Exon 14 Deleted MET Receptor as a New Biomarker and Target in Cancers

摘要: Inhibitors of the receptor tyrosine kinase (RTK) MET have been ineffective at treating cancer, possibly because lack knowledge that would allow selection tumors likely to respond this treatment. In contrast, specific epidermal growth factor (EGFR) inhibitors used successfully against lung displaying activating mutations in domain EGFR. Recent publications describe a set causing exon 14 skipping, and importantly, several case reports objective responses MET-targeting patients with such mutations. These observations suggest novel therapeutic strategy for fighting especially lung. Exon encodes juxtamembrane targeted by mechanisms negatively regulate stability activity. review, we molecular leading first skipping then activation how process differs from triggered classical RTK-activating domain. We detail clinical characteristics carrying these sensitivity their inhibitors. Lastly, discuss future challenges related cancers, including patient screening anticipating resistance