非小细胞肺癌对EGFR-TKIs产生获得性耐药后发生小细胞肺癌转化的研究进展  

Small cell lung cancer transformation in non-small cell lung cancer with acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors

作　　者：孟淑燕[1] 郁佳[1] 方启宇[1] 吕梅君[1] 

机构地区：[1]同济大学附属上海市肺科医院肿瘤内科,上海200433

出　　处：《肿瘤》2016年第9期1070-1074,共5页Tumor

摘　　要：小细胞肺癌转化是非小细胞肺癌（non—small cell lung cancer，NSCLC）对表皮生长因子受体（epidermal growth factor receptor，EGFR）酪氨酸激酶抑制剂（tyrosine kinase inhibitors，TKIs）产生获得性耐药的机制之一。据报道，小细胞肺癌转化的发生率为2％～14％。目前，小细胞肺癌转化的发生机制尚不十分明确。有些NSCLC可直接转化成小细胞癌，还是初诊时即为复合性小细胞癌，尚存在争议。报道显示，NSCLC仅有部分病灶发生小细胞癌转化，转化的小细胞癌与原发性小细胞肺癌在细胞形态及蛋白表达上尚未见明显差异，但多有与初始NSCLC相同的EGFR基因突变型；而且，经典的抗原发性小细胞肺癌的放化疗方案对转化的小细胞肺癌一般也有较好的疗效。本文对近年来有关小细胞肺癌转化的发生机制、临床特点及处理策略进行综述。Small cell lung cancer （SCLC） transformation is one of the mechanisms of acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors （EGFR-TKIs） in non-small cell lung cancer （NSCLC）. According to reports, the incidence rates of SCLC transformation range from 2% to 14%. However, the mechanisms underlying SCLC transformation are not clear at present. There is still a controversy whether the SCLC can be directly originated from NSCLC, or only a combination of SCLC and NSCLC at the time of initial diagnosis. Many reports have showed that SCLC transformation may just occur to part of the lesions; the morphology and protein expression of transformed SCLC are similar to the de-novo SCLC, but the transformed SCLC has similar genetic profile of EGFR as the primary NSCLC tissues in most cases; the patients with transformed SCLC may benefit from the classic radiotherapy and chemotherapy regiments for SCLC. This paper reviews the occurrence mechanisms, clinical features and treatment strategies of SCLC transformation in recent years.

关 键 词：癌 非小细胞肺 受体 表皮生长因子 抗药性 肿瘤 细胞转化 肿瘤 

分 类 号：R734.2[医药卫生—肿瘤]