期刊
ONCOTARGETS AND THERAPY
卷 13, 期 -, 页码 5691-5706出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S219959
关键词
non-small-cell lung cancer; MET exon 14; MET amplification; MET pathway
The c-MET proto-oncogene (MET) plays an important role in lung oncogenesis, affecting cancer-cell survival, growth and invasiveness. The MET receptor in non-small-cell lung cancer (NSCLC) is a potential therapeutic target. The development of high-output next-generation sequencing techniques has enabled better identification of anomalies in the MET pathway, like the MET exon-14 (METex14) mutation. Moreover, analyses of epidermal growth factor-receptor (EGFR) and mechanisms of resistance to tyrosine-kinase inhibitors (TKIs) demonstrated the importance of MET amplification as an escape mechanism in patients with TKI-treated EGFR-mutated NSCLCs. This review summarizes the laboratory findings on METand its anomalies, trial results on METex14 alterations and MET amplification in non-EGFRmutated NSCLCs, and acquired resistance to TKI in EGFR-mutated NSCLCs. The outcomes of the first trials with anti-MET agents on non-selected NSCLC patients or those selected for METoverexpression were disappointing. Two situations seem themost promising today for the use of anti-METagents to treat these patients: tumors harboringMETex14 and those EGFR-sensitivemutationmutated under TKI-EGFR with a MET-amplification mechanism of resistance or EGFR-resistance mutation.
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