期刊
CANCER DISCOVERY
卷 5, 期 8, 页码 842-849出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2159-8290.CD-14-1467
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- NCI NIH HHS [P01 CA129243, P30 CA008748] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA129243, P30CA008748] Funding Source: NIH RePORTER
Mutations in the MET exon 14 RNA splice acceptor and donor sites, which lead to exon skipping, deletion of the juxtamembrane domain containing the CBL E3-ubiquitin ligase-binding site, and decreased turnover of the resultant aberrant MET protein, were previously reported to be oncogenic in preclinical models. We now report responses to the MET inhibitors crizotinib and cabozantinib in four patients with stage IV lung adenocarcinomas harboring mutations leading to MET exon 14 skipping, highlighting a new therapeutic strategy for the 4% of lung adenocarcinoma patients whose tumors harbor this previously underappreciated genetic alteration. SIGNIFICANCE: Oncogenic mutations in the MET exon 14 splice sites that cause exon 14 skipping occur in 4% of lung adenocarcinomas. We report responses to the MET inhibitors crizotinib and cabozantinib in patients with lung adenocarcinomas harboring MET exon 14 splice site mutations, identifying a new potential therapeutic target in this disease. (C) 2015 AACR.
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