High Frequency of Mutations of the PIK3CA Gene in Human Cancers
By Yardena Samuels, Zhenghe Wang, A. Bardelli, Natalie Silliman, Janine Ptak, Steve Szabo, Hai Yan, Adi F. Gazdar, S. Powell, G. Riggins and 5 more. Science, 2004
3,682 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/0ff3e796af4df608ea968078e102ff1a1e7a2c2f
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In Genetics
In Molecular Biology
- Lewis C. Cantley
- David M. Sabatini
- R. Weinberg
- T. Franke
- R. Shaw
- J. Engelman
- Craig B. Thompson
- T. Balla
Citations in the corpus
- A Pharmacological Map of the PI3-K Family Defines a Role for p110α in Insulin Signaling (2006, positive): “This interest has been fueled by the recent discovery that p110a is frequently mutated in primary tumors (Samuels et al., 2004) and evidence that the lipid phosphatase PTEN, an inhibitor of PI3-K signaling, is a commonly inactivated tumor suppressor (Cantley and Neel, 1999).”
- PI3K pathway alterations in cancer: variations on a theme (2008, positive): “Activating mutations in PIK3CA, the gene encoding the p110a catalytic subunit of PI3K, were recently identified as novel mechanisms of inducing oncogenic PI3K signaling (Samuels et al., 2004).”
- Cancer genomics: from discovery science to personalized medicine (2011, background): “On the heels of BRAF , it was discovered that PIK3CA is frequently mutated in colorectal cancer”
- Perturbations of the AKT signaling pathway in human cancer (2005, background): “The locations of the mutations within PIK3CA coincided with their potential to increase PI3K activity, because expression of a ‘hot spot’ p110a mutant in NIH3T3 cells conferred more lipid kinase activity than did expression of the wild-type protein (Samuels et al., 2004).”
- PIK3CA mutations correlate with hormone receptors, node metastasis, and ERBB2, and are mutually exclusive with PTEN loss in human breast carcinoma. (2005, methodology): “Sequencing of PIK3CA exons 1, 2, 4, 5, 7, 9, 12, 13, 18, 20, including intron-exon boundaries was done by PCR amplification and direct sequencing of both strands for all tumors as previously described (6) with some modifications.”
- Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity (2008, background): “First, systemic sequencing of the PIK3CA gene has revealed the presence of somatic mutations (11), occurring along the coding region of the gene but with most of them present in two hotspots.”
- Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “Strikingly, a large-scale effort to sequence exons of PI(3)K genes from human tumours revealed clustered regions of point mutations in the p110α catalytic subunit in 20–30p of breast, colon, brain and gastric tumours examine”
- Brick by brick: metabolism and tumor cell growth. (2008, background): “Augmentation of this pathway by mutations activating PI3K or eliminating negative regulators like PTEN comprises a prevalent category of mutation in human cancer [35,36].”
- The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “From the top of the pathway, PI3K class IA is mutated and amplified in a variety of cancers (Samuels et al., 2004).”
- Autophagy: dual roles in life and death? (2005, background): “Mutations in both positive and negative regulators of autophagy that are components of the class I PI3K pathway are associated with human cancer”
- ErbB receptors and signaling pathways in cancer. (2009, background): “In NSCLC, Akt mutations appear to be rare [36] and p110a mutations have been reported only in 4% of the cases [45,46].”