c-MET通路和抑制剂在非小细胞肺癌中的研究进展  

Progress of c-MET Signaling Pathway and TKIs in Non-small Cell Lung Cancer

作　　者：俞晓晴 徐艳珺[2] 范云[2] Xiaoqing YU Yanjun XU Yun FAN(Zhejiang Chinese Medical University, Hangzhou 310053, China Department of Thoracic Oncology, Zhejiang Cancer Hospital, Hangzhou 310022, China)

机构地区：[1]浙江中医药大学,杭州310053 [2]浙江省肿瘤医院胸部肿瘤内科,杭州310022

出　　处：《中国肺癌杂志》2017年第4期287-292,共6页Chinese Journal of Lung Cancer

摘　　要：c-MET被认为是继表皮生长因子受体(epidermal growth factor receptor,EGFR)基因突变和间变性淋巴瘤激酶(anaplastic lymphoma kinase,ALK)基因融合之后,非小细胞肺癌(non-small cell lung cancer,NSCLC)又一个重要的驱动基因。MET的激活包括突变、扩增和蛋白质过表达,是NSCLC潜在的治疗靶点,并提示与预后相关。临床证据表明,MET既可以作为肺癌的原发致癌驱动基因,也是EGFR靶向治疗获得性耐药的原因之一。本文主要对c-MET通路在NSCLC中的活性形式及治疗的研究进展进行综述。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.

关 键 词：肺肿瘤 C-MET 扩增 克唑替尼 

分 类 号：R734.2[医药卫生—肿瘤]