Phosphatidylinositol 3-kinase mutations identified in human cancer are oncogenic.

By Sohye Kang, A. Bader, P. Vogt. Proceedings of the National Academy of Sciences of the United States of America, 2005

851 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/dc05b8d5c155d66d9505f968eba57c2944f56acb

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Citations in the corpus

An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer (2008, background): “These mutations have been reported to activate AKT and downstream signaling in model systems but their effects in patient tumors are unknown (5).”
Mutational Analysis Reveals the Origin and Therapy-driven Evolution of Recurrent Glioma (2013, neutral): “recurrent tumor of patient 18 that drives Akt hyperactivation and induces mTOR-dependent oncogenic transformation (35).”
Oncogenic mutations of PIK3CA in human cancers. (2004, background): “Indeed, follow-up functional analyses of the PIK3CA mutations confirmed them to be constitutively kinase activating and oncogenic (Bader et al. 2006; Kang et al. 2005; Samuels et al. 2004, 2005; Zhao and Vogt 2008).”
Perturbations of the AKT signaling pathway in human cancer (2005, background): “Moreover, recently the growth-regulatory and signaling properties of the three most common PIK3CA mutations seen in tumors, namely E542K, E545K and H1047R, were each found to induce oncogenic transformation with high efficiency (Kang et al., 2005).”
Spatial and temporal diversity in genomic instability processes defines lung cancer evolution (2014, background): “For instance, L008 presented with an activating BRAF (G469A) mutation (30) in all regions and an activating PIK3CA (E542K) mutation (31) only in region R3.”
Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, background): “Transfected with mutated PI3Kα, these cells show constitutive phosphorylation of PKB/Akt and of downstream proteins S6K, 4E-BP1 and forkhead transcription factors [155–157].”
A central role for HER3 in HER2-amplified breast cancer: implications for targeted therapy. (2008, background): “B, the extent of phosphorylation of HER3 (top ) and EGFR (bottom ) normalized to total receptor level for the entire sample set was quantified by densitometry. a frequently observed gain-of-function mutation in the kinase domain of PIK3CA (33), which could potentially affect response to knockdown.”