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• W4361952061 abstract "<div>Abstract<p><b>Purpose:</b> <i>MET</i> amplification, responsible for 20% of acquired resistance to EGFR tyrosine kinase inhibitor (TKI) in patients with advanced non–small cell lung cancer (NSCLC), presents an attractive target. Numerous studies have conferred susceptibility of <i>MET</i> mutations and focal amplification to targeted MET-TKIs. However, the mechanism underlying MET-TKIs–induced resistance remains elusive.</p><p><b>Experimental Design:</b> We conducted a cohort of 12 patients with advanced NSCLC who developed resistance to a combinatorial therapy consisting of gefitinib and a type I MET-TKI. We performed capture-based targeted ultra-deep sequencing on serial tumor biopsies and plasmas ctDNA samples to detect and quantify genetic alterations.</p><p><b>Results:</b> We identified 2 newly acquired <i>MET</i> mutations, Y1248H and D1246N, in 2 patients and further confirmed their resistance against type I MET-TKIs <i>in silco, in vitro</i>, and <i>in vivo</i>. Interestingly, NIH3T3 cells harboring either mutation exhibited responses to type II MET-TKIs, suggesting sequential use of MET-TKIs may offer a more durable response. In addition, we also discovered that EGFR amplification may act as an alternative MET-TKI resistance mechanism.</p><p><b>Conclusions:</b> Our study provides insight into the diversity of mechanisms underlying MET-TKI–induced resistance and highlights the potential of sequential use of MET-TKIs. <i>Clin Cancer Res; 23(16); 4929–37. ©2017 AACR</i>.</p></div>" @default.
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• W4361952061 date "2023-03-31" @default.
• W4361952061 modified "2023-10-17" @default.
• W4361952061 title "Data from Acquired <i>MET</i> Y1248H and D1246N Mutations Mediate Resistance to MET Inhibitors in Non–Small Cell Lung Cancer" @default.
• W4361952061 doi "https://doi.org/10.1158/1078-0432.c.6525294.v1" @default.
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