Literature summary for 2.7.1.137 extracted from

Eichhorn, P.J.; Gili, M.; Scaltriti, M.; Serra, V.; Guzman, M.; Nijkamp, W.; Beijersbergen, R.L.; Valero, V.; Seoane, J.; Bernards, R.; Baselga, J.
Phosphatidylinositol 3-kinase hyperactivation results in lapatinib resistance that is reversed by the mTOR/phosphatidylinositol 3-kinase inhibitor NVP-BEZ235 (2008), Cancer Res., 68, 9221-9230.

Search for more literature for 2.7.1.137

Protein Variants

Protein Variants	Comment	Organism
E545K	a dominant activating mutation of the catalytic subunit PIK3CA that is prevalent in breast cancer and confers resistance to lapatinib, lapatinib effectively inhibits the transactivation of EGFR and HER2 by IGF-I signaling	Homo sapiens
H1047R	a dominant activating mutation of the catalytic subunit PIK3CA that is prevalent in breast cancer and confers resistance to lapatinib, lapatinib effectively inhibits the transactivation of EGFR and HER2 by IGF-I signaling	Homo sapiens
additional information	deregulation of the PI3K pathway, either through loss-of-function mutations in PTEN or dominant activating mutations in PIK3CA, leads to lapatinib resistance, which can be effectively reversed by NVP-BEZ235. Constitutive activation of the PI3K pathway decreases sensitivity to trastuzumab and lapatinib, overview	Homo sapiens

Inhibitors

Inhibitors	Comment	Organism	Structure
NVP-BEZ235	a mTOR/phosphatidylinositol 3-kinase inhibitor. Effector lapatinib and the PI3K inhibitor NVP-BEZ235 collaborate to suppress the PI3K-AKT-mTOR axis driven by loss-offunction PTEN mutations, overview	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
breast cancer cell	-	Homo sapiens	-
BT-474 cell	-	Homo sapiens	-
carcinoma cell	-	Homo sapiens	-
SK-BR-3 cell	a cell line overexpressing the HER2/c-erb-2 gene product	Homo sapiens	-

Synonyms

Synonyms	Comment	Organism
PI3K	-	Homo sapiens

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)