MET14外显子跳跃突变与非小细胞肺癌

doi:10.3760/cma.j.cn371439-20201207-00070

摘要/Abstract

摘要：

MET14外显子(METex14)跳跃突变的分子机制主要是METex14跳跃导致c-Cbl酪氨酸结合位点丢失,从而引起蛋白酶体介导的MET蛋白降解率降低,使MET信号持续激活,最终导致肿瘤发生。METex14跳跃突变在非小细胞肺癌中的发生率为3%~4%。作用于METex14跳跃突变的药物包括克唑替尼、卡马替尼、特泊替尼、沃利替尼等,且客观缓解率均较高,安全性良好。但是由于存在基因扩增、第二位点突变、旁路激活和病理类型转化等,经靶向药物治疗后出现药物耐药需引起注意。

关键词: 癌, 非小细胞肺, MET14外显子跳跃突变, 酪氨酸激酶抑制剂

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.

Key words: Carcinoma, non-small-cell lung, MET exon 14 skipping mutation, Tyrosine kinase inhibitors

周晔, 于雁. MET14外显子跳跃突变与非小细胞肺癌[J]. 国际肿瘤学杂志, 2021, 48(6): 366-369.

Zhou Ye, Yu Yan. MET14 exon skipping mutation and non-small cell lung cancer[J]. Journal of International Oncology, 2021, 48(6): 366-369.

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