表皮生长因子受体突变诱导吉非替尼获得性耐药机制分析  

Analysis of the mechanism of gefitinib induced drug resistance induced by EGFR mutatio

作　　者：曾军[1] 黄强[1] 李跃程[1] 

机构地区：[1]新余钢铁集团有限公司中心医院,江西新余338001

出　　处：《中国医院药学杂志》2017年第4期397-401,共5页Chinese Journal of Hospital Pharmacy

摘　　要：吉非替尼作为表皮生长因子受体络氨酸激酶抑制剂(EGFR-TKI)类靶向药物,广泛用于临床非小细胞肺癌(NSCLC)的治疗,但近几年的临床应用发现,肿瘤细胞对该类药物的敏感度逐渐下降,药物作用疗效呈现减低趋势,临床耐药问题逐渐凸显。近几年的深入研究表明,吉非替尼的耐药机制可能与表皮生长因子受体(EGFR)旁路效应、EGFR信号传导路径和EGFR靶基因的二次突变有关,基于此以吉非替尼作用机制为出发点对其获得性耐药机制进行归纳总结。Epidermal growth gactor receptor tyrosine kinase inhibitor（ EGFR-TKI）,such as gefitinib,was widely used in the treatment of non-small cell lung cancer（ NSCLC）,However,with the continuous application of EGFR-TKI,the sensitivity to tumor cells and the efficacy were reduced and drug resistance increased. In recent years,The mechanism of drug resistance may be related to the EGFR side-channel effect,EGFR signal transduction and the two mutations in target genes of EGFR. Based on this,this paper summarizes the mechanism of the effect of the drug resistance mechanism of the starting point.

关 键 词：吉非替尼 表皮生长因子受体络氨酸激酶抑制剂 获得性耐药 

分 类 号：R969[医药卫生—药理学]