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- W2012871610 abstract "MET receptor tyrosine kinase and its natural ligand, hepatocyte growth factor, have been implicated in a variety of cancers, including non-small cell lung cancer (NSCLC). Mechanisms by which cellular deregulation of MET occurs include overexpression, genomic amplification, mutation, or alternative splicing. MET overexpression or activation is a known cause of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in NSCLC. Inhibition of MET signaling in these EGFR tyrosine kinase inhibitor-resistant cells may potentially restore sensitivity to EGFR inhibitors. Tivantinib (ARQ 197), reported as a small-molecule MET inhibitor, has demonstrated antitumor activity in early clinical studies. This review focuses on MET and lung cancer, the clinical development of tivantinib, the clinical trials of tivantinib in NSCLC to date, its current/emerging role in the management of NSCLC, and future directions." @default.
- W2012871610 created "2016-06-24" @default.
- W2012871610 creator A5035198996 @default.
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- W2012871610 date "2014-10-01" @default.
- W2012871610 modified "2023-09-26" @default.
- W2012871610 title "Targeting the MET receptor tyrosine kinase in non-small cell lung cancer: emerging role of tivantinib" @default.
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- W2012871610 doi "https://doi.org/10.2147/cmar.s37345" @default.
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