Pan Sisi, Wang Na, Song Xia
The Second Clinical Medical College of Shanxi Medical University, Taiyuan 030001, China.
The Second Department of Respiratory, Shanxi Provincial Cancer Hospital, Taiyuan 030013, China.
Zhongguo Fei Ai Za Zhi. 2022 Aug 20;25(8):615-621. doi: 10.3779/j.issn.1009-3419.2022.102.23.
Mesenchymal-epithelial transition factor (MET) amplification is an important driver of resistance in epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC), and the combination of MET proto-oncogene (MET) and EGFR-tyrosine kinase inhibitors (TKIs) has shown promise in overcoming this molecularly defined acquired resistance. Emerging data also demonstrate MET amplification as a resistance driver to TKIs-treated anaplastic lymphoma kinase (ALK)-, RET-, and ROS1-fusion NSCLC. Here, we review the literature on recent research progress of MET amplification as a resistance driver to targeted therapy in oncogene-driven NSCLC and summarize the progress of clinical strategies to overcome the resistance mechanism. .
间充质-上皮转化因子(MET)扩增是表皮生长因子受体(EGFR)突变的非小细胞肺癌(NSCLC)耐药的重要驱动因素,MET原癌基因(MET)与EGFR酪氨酸激酶抑制剂(TKIs)联合使用在克服这种分子定义的获得性耐药方面已显示出前景。新出现的数据还表明,MET扩增是TKIs治疗的间变性淋巴瘤激酶(ALK)、RET和ROS1融合NSCLC的耐药驱动因素。在此,我们综述了关于MET扩增作为致癌基因驱动的NSCLC靶向治疗耐药驱动因素的最新研究进展文献,并总结了克服耐药机制的临床策略进展。