Yu Xiaoqing, Xu Yanjun, Fan Yun
Zhejiang Chinese Medical University, Hangzhou 310053, China.
Department of Thoracic Oncology, Zhejiang Cancer Hospital, Hangzhou 310022, China.
Zhongguo Fei Ai Za Zhi. 2017 Apr 20;20(4):287-292. doi: 10.3779/j.issn.1009-3419.2017.04.10.
c-MET is considered a promising oncogenic driver in non-small cell lung cancer (NSCLC) after the discovery of epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK). MET activation including gene mutation, amplification and protein overexpression, all of these are potential therapeutic targets and are associated with poor prognosis. Clinical evidence suggests a role for MET activation as both a primary oncogenic driver in subsets of lung cancer, and as a secondary driver of acquired resistance to EGFR-tyrosine kinase inhibitor (TKI). This review focuses on the MET activation in NSCLC and the latest trials of its treatment.
在表皮生长因子受体(EGFR)和间变性淋巴瘤激酶(ALK)被发现之后,c-MET被认为是非小细胞肺癌(NSCLC)中一个有前景的致癌驱动因子。MET激活包括基因突变、扩增和蛋白过表达,所有这些都是潜在的治疗靶点,并且与预后不良相关。临床证据表明,MET激活在肺癌亚组中既是主要致癌驱动因子,也是对EGFR-酪氨酸激酶抑制剂(TKI)获得性耐药的次要驱动因子。本综述聚焦于NSCLC中的MET激活及其治疗的最新试验。