MET14 exon skipping mutation and non-small cell lung cancer / 国际肿瘤学杂志

ABSTRACT

The molecular mechanism of the skipping mutation of MET14 exon (METex14) is mainly that the skipping of METex14 leads to the loss of the c-Cbl tyrosine binding site, which causes the proteasome-mediated degradation of MET protein to decrease, which continuously activates the MET signal, and finally leads to tumorigenesis. The incidence of METex14 skipping mutations in non-small cell lung cancer is 3%-4%. Drugs that act on skipping mutations of METex14 include crizotinib, capmatinib, tepotinib, savolitinib, and have a high objective remission rate and good safety. However, due to gene amplification, second site mutations, bypass activation and pathological type conversion, drug resistance after targeted drug therapy requires attention.