratory properties of cervical cancer cells. diagnostic usage 3 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/31434093/ Inhibition of Euchromatic Histone Lysine Methyltransferase 2 (EHMT2) Suppresses the Proliferation and Invasion of Cervical Cancer Cells. diagnostic usage 3 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/25739318/ The polycomb group protein EZH2 is a novel therapeutic target for cervical cancer. therapeutic application 1 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. therapeutic application 1 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. therapeutic application 2 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/31434093/ Inhibition of Euchromatic Histone Lysine Methyltransferase 2 (EHMT2) Suppresses the Proliferation and Invasion of Cervical Cancer Cells. therapeutic application 4 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. ongoing research 3 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/30772380/ A SUV39H1-low chromatin state characterises and promotes migratory properties of cervical cancer cells. ongoing research 4 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/31434093/ Inhibition of Euchromatic Histone Lysine Methyltransferase 2 (EHMT2) Suppresses the Proliferation and Invasion of Cervical Cancer Cells. ongoing research 4 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/26622583/ Prognostic significance of histone methyltransferase enhancer of zeste homolog 2 in patients with cervical squamous cell carcinoma. unassigned - 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/26889659/ Novel strategies for molecular targeting to cancer. unassigned - 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/30772380/ A SUV39H1-low chromatin state characterises and promotes migratory properties of cervical cancer cells. unassigned - 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/32698743/ SUV39H1-Mediated DNMT1 is Participated in the Epigenetic Regulation of Smad3 in Cervical Cancer. unassigned - 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/32699524/ SUV39H1-DNMT3A-mediated epigenetic regulation of Tim-3 and galectin-9 in the cervical cancer. unassigned - 2.1.1.355 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/25739318/ The polycomb group protein EZH2 is a novel therapeutic target for cervical cancer. unassigned - 2.1.1.355 Vascular Diseases https://pubmed.ncbi.nlm.nih.gov/29077881/ Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. causal interaction 1 2.1.1.355 Vascular Diseases https://pubmed.ncbi.nlm.nih.gov/29077881/ Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. therapeutic application 1 2.1.1.355 Vascular Diseases https://pubmed.ncbi.nlm.nih.gov/29077881/ Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. ongoing research 4 2.1.1.355 Vascular Diseases https://pubmed.ncbi.nlm.nih.gov/29077881/ Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. unassigned - 2.1.1.355 Vascular System Injuries https://pubmed.ncbi.nlm.nih.gov/31736204/ Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats. causal interaction 4 2.1.1.355 Vascular System Injuries https://pubmed.ncbi.nlm.nih.gov/31736204/ Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats. therapeutic application 4 2.1.1.355 Vascular System Injuries https://pubmed.ncbi.nlm.nih.gov/31736204/ Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats. ongoing research 2 2.1.1.355 Vascular System Injuries https://pubmed.ncbi.nlm.nih.gov/31330382/ Suv39h1 downregulation inhibits neointimal hyperplasia after vascular injury. unassigned - 2.1.1.355 Vascular System Injuries https://pubmed.ncbi.nlm.nih.gov/31736204/ Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats. unassigned - 2.1.1.355 Vesicular Stomatitis https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. therapeutic application 4 2.1.1.355 Vesicular Stomatitis https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. ongoing research 4 2.1.1.355 Vesicular Stomatitis https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. unassigned - 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/25669152/ Epigenetic control of Foxp3 by SMYD3 H3K4 histone methyltransferase controls iTreg development and regulates pathogenic T-cell responses during pulmonary viral infection. causal interaction 3 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/30842630/ The histone methyltransferase EZH2 primes the early differentiation of follicular helper T cells during acute viral infection. causal interaction 3 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. therapeutic application 4 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/25880195/ The epigenetic regulator G9a mediates tolerance to RNA virus infection in Drosophila. therapeutic application 1 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/25669152/ Epigenetic control of Foxp3 by SMYD3 H3K4 histone methyltransferase controls iTreg development and regulates pathogenic T-cell responses during pulmonary viral infection. ongoing research 3 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. ongoing research 4 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/25880195/ The epigenetic regulator G9a mediates tolerance to RNA virus infection in Drosophila. ongoing research 1 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/26418342/ Inhibition of EHMT2 Induces a Robust Antiviral Response Against Foot-and-Mouth Disease and Vesicular Stomatitis Virus Infections in Bovine Cells. unassigned - 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/25880195/ The epigenetic regulator G9a mediates tolerance to RNA virus infection in Drosophila. unassigned - 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/25669152/ Epigenetic control of Foxp3 by SMYD3 H3K4 histone methyltransferase controls iTreg development and regulates pathogenic T-cell responses during pulmonary viral infection. unassigned - 2.1.1.355 Virus Diseases https://pubmed.ncbi.nlm.nih.gov/30842630/ The histone methyltransferase EZH2 primes the early differentiation of follicular helper T cells during acute viral infection. unassigned - 2.1.1.355 Wiskott-Aldrich Syndrome https://pubmed.ncbi.nlm.nih.gov/11018264/ Gene regulation of Wiskott-Aldrich syndrome protein and the human homolog of the Drosophila Su(var)3-9: WASP and SUV39H1, two adjacent genes at Xp11.23. ongoing research 2 2.1.1.355 Wiskott-Aldrich Syndrome https://pubmed.ncbi.nlm.nih.gov/11018264/ Gene regulation of Wiskott-Aldrich syndrome protein and the human homolog of the Drosophila Su(var)3-9: WASP and SUV39H1, two adjacent genes at Xp11.23. unassigned - 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23011637/ The histone methyltransferase Wolf-Hirschhorn syndrome candidate 1-like 1 (WHSC1L1) is involved in human carcinogenesis. causal interaction 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23955539/ Lung tumor-associated dendritic cell-derived resistin promoted cancer progression by increasing Wolf-Hirschhorn syndrome candidate 1/Twist pathway. causal interaction 3 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/25677622/ Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. causal interaction 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. causal interaction 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/33589522/ WHSC1/NSD2 regulates immune infiltration in prostate cancer. causal interaction 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/34428935/ Wolf-Hirschhorn syndrome candidate 1 facilitates alveolar macrophage pyroptosis in sepsis-induced acute lung injury through NEK7-mediated NLRP3 inflammasome activation. causal interaction 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23011637/ The histone methyltransferase Wolf-Hirschhorn syndrome candidate 1-like 1 (WHSC1L1) is involved in human carcinogenesis. diagnostic usage 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. diagnostic usage 1 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/33589522/ WHSC1/NSD2 regulates immune infiltration in prostate cancer. diagnostic usage 3 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23011637/ The histone methyltransferase Wolf-Hirschhorn syndrome candidate 1-like 1 (WHSC1L1) is involved in human carcinogenesis. therapeutic application 3 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23921552/ WHSC1 links transcription elongation to HIRA-mediated histone H3.3 deposition. therapeutic application 1 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/25677622/ Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. therapeutic application 3 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/33589522/ WHSC1/NSD2 regulates immune infiltration in prostate cancer. therapeutic application 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23011637/ The histone methyltransferase Wolf-Hirschhorn syndrome candidate 1-like 1 (WHSC1L1) is involved in human carcinogenesis. ongoing research 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23921552/ WHSC1 links transcription elongation to HIRA-mediated histone H3.3 deposition. ongoing research 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/25677622/ Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. ongoing research 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. ongoing research 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/33589522/ WHSC1/NSD2 regulates immune infiltration in prostate cancer. ongoing research 4 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/34428935/ Wolf-Hirschhorn syndrome candidate 1 facilitates alveolar macrophage pyroptosis in sepsis-induced acute lung injury through NEK7-mediated NLRP3 inflammasome activation. ongoing research 1 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23921552/ WHSC1 links transcription elongation to HIRA-mediated histone H3.3 deposition. unassigned - 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/32472076/ H3K36 dimethylation by MMSET promotes classical non-homologous end-joining at unprotected telomeres. unassigned - 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/23955539/ Lung tumor-associated dendritic cell-derived resistin promoted cancer progression by increasing Wolf-Hirschhorn syndrome candidate 1/Twist pathway. unassigned - 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/25677622/ Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. unassigned - 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/34428935/ Wolf-Hirschhorn syndrome candidate 1 facilitates alveolar macrophage pyroptosis in sepsis-induced acute lung injury through NEK7-mediated NLRP3 inflammasome activation. unassigned - 2.1.1.355 Wolf-Hirschhorn Syndrome https://pubmed.ncbi.nlm.nih.gov/31092221/ The histone methyltransferase WHSC1 is regulated by EZH2 and is important for ovarian clear cell carcinoma cell proliferation. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. causal interaction 3 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. causal interaction 4 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. causal interaction 4 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/31666522/ Neuronal network dysfunction in a model for Kleefstra syndrome mediated by enhanced NMDAR signaling. causal interaction 3 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/25228647/ Setdb1 is required for germline development and silencing of H3K9me3-marked endogenous retroviruses in primordial germ cells. causal interaction 4 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33133132/ The Histone Methyltransferase SETDB1 Modulates Survival of Spermatogonial Stem/Progenitor Cells Through NADPH Oxidase. causal interaction 3 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. causal interaction 4 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/27070551/ Maternal Setdb1 Is Required for Meiotic Progression and Preimplantation Development in Mouse. causal interaction 4 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/27767173/ Euchromatin histone methyltransferase 1 regulates cortical neuronal network development. causal interaction 3 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. diagnostic usage 4 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/27767173/ Euchromatin histone methyltransferase 1 regulates cortical neuronal network development. diagnostic usage 3 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. therapeutic application 1 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. therapeutic application 4 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. therapeutic application 4 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/31666522/ Neuronal network dysfunction in a model for Kleefstra syndrome mediated by enhanced NMDAR signaling. therapeutic application 1 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. therapeutic application 2 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. ongoing research 1 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/31914391/ SETDB1-Mediated Cell Fate Transition between 2C-Like and Pluripotent States. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/28059589/ An HP1 isoform-specific feedback mechanism regulates Suv39h1 activity under stress conditions. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/23340989/ Histone methyltransferase Suv39h1 deficiency prevents Myc-induced chromosomal instability in murine myeloid leukemias. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/28271186/ SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/31666522/ Neuronal network dysfunction in a model for Kleefstra syndrome mediated by enhanced NMDAR signaling. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/25228647/ Setdb1 is required for germline development and silencing of H3K9me3-marked endogenous retroviruses in primordial germ cells. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33133132/ The Histone Methyltransferase SETDB1 Modulates Survival of Spermatogonial Stem/Progenitor Cells Through NADPH Oxidase. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33252038/ EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/27070551/ Maternal Setdb1 Is Required for Meiotic Progression and Preimplantation Development in Mouse. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/27767173/ Euchromatin histone methyltransferase 1 regulates cortical neuronal network development. unassigned - 2.1.1.355 [histone h3]-lysine9 n-trimethyltransferase deficiency https://pubmed.ncbi.nlm.nih.gov/33643820/ SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. unassigned -