Cellular function of phosphoinositide 3-kinases: implications for development, homeostasis, and cancer.
By R. Katso, K. Okkenhaug, K. Ahmadi, S. White, J. Timms, M. Waterfield. Annual Review of Cell and Developmental Biology, 2001
718 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/bb6735e315e479a9a8c331ffb2ad54de7e688f2f
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Citations in the corpus
- Phase I, dose-escalation study of BKM120, an oral pan-Class I PI3K inhibitor, in patients with advanced solid tumors. (2012, background): “signaling; inhibition blocks the metabolic actions of insulin, including glucose transport and glycogen synthesis,(2,3,28-30) resulting in increased blood glucose and compensatory release of insulin (and C-peptide) from pancreatic -cells.(3) Disturbance of glucose homeostasis as evidenced by hypergl”
- Targeting PI3K/Akt signal transduction for cancer therapy (2021, background): “PI3K forms a complex with E-cadherin, β-catenin, and VEGFR-2 and is involved in endothelial signaling mediated by VEGF through the activation of the PI3K/Akt pathway.(160) The PI3K/Akt signaling pathway also promotes TNF-induced endothelial cell migration and regulates tumor angiogenesis.”
- A Pharmacological Map of the PI3-K Family Defines a Role for p110α in Insulin Signaling (2006, unknown): “In the appropriate cellular context, these three lipids control diverse physiological processes including cell growth, survival, differentiation, and chemotaxis (Katso et al., 2001).”
- The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “Data coming from mice lacking p110a regulatory subunits have shed light on the dual role of p85 in PI3K regulation in response to insulin (Katso et al., 2001).”
- The PI3K pathway as drug target in human cancer. (2010, background): “forms, p110 , p110 , and p110 , are the products of three genes, PIK3CA, PIK3CB, and PIK3CD.(5,8) As”
- Targeting PI3K in cancer: mechanisms and advances in clinical trials (2019, background): “In a global, randomised, phase III trial, idelalisib plus atumumab (a second-generation anti-CD20 antibody) resulted in better PFS (16.3 months vs.8.0months, HR 0·27, p 0·0001) compared with atumumab alone in patients with relapsed chronic lymphocytic leukaemia progressing less than 24 months from”