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Literature summary for 2.7.10.1 extracted from

  • Liu, Z.; Hou, P.; Ji, M.; Guan, H.; Studeman, K.; Jensen, K.; Vasko, V.; El-Naggar, A.K.; Xing, M.
    Highly prevalent genetic alterations in receptor tyrosine kinases and phosphatidylinositol 3-kinase/akt and mitogen-activated protein kinase pathways in anaplastic and follicular thyroid cancers (2008), J. Clin. Endocrinol. Metab., 93, 3106-3116.
    View publication on PubMed

Application

Application Comment Organism
drug development genetically altered RTKs and their coupled PI3K/Akt and MAPK pathways may play an extensive role in the tumorigenesis and aggressiveness of anaplastic thyroid cancer, thus specific genotype-based targeting at these signaling pathways may be an effective therapeutic strategy for anaplastic thyroid cancer Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information mutations in RTK genes are uncommon in anaplastic thyroid cancer, but there are genomic copy number gains in many RTK genes with relatively high prevalences in these thyroid cancers. The prevalences of these copy gains are generally higher in anaplastic thyroid cancer than follicular thyroid cancer Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
anaplastic thyroid cancer cell genetic alterations of RTKs are relatively common in anaplastic thyroid cancer cells Homo sapiens
-
follicular thyroid cancer cell genetic alterations of RTKs are somewhat less common in follicular thyroid cancer cells Homo sapiens
-

Synonyms

Synonyms Comment Organism
Egfr
-
Homo sapiens
KIT
-
Homo sapiens
PDGFRalpha
-
Homo sapiens
PDGFRbeta
-
Homo sapiens
receptor tyrosine kinase
-
Homo sapiens
RTK
-
Homo sapiens
VEGFR1
-
Homo sapiens
VEGFR2
-
Homo sapiens