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表皮生长因子受体(epidermal growth factor receptor,EGFR)是非小细胞肺癌(non-small-cell lung cancer,NSCLC)的重要诊疗靶点,指南和专家共识首选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EGFR敏感突变的晚期NSCLC。然而,有些EGFR敏感突变的患者使用一段时间的EGFR-TKI后疾病进展,即获得性耐药,这是治疗晚期NSCLC患者的难点之一。获得性耐药机制包括EGFR T790M突变,细胞间质上皮转化因子(cellular-mesenchymal to epithelial transition factor,c-MET)扩增,上皮间质化(epithelial mesenchymal transition,EMT)及肿瘤干细胞机制等,但还有部分耐药机制尚不清楚。该文阐述了近年来NSCLC对EGFR-TKI的获得性耐药机制的研究进展及其克服EGFR-TKI耐药的新方法。
Epidermal growth factor receptor (EGFR) is an important target for diagnosis and treatment of non-small-cell lung cancer (NSCLC). Guidelines and expert consensus are the first choice epidermal growth factor receptor tyrosine kinase inhibitors (epidermal growth factor receptor tyrosine kinase inhibitor, EGFR-TKI) for the treatment of advanced NSCLC with EGFR-sensitive mutations. However, some EGFR-sensitive mutations in patients with advanced stage EGFR-TKI disease progression, that is, acquired resistance, which is one of the difficulties in the treatment of advanced NSCLC patients. Acquired resistance mechanisms include EGFR T790M mutation, c-MET expansion, epithelial mesenchymal transition (EMT) and tumor stem cell mechanisms There are still some mechanisms of resistance is not clear. This article describes the progress of acquired resistance mechanism of NSCLC to EGFR-TKI in recent years and a new method to overcome the resistance of EGFR-TKI.