Ras, PI(3)K and mTOR signalling controls tumour cell growth

By R. Shaw, Lewis C. Cantley. Nature, 2006

2,120 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/657b9110e5bf0f844d72de6ed0043af3bc9070a7

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In Molecular Biology

Citations in the corpus

With TOR less is more: a key role for the conserved nutrient sensing TOR pathway in aging (2010, positive): “This has led to the view that TOR signaling serves as a ‘‘growth checkpoint,’’ surveying the extra and intracellular milieu for favorable conditions to mediate growth accordingly (Shaw and Cantley, 2006).”
Rare de novo variants associated with autism implicate a large functional network of genes involved in formation and function of synapses (2011, background): “See also Table S4. target of rapamycin (mTOR) pathway (Kumar et al., 2005; Shaw and Cantley, 2006).”
Hypoxic and Ras-transformed cells support growth by scavenging unsaturated fatty acids from lysophospholipids (2013, background): “Two of the most commonly activated pathways in human cancer are the PI3K-Akt and the Ras pathways (3).”
Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “The mTOR receives stimulatory signals from growth factors through RAS and PI3K, as well as from nutrient inputs through amino acids, glucose, and oxygen availability [286].”
ERK promotes tumorigenesis by inhibiting FOXO3a via MDM2-mediated degradation (2008, background): “Results Erk suppresses FOXO3a stability and induces its nuclear exclusion The RAS–ERK is an essential oncogenic signalling cascade that promotes tumour cell growth and developmen”
Digoxin and other cardiac glycosides inhibit HIF-1α synthesis and block tumor growth (2008, neutral): “Whereas VHL loss-of-function leading to dysregulated HIF-1 expression is restricted to renal cell carcinoma and cerebellar hemangioblastoma, many common human cancers have mutations in phosphatidylinositol 3-kinase or upstream signaling pathways (13).”
The LKB1-AMPK pathway: metabolism and growth control in tumor suppression (2009, background): “Cancer genetics and Drosophila melanogaster genetics led to the discovery of upstream components of mTORC1, including the tuberous sclerosis complex 2 ( TSC2 ) tumour suppressor and its obligate partner TSC1 (Ref”
Post operative radiation therapy in endometrial carcinoma : reducing overtreatment and improving quality of life (2013, background): “PTEN, KRAS and PIK3CA converge in the PI3K-AKT signalling pathway, which has been implicated in nearly all aspects of tumor biology.(22,23) ß-catenin is a key component of the Wnt signaling pathway, interacting with the TCF/LEF family of transcription factors.”
Oncogenic activation of the RAS/RAF signaling pathway impairs the response of metastatic colorectal cancers to anti-epidermal growth factor receptor antibody therapies. (2007, background): “The second involves the lipid kinase phosphatidylinositol 3-kinase that triggers activation of the PDK1-AKT signaling machinery (13).”
The PI3K pathway as drug target in human cancer. (2010, background): “PI3K also can be activated by genetic mutation and/or amplification of upstream RTKs, and possibly by mutationally activated Ras.(7,17) The”
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): “Overactivation of the PI3K pathway could be the result of different genetic alterations (10).”
Melanoma biology and new targeted therapy (2007, background): “Phosphoinositides are membrane lipids that are converted to second messengers through hyper-phosphorylation by one of a family of PI(3)K”