EGFR TKIs在非小细胞肺癌中的耐药机制及治疗进展  

Mechanisms of resistance to EGFR TKIs and therapeutic perspectives in non-small cell lung cancer

作　　者：王珊珊[1] 常建华[1] 

机构地区：[1]复旦大学附属肿瘤医院化疗科,复旦大学上海医学院肿瘤学系,上海200032

出　　处：《中国癌症杂志》2013年第4期308-314,共7页China Oncology

摘　　要：吉非替尼和厄洛替尼是表皮生长因子受体(epidermal growth factor receptor,EGFR)酪氨酸激酶抑制剂(tyrosine kinase inhibitors,TKIs),广泛用于非小细胞肺癌的治疗。但随着应用的深入,耐药问题开始凸显。过去几年,针对继发性耐药和原发性耐药的深入研究,发现EGFR二次突变,MET基因扩增,K-ras基因突变等是EGFR TKIs耐药的主要原因。本文就EGFR-TKIs原发耐药与继发耐药的机制,以及克服此类耐药的新型药物及其临床试验数据作一综述。Gefitinib and erlotinib, which are epidermal growth factor receptor （EGFR） specific tyrosine kinase inhibitors （TKIs）, are widely used as molecularly targeted drugs for non-small-cell lung cancer （NSCLC）. However, many patients ultimately develop resistance to these drugs. Mechanisms of acquired and primary resistance have been reported in the past few years, such as secondary mutation of the EGFR gene, amplification of the MET gene and mutations of the K-ras gene. Novel pharmaceutical agents are currently being developed to overcome resistance. This review focuses on these mechanisms of resistance to EGFR-TKIs and discusses how can be overcome.

关 键 词：耐药 突变 信号通路 治疗 

分 类 号：R734.2[医药卫生—肿瘤]