晚期非小细胞肺癌靶向治疗的研究进展  

Research progress on target therapy of advanced non-small cell lung cancer

作　　者：姜文丽[1] 黄才国[1] 

机构地区：[1]第二军医大学基础部生物化学与分子生物学教研室,上海200433

出　　处：《药学实践杂志》2016年第4期301-304,333,共5页Journal of Pharmaceutical Practice

基　　金：国家自然科学基金面上项目(41576160;81473239)

摘　　要：生物标志物检测使得许多晚期非小细胞肺癌(NSCLC)患者获益。近年来,针对表皮生长因子受体(EGFR)和间变性淋巴瘤激酶(ALK)突变呈阳性的NSCLC患者,以吉非替尼、厄洛替尼、阿法替尼为代表的表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)和以克唑替尼为代表的ALK-TKI取得了卓越的疗效。但是,大多数第一代EGFR-TKI和ALK-TKI的疗效因为不可避免的继发性耐药而被减弱。目前,第三代EGFR-TKI正是基于第二代EGFR-TKI的耐药机制研发而成。除此之外,还有许多针对其他突变位点的晚期NSCLC维持治疗的靶向抑制剂。遗憾的是,针对突变比例最大的K-RAS突变,尚无疗效确切的靶向药物。因此,基于肿瘤驱动基因突变机制的探索和靶向药物的开发是目前NSCLC的研究热点。Detection of biomarkers benefited many advanced non-small cell lung cancer （NSCLC） patients. In recent years, epidermal growth factor （EGFR） tyrosine kinase inhibitors （TKIs） represented by Gefitinib, Erlotinib, Afatinib and an- aplastic lymphoma kinase （ALK） TKIs represented by Crizotinib have remarkable efficacy. However, the efficacy for most first-generation EGFR-TKI and ALK-TKI is weakened due to secondary resistance. Currently, the third-generation EGFR-TKI which successfully against drug resistance is based on research and development of the second-generation. In addition, there are many other targeted inhibitors of mutation sites for advanced NSCLC. Unfortunately, the largest proportion of Kirsten rat sar- coma viral oncogene homolog （K-RAS） mutation is not targetable with small molecule inhibitors currently. Therefore, based on mechanisms exploration of tumor driven gene mutation, its target drug research and development will be greatly addressed in the future.

关 键 词：非小细胞肺癌 靶向药物 肿瘤 

分 类 号：R979.1[医药卫生—药品]