Oncogenic kinase signalling

By P. Blume-Jensen, T. Hunter. Nature, 2001

3,795 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/3259fa0b3c6039fe70f124aba9752a2c42a9a50a

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In Oncology

Citations in the corpus

Transcription factors as targets for cancer therapy (2002, background): “gif" NDATA ITEM> ]> The initial flurry (1976–1985) in the discovery of oncogenes — mutated genes that allow unregulated cell growth — yielded a large number of proteins that are involved in cell signallin”
Temporal analysis of phosphotyrosine-dependent signaling networks by quantitative proteomics (2004, background): “In growth factor signaling, stimulation of cell-surface receptors first triggers activation of the receptor itself and then of a large number of intracellular effector molecule”
The discovery of receptor tyrosine kinases: targets for cancer therapy (2004, background): “More than half of these have been found to be overexpressed or mutated in human hyperproliferative or hypoproliferative diseases and are therefore considered to be targets for cancer therap”
Vascular endothelial growth factor in eye disease. (2008, neutral): “1A) (Hanks and Quinn, 1991; Blume-Jensen and Hunter, 2001).”
Exploiting the PI3K/AKT Pathway for Cancer Drug Discovery (2005, background): “Recruitment to the membrane results in a conformational change that exposes two crucial amino acids that are phosphorylated and necessary for activation: one in the kinase domain (threonine 308 in AKT1) is phosphorylated by constitutively active phosphoinositide-dependent kinase 1 (PDK1), stabilizin”
Molecular mechanisms of drug resistance (2005, background): “Protein tyrosine kinases (PTKs) can have an important impact on drug resistance through their regulation of anti-apoptotic signal transduction pathways [206].”
Intercellular transfer of the oncogenic receptor EGFRvIII by microvesicles derived from tumour cells (2008, background): “Although the present study focuses on EGFRvIII and human glioma cells, a similar microvesicular transfer mechanism could also involve other mutant, upregulated or otherwise activated membrane-associated oncogenic tyrosine kinases (for example, HER-2, wtEGFR, cKit or MET”
An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms. (2007, background): “An emerging paradigm in oncology is that robust clinical efficacy can be obtained with inhibitors directed toward oncogenic receptor tyrosine kinases (RTK) that are mutated or otherwise dysregulated in selected advanced tumors (1, 2).”
Protein-tyrosine phosphatases and cancer (2006, background): “Perturbation of PTK activity by mutations or over-expression results in malignant transformatio”
Nuclear retinoid receptors and the transcription of retinoid-target genes. (2004, background): “, 2002b), one can postulate that the retinoid resistance of some cancer cells would result from aberrant kinome signaling (Blume-Jensen and Hunter, 2001; Tari et al., 2002).”
Ageing as a risk factor for disease. (2012, background): “Accordingly, hyperinsulinaemia stimulates cell division and can induce cancer [46] and positive regulators of IIS signalling are usually oncogenic whereas negative regulators are tumour suppressors [47].”
The role of autophagy in cancer development and response to therapy (2005, background): “Recent evidence indicates that the phosphatidylinositol 3-kinase (PI3K)–AKT–mTOR pathway, which is activated in many types of cance”
The crucial role of protein phosphorylation in cell signaling and its use as targeted therapy (Review) (2017, neutral): “To date, more than 1,000 variations in the expression of protein kinases have been detected in human tumors (108-111).”