摘要
表皮生长因子受体-酪氨酸激酶抑制剂(EGFR-TKI)治疗晚期非小细胞肺癌(NSCLC)的耐药分子机制逐渐明了,其中小细胞肺癌(SCLC)转化引发了学者极大关注。这种表型转化和伴发EGFR突变是肿瘤细胞异质性,或是肿瘤干细胞,或是某些分子事件使然,但无论那种机制均是推测且无直接证据。目前临床实践中对这种EGFR-TKI耐药转化为SCLC患者的治疗仅是经验分享,亦无更高级别的证据推荐。
The genetics mechanisms of drug resistance in non-small cell lung cancer（NSCLC） patients treated with epidermal growth factor receptor-tyrosine kinase inhibitors（EGFR-TKI） were revealed gradually,one of them was surprising-NSCLC transformation into small cell lung cancer（SCLC）.This phenotype transformation associated with EGFR gene mutation was resulted from tumor heterogeneity,cancer stem cell or some molecular events,but there was no confirmed evidence for them.Currently,the treatment of the transformation of NSCLC into SCLC after failure of EGFR-TKI therapy is empirical in clinical practice,no higher-level evidence to recommend.
出处
《临床药物治疗杂志》
2013年第5期1-3,25,共4页
Clinical Medication Journal
