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• W2090920004 abstract "Target-based therapeutic development has significantly changed cancer treatment and has generated new sense of optimism. Cancers that contain multiple genetic and epigenetic abnormalities remain addicted to one or few genes for their malignant phenotype and cell survival. Inhibition of these abnormalities via monoclonal antibodies (mAbs) and small-molecule inhibitors (SMIs) have brought about new hope in NSCLC. MET gene was initially discovered in the laboratory of George Vande Woude as part of a transforming fusion gene between transforming promoter region (TPR) and MET which was derived from a chromosomal translocation after treatment with N-methyl-N-nitro-N-nitrosoguanidine. 1 MET is located on chromosome 7, encodes for a single precursor which is post-transcriptionally digested, forming an extracellular -chain and a transmembrane s-chain linked by disulfide bonds. The ligand for MET is hepatocyte growth factor (HGF)/Scatter Factor (SF), which is synthesized as a single inactive polypeptide chain (pro-HGF/SF) and cleaved to an active, disulfide-linked dimer by serine proteases including uPA, tPA, and then binds to the MET Sema domain. 2 Ligation of the MET receptor by HGF leads to receptor dimerization and activation of its intrinsic tyrosine kinase and further autophosphorylation or phosphorylation of downstream intermediates and activation of signaling pathways. MET can be activated by mutations, autocrine/paracrine growth, overexpression by gene amplification, or decreased degradation. Germline and somatic MET gene mutations have been reported in hereditary and sporadic papillary renal cell cancers. 3‐5 Both MET gene mutations and amplifications have now been reported in other cancers, although at low frequencies but as genetic predictors of therapeutic sensitivity. 6 Expression of MET and phosphoMET has been studied in lung cancer, and recently it was shown that 40% of lung cancer tissues overexpressed MET. 7 Summary of Presentations MET as a therapeutic target in NSCLC Dr. Robert C. Doebele discussed some of the key background points surrounding MET inhibition in NSCLC. He noted that survival in NSCLC patients with 5 copies/cell is worse than those with less than 5 copies/cell and that MET gene amplification leads to EGFR tyrosine kinase resistance in EGFR mutant patients.8 Anti-HGF Abs, anti-MET Abs, and small-molecule MET TKI inhibitors are all in various stages of development, and predictive biomarkers for MET inhibitors will be important to elucidate for future trials and treatment decisions." @default.
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• W2090920004 date "2011-11-01" @default.
• W2090920004 modified "2023-10-18" @default.
• W2090920004 title "Inhibition of MET Receptor Tyrosine Kinase and Its Ligand Hepatocyte Growth Factor" @default.
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• W2090920004 doi "https://doi.org/10.1097/01.jto.0000407568.45147.43" @default.
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