The PIK3CA gene is mutated with high frequency in human breast cancers

By K. Bachman, P. Argani, Yardena Samuels, Natalie Silliman, Janine Ptak, Steve Szabo, H. Konishi, B. Karakas, B. Blair, Clarence Lin and 3 more. Cancer Biology & Therapy, 2004

714 citations recorded by the source corpus.

Subfields: Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/2b69625553b8004e67fb8e618ca7689aacd37340

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Citations in the corpus

A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma. (2006, positive): “Gain-of-function mutations in the p110 a gene ( PIK3CA ) are found in cancers of the colon, breast, and brain (Bachman et al., 2004; Broderick et al., 2004; Samuels et al., 2004).”
Exploiting the PI3K/AKT Pathway for Cancer Drug Discovery (2005, background): “PI3K itself is a frequent target of mutational activatio”
Cancer genomics: from discovery science to personalized medicine (2011, background): “and other tumor types, most notably in breast cancer where it is the most commonly mutated gen”
The crucial role of protein phosphorylation in cell signaling and its use as targeted therapy (Review) (2017, neutral): “This drug also targets against PI3K in solid tumors (124,125), serine/threonine kinase BRAF to treat melanoma (126-128), the receptor tyrosine kinase EGFR for lung cancer (129,130), and serine/threonine kinase mTOR for the treatment of renal tumors (131).”
Mutation of the PIK3CA Gene in Ovarian and Breast Cancer (2004, background): “(9) suggested that exon 20 mutations predominate in breast cancers in contrast to colorectal cancers where exon 9 mutations are more common.”
Oncogenic mutations of PIK3CA in human cancers. (2004, background): “However, due to the relatively small number of samples studied and the fact that, despite years of effort, a commonly mutated breast cancer oncogene had not yet been discovered, several groups immediately initiated more comprehensive mutational analyses of PIK3CA in breast cancer (Bachman et al. 200”
Stem cell and epithelial-mesenchymal transition markers are frequently overexpressed in circulating tumor cells of metastatic breast cancer patients (2009, background): “Also involved is PI3Kα, which activates the Akt1 and Akt2 Ser/Thr kinase, responsible for proliferation and antiapoptotic function [ 19-22 ].”
ErbB receptors and signaling pathways in cancer. (2009, background): “Considering breast tumors, somatic activating mutations in Akt [35,36] and the p110a subunit of the PI3K [35,37,38] have been detected in 3–5% and 20–25% of primary breast tumors, respectively.”
Targeting cancer with small molecule kinase inhibitors (2009, positive): “Perhaps the most notable success from these efforts was the discovery that PI3KCA is frequently mutated in numerous cancers and that these mutations impart transforming potential in vitro as well as in vivo”
PI3K/Akt: getting it right matters (2008, background): “One caveat for targeting Akt, however, is that genetic changes in upstream signaling molecules (for example, PIK3CA) will not only affect Akt signaling, but also other parallel pathways that are regulated by these upstream activators.”
PIK3CA mutations correlate with hormone receptors, node metastasis, and ERBB2, and are mutually exclusive with PTEN loss in human breast carcinoma. (2005, background): “who found no correlation to ERBB2 staining (8).”
Improved classification of breast cancer by analysis of genetic alterations and gene expression profiling (2011, background): “[11] Bachman KE, Argani P, Samuels Y, et al.”