Mutant PIK3CA promotes cell growth and invasion of human cancer cells.
By Yardena Samuels, L. Diaz, O. Schmidt-Kittler, Jordan M. Cummins, Laura Delong, I. Cheong, C. Rago, D. Huso, Christoph Lengauer, Kenneth W. Kinzler and 2 more. Cancer Cell, 2005
938 citations recorded by the source corpus.
Subfields: Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/20e85e0e5f426c301351fd7d668e814e5517cacd
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In Molecular Biology
- David M. Sabatini
- Lewis C. Cantley
- R. Shaw
- J. Engelman
- M. Wymann
- D. Guertin
- Bernd Giese
- Romina Marone
In Pathology and Forensic Medicine
Citations in the corpus
- Defining the role of mTOR in cancer. (2007, background): “Because ablation of mTORC2 activity reduces FOXO1/3 T24/32 phosphorylation in MEFs, this might suggest that FOXOs are important targets of AKT in development.”
- PI3K pathway alterations in cancer: variations on a theme (2008, neutral): “These ‘hot spot’ mutations, H1047R, E545K and E542K, are non-synonymous missense mutations that confer constitutive kinase activity (Samuels et al., 2004, 2005).”
- A genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene. (2009, neutral): “In addition, a significant number of patients that do not have activating mutations in Ras have an activated Ras pathway through IL-6 signaling (Ogata et al., 1997; Rowley and Van Ness, 2002 ).”
- Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. (2007, neutral): “Imatinib also suppressed tyrosine phosphorylation of a number of important downstream signaling proteins including phospholipase Cg 1, the regulatory subunit of PI3K, Stat5, and SHP-2 (see Figure 5F and Table S6).”
- Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, background): “As a result, these cells are able to proliferate better in 2D and in 3D culture settings, and display reduced levels of apoptosis as compared to wild type cells, when grown in the absence of fetal calf serum [157].”
- PIK3CA mutations in colorectal cancer are associated with clinical resistance to EGFR-targeted monoclonal antibodies. (2009, background): “With regard to the role of PIK3CA mutations in affecting tumor progression, a number of functional evidences suggest that PIK3CA mutations might have a relatively mild effect on the growth of the tumor (12).”
- The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism (2006, background): “The expression of these p110α mutants in cells confers AKT activation in the absence of growth factor stimulatio”
- Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “Investigations of the most frequent p110α tumour mutations have shown that they enhance PI(3)K activity and drive cell transformatio”