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Acquired Resistance Mechanisms to Combination Met-TKI/EGFR-TKI Exposure in Met-Amplified EGFR-TKI-Resistant Lung Adenocarcinoma Harboring an Activating EGFR Mutation.

Molecular cancer therapeutics - 1 Dec 2016

Yamaoka Toshimitsu, Ohmori Tohru, Ohba Motoi, Arata Satoru, Kishino Yasunari, Murata Yasunori, Kusumoto Sojiro, Ishida Hiroo, Shirai Takao, Hirose Takashi, Ohnishi Tsukasa, Sasaki Yasutsuna

Abstract excerpt

Met-amplified EGFR-tyrosine kinase inhibitor (TKI)-resistant non-small cell lung cancer (NSCLC) harboring an activating EGFR mutation is responsive to concurrent EGFR-TKI and Met-TKI treatment in a preclinical model. Here, we determined that Met-amplified gefitinib-resistant cells acquire dual resistance to inhibition of EGFR and Met tyrosine kinase activities. PC-9 lung adenocarcinoma cells harboring 15-bp...

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PMID: 27612490
DOI: 10.1158/1535-7163.MCT-16-0313

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EGFR
IGF1
SET
SMYD3

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Acquired Resistance Mechanisms to Combination Met-TKI/EGFR-TKI Exposure in Met-Amplified EGFR-TKI-Resistant Lung Adenocarcinoma Harboring an Activating EGFR Mutation.PMID 27612490Read ↗

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Strategies to Overcome Bypass Mechanisms Mediating Clinical Resistance to EGFR Tyrosine Kinase Inhibition in Lung Cancer.Semantic proximity Read ↗

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