晚期非小细胞肺癌EGFR-TKI获得性耐药机制

摘要/Abstract

摘要：随着分子生物学的发展，晚期非小细胞肺癌的治疗由传统的化疗转向以基因分型为指导的分子靶向治疗。其中应用较多的是表皮生长因子受体酪氨酸激酶抑制剂（EGFRTKI）类药物。然而EGFR-TKI的耐药问题近年来受到越来越多的关注，其机制主要有EGFR基因二次突变，c-MET、人类表皮生长因子受体2（Her2）等靶基因的扩增，组织表型的改变，旁路途径的激活，p53基因的缺失，细胞信号通路负反馈的减弱以及多重机制叠加等。

关键词:癌,非小细胞肺,抗药性,肿瘤,分子靶向治疗

Abstract:Since the development of molecular biology, the treatment of advanced non-small cell cancer is shifting from traditional chemotherapy into molecular targeted therapy with genotyping as a guide′s help. The most widely used is epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs). With the application of EGFRTKIs, the resistances to EGFR inhibitors are paid more and more attention, in recent years. The main mechanisms of acquired resistances are as follows: secondary mutation of the EGFR gene, amplification of c-MET, Her2 and other target genes, histological transformation, activation of the bypass mechanisms, loss of p53, the relief of negative feedback loops, overlap of mechanisms, etc.

Key words:Carcinoma, non-small cell lung,Drug resistance, neoplasm,Molecular targeted therapy

郑悦,魏素菊. 晚期非小细胞肺癌EGFR-TKI获得性耐药机制[J]. 国际肿瘤学杂志, 2015, 42(6): 458-461.

Zheng Yue, Wei Suju. Acquired resistance mechanisms of EGFR-TKI in advanced non-small cell lung cancer[J]. Journal of International Oncology, 2015, 42(6): 458-461.

参考文献

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