非小细胞肺癌EGFR-TKIs耐药--小细胞肺癌转化的机制和治疗

摘要

肺癌是当前死亡率最高的恶性肿瘤之一。表皮生长因子受体酪氨酸激酶抑制剂（ EGFR-TKIs）明显提高了晚期非小细胞肺癌（ NSCLC）患者的生活质量，延长了生存期。 EGFR基因优势突变的NSCLC患者临床获益明显，然而由于耐药产生，患者的中位无进展生存期（ PFS）仅1年左右。最近，有文献报道EGFR-TKIs耐药的机制之一是NSCLC转化为小细胞肺癌（ SCLC）。本文对这种现象进行了分析总结，探讨了其转化的可能机制。根据EGFR-TKIs耐药后的处理方法和病理表型转化患者的治疗报道，探讨NSCLC EGFR-TKIs耐药后转化为SCLC患者的治疗策略。%Lung cancer is one of the malignant tumors with the highest mortality in the world. Epidermal growth factor receptor tyrosine kinase inhibitors( EGFR-TKIs) significantly improve the quality of life of advanced non-small cell lung cancer( NSCLC) , and prolong the overall survival. However, only a certain subpopulation of lung cancer patients carrying specific activating mutations in EG-FR respond clinically to EGFR-TKIs. Even among these patients, The median progression-free survival( PFS) is about 12 months owing to drug resistance. Recently, quite a few patients acquired drug resistance with NSCLC transitioned to small cell lung cancer( SCLC) were reported. In this review, we discuss the recent advances in the understanding of the phenomenon and possible mechanisms for the conversion of NSCLC into SCLC. The treatment strategies of patients with EGFR mutations in SCLC will be recommended according to the therapy scheme after EGFR-TKIs resistance of NSCLC and treatment proposal of the individual reported.