T790M突变与EGFR-TKI耐药后治疗策略

表皮生长因子受体酪氨酸激酶抑制剂（epidermal growth factor receptor-tyrosine kinase inhibitor,EGFR-TKI）治疗非小细胞肺癌已获得较好的疗效，患者生活质量明显改善。但EGFR-TKI耐药似乎成为了靶向治疗的瓶颈，耐药的产生可能存在多种机制，包括T790M突变、K-ras基因突变、C-Met基因扩增、BRAF基因突变、BIM多态性缺失、EML4-ALK融合基因突变及上皮间充质转化等,其中最常见的是T790M基因突变。目前研究表明，T790M基因还可能具有一定预测疗效和预后的作用。本文将简要介绍T790M基因的发现、起源、作用机制及预后，并主要针对EGFR-TKIs耐药后的治疗策略进行综述。

T790M mutation and therapeutic strategy after EGFR - TKI resistance

Tyrosine kinase inhibitors (EGFR-TKI) have shown favorable efficacy in non -small cell lung cancer，the patient's quality of life improved significantly.However，resistance to EGFR-TKI has become a problem of the targeted therapy.The resistance to EGFR-TKI have identified several mechanisms，which including T790M mutation，K-ras gene mutation，C-Met gene amplification，BRAF mutations，BIM deletion polymorphism，EML4-ALK fusion gene mutation and epithelial-mesenchy-mal transition of small-cell lung cancer etc，of which the most common is the T790M mutation .The present study indicates that，T790M mutation may play a important role in predicting the efficacy and prognosis.This review will introduce the discovery,origin,mechanism and prognosis of T790M，and mainly discusses the therapeutic strategy after EGFR-TKI resistance.