非小细胞肺癌EML4-ALK靶向药物耐药机制及逆转耐药的研究进展  

Research advance of resistance mechanism of EML4-ALK related targeted drug and reversal resistance in non-small cell lung cancer

作　　者：刘晓[1,2] 贾燕花[1] 张可[1] 刘皈阳[1] 

机构地区：[1]解放军总医院第一附属医院,北京100048 [2]河北北方学院,张家口075000

出　　处：《中国新药杂志》2016年第9期1018-1023,共6页Chinese Journal of New Drugs

摘　　要：非小细胞肺癌是危害人类生命最常见的恶性肿瘤之一,棘皮动物微管蛋白样4-间变性淋巴瘤激酶（echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase,EML4-ALK）融合基因是新发现的非小细胞肺癌驱动基因,是非小细胞肺癌治疗的新靶点。EML4-ALK融合基因在非小细胞肺癌患者中的发生率约为4%-5%,并且在不伴有表皮生长因子受体（epidermal growth factor receptor,EGFR）突变或KRas突变的腺癌患者中的表达率约为42.80%。目前临床上用于治疗ALK阳性肺癌的药物为克唑替尼,同其他酪胺酸激酶抑制剂（tyrosine kinase inhibitors,TKIs）相似,使用一段时间后也出现耐药。本文旨在介绍EML4-ALK融合基因结构特点、检测方法、ALK靶向药物的耐药机制以及逆转耐药的策略。Non-small cell lung cancer（ NSCLC） is one of the most life-threatening human malignancies,and EML4-ALK（ echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase） fusion gene being a new drive gene is a new therapeutic target for NSCLC. The positive rate of EML4-ALK fusion gene is about 4% -5% in patients with NSCLC. However,the positive rate of EML4-ALK fusion gene is about 42. 80% in the NSCLC patients without EGFR（ epidermal growth factor receptor） mutation or K-Ras mutation. Currently,crizotinib was used for the treatment of patients with EML4-ALK fusion gene in clinical. Similar to other TKIs,crizotinib appears resistance after a period of time. The purpose of this review is to introduce EML4-ALK structure,detection methods,resistance mechanisms and the strategies of solving the resistance.

关 键 词：非小细胞肺癌 EML4-ALK 检测方法 耐药机制 

分 类 号：R979.1[医药卫生—药品]