中药抑制非小细胞肺癌PI3K/Akt/mTOR信号通路克服EGFR-TKIs获得性耐药研究进展  

Research progress on Chinese materia medica in overcoming EGFR-TKIs acquired drugs resistance through PI3K/Akt/mTOR pathway

作　　者：蔡鹏涛 吴志强[1] 郭会[1] 舒琦瑾[2] 

机构地区：[1]浙江中医药大学,浙江杭州310053 [2]浙江中医药大学附属第一医院肿瘤科,浙江杭州310006

出　　处：《中草药》2015年第12期1849-1852,共4页Chinese Traditional and Herbal Drugs

基　　金：国家自然科学基金面上项目(81173247)

摘　　要：随着对肺癌发病机制及其生物学特性研究的不断深入,分子靶向治疗尤其是表皮生长因子受体-酪氨酸激酶抑制剂（EGFR-TKIs）在非小细胞肺癌治疗方面取得了突破性进展,然而经过6-12个月的治疗后,大部分患者会对EGFR-TKIs产生获得性耐药。PI3K/Akt/mTOR信号通路在非小细胞肺癌的发生发展中具有重要的作用,该通路在肿瘤治疗方面已经有了比较广泛的研究。中药在对抗EGFR-TKIs耐药方面有很大的前景。就近年来中药通过抑制非小细胞肺癌PI3K/Akt/mTOR信号通路来克服EGFR-TKIs获得性耐药的研究进展进行综述。With in-depth study of the pathogenesis of lung cancer and its biological behaviour,molecular targeted therapy,especially the epidermal growth factor receptor-tyrosine kinase inhibitors（EGFR-TKIs） made a breakthrough in non-small cell lung cancer treatment.However,the majority of patients can produce the resistance to EGFR-TKIs after 6 to 12 months treatment,which called acquired drug resistance.PI3K/Akt/mTOR pathway plays an important role in the development of non-small cell lung cancer,this pathway in cancer treatment has been widely studied.Chinese materia medica（CMM） in overcoming EGFR-TKIs resistance has a bright future,In this review,we show the developments on CMM in overcoming EGFR-TKIs acquired drugs resistance through PI3K/Akt/mTOR pathway.

关 键 词：表皮生长因子受体-酪氨酸激酶抑制剂 获得性耐药 PI3K/Akt/mTOR信号通路 非小细胞肺癌 中药 

分 类 号：R285[医药卫生—中药学]