Amplification of Wild-type KRAS Imparts Resistance to Crizotinib in MET Exon 14 Mutant Non-Small Cell Lung Cancer.

doi:10.1158/1078-0432.CCR-18-0876

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Article

Amplification of Wild-type KRAS Imparts Resistance to Crizotinib in MET Exon 14 Mutant Non-Small Cell Lung Cancer.

Clinical cancer research : an official journal of the American Association for Cancer Research - 1 Dec 2018

Bahcall Magda, Awad Mark M, Sholl Lynette M, Wilson Frederick H, Xu Man, Wang Stephen, Palakurthi Sangeetha, Choi Jihyun, Ivanova Elena V, Leonardi Giulia C, Ulrich Bryan C, Paweletz Cloud P, Kirschmeier Paul T, Watanabe Masayuki, Baba Hideo, Nishino Mizuki, Nagy Rebecca J, Lanman Richard B, Capelletti Marzia, Chambers Emily S, Redig Amanda J, VanderLaan Paul A, Costa Daniel B, Imamura Yu, Jänne Pasi A

Abstract excerpt

PURPOSE: MET inhibitors can be effective therapies in patients with MET exon 14 (METex14) mutant non-small cell lung cancer (NSCLC). However, long-term efficacy is limited by the development of drug resistance. In this study, we characterize acquired amplification of wild-type (WT) KRAS as a molecular mechanism behind crizotinib resistance in three cases of METex14-mutant NSCLC and propose a combination therapy...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 30072474
DOI: 10.1158/1078-0432.CCR-18-0876
PMCID: PMC6279568

Genes

KRAS
MET
EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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