Impact of somatic PI3K pathway and ERBB family mutations on pathological complete response (pCR) in HER2-positive breast cancer patients who received neoadjuvant HER2-targeted therapies.
Eustace, Alexander J
Sheehan, Katherine M
Madden, Stephen F
Kay, Elaine W
Kennedy, M John
Hill, Arnold D
Hennessy, Bryan T
Local subject classificationBREAST CANCER
Antineoplastic Combined Chemotherapy Protocols
Class I Phosphatidylinositol 3-Kinases
Gene Expression Regulation, Neoplastic
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CitationImpact of somatic PI3K pathway and ERBB family mutations on pathological complete response (pCR) in HER2-positive breast cancer patients who received neoadjuvant HER2-targeted therapies. 2017, 19 (1):87 Breast Cancer Res.
JournalBreast cancer research : BCR
AbstractThe Cancer Genome Atlas analysis revealed that somatic EGFR, receptor tyrosine-protein kinase erbB-2 (ERBB2), Erb-B2 receptor tyrosine kinase 3 (ERBB3) and Erb-B2 receptor tyrosine kinase 4 (ERBB4) gene mutations (ERBB family mutations) occur alone or co-occur with somatic mutations in the gene encoding the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (PIK3CA) in 19% of human epidermal growth factor receptor 2 (HER2)-positive breast cancers. Because ERBB family mutations can activate the PI3K/AKT pathway and likely have similar canonical signalling effects to PI3K pathway mutations, we investigated their combined impact on response to neoadjuvant HER2-targeted therapies.
SponsorsThis work was supported by the Irish Cancer Society Collaborative Cancer Research Centre under BREAST-PREDICT grant CCRC13GAL (www.breastpredict.com), the Health Research Board (HRA/POR2012/054), the North East Cancer Research and Education Trust, and the Science Foundation Ireland-funded Molecular Therapeutics for Cancer Ireland (08-SRC-B1410)