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Targeting the MET receptor tyrosine kinase in non-small cell lung cancer: emerging role of tivantinib

Authors Agwa E, Ma P

Received 22 April 2014

Accepted for publication 27 June 2014

Published 4 October 2014 Volume 2014:6 Pages 397—404

DOI https://doi.org/10.2147/CMAR.S37345

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3


Eberechi S Agwa, Patrick C Ma

Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA

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.

Keywords: MET inhibitor, tivantinib, ARQ 197, non-small cell lung cancer

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