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FP14.04 Resistance to MET Inhibition in MET Driven NSCLC and Response after Switching from Type I to Type II MET Inhibitors

R. Riedel,C. Heydt,A. Scheel, H. Tumbrink,J. Brägelmann,J. Fassunke,L. Nogova,S. Michels,M. Scheffler,R. Fischer,S. Koleczko,J. Weber,T. Westphal,D. Abdulla,S. Merkelbach-Bruse,M. Sos,R. Büttner,J. Wolf

Journal of Thoracic Oncology（2021）

Cited 3|Views14
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Abstract
Molecular aberrations of the MET gene including MET Exon 14 skipping mutations (METΔex14), amplifications and translocations activate oncogenic signaling in lung cancer and are sensitive to MET inhibition. Resistance to targeted therapy with MET tyrosine kinase inhibitors (TKI) occurs inevitably and is poorly understood.
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Key words
Targeted therapy, aquired resistance, MET
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