title: Oncogenic MET as an Effective Therapeutic Target in Non-Small Cell Lung Cancer Resistant to EGFR Inhibitors: The Rise of the Phoenix.
abstract: Anecdotal reports have shown that concomitant inhibition of EGFR and MET can be clinically effective in patients with non-small cell lung cancer carrying EGFR mutations and MET amplification, but large phase III trials in genetically unselected individuals have failed to confirm the benefit of this combination therapy. A new study corroborates the evidence that lung cancer susceptibility to EGFR and MET blockade is sustained by genetically based activation of both targets and identifies a mutation in MET that confers acquired resistance to standard MET inhibitors hitting the active kinase, yet is vulnerable to other MET-directed compounds with a different binding mode. Cancer Discov; 6(12); 1306-8. ©2016 AACR.See related article by Bahcall and colleagues, p. 1334.
authors.affiliation: Laboratory of Translational Cancer Medicine, Candiolo Cancer Institute IRCCS, and Department of Oncology, University of Torino School of Medicine, Candiolo, Torino, Italy. livio.trusolino@ircc.it.
authors.forename: Livio
authors.initials: L
authors.lastname: Trusolino
mesh_terms: D002289:Carcinoma, Non-Small-Cell Lung; D019008:Drug Resistance, Neoplasm / Q000187:drug effects; D066246:ErbB Receptors / Q000037:antagonists & inhibitors*; D006801:Humans; D008175:Lung Neoplasms; D047428:Protein Kinase Inhibitors / Q000737:chemistry; D019859:Proto-Oncogene Proteins c-met / Q000037:antagonists & inhibitors
chemical_list: D047428:Protein Kinase Inhibitors; D066246:ErbB Receptors; D019859:Proto-Oncogene Proteins c-met