The resistance mechanism and coping strategy of the third-generation EGFR-TKIs in NSCLC

秦闪闪; 常建华

doi:10.19401/j.cnki.1007-3639.2017.11.013

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The resistance mechanism and coping strategy of the third-generation EGFR-TKIs in NSCLC

更新时间：2025-12-31

- The resistance mechanism and coping strategy of the third-generation EGFR-TKIs in NSCLC
- China Oncology Vol. 27, Issue 11, Pages: 913-916(2017)
- 作者机构：
  
  复旦大学附属肿瘤医院肿瘤内科，复旦大学上海医学院肿瘤学系,上海,200032
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2017.11.013
  CLC：
- Published Online：12 December 2017，
  
  Published：12 December 2017
- 稿件说明：
移动端阅览
秦闪闪,常建华. 第三代EGFR-TKIs在非小细胞肺癌中的耐药机制及应对策略[J]. 中国癌症杂志, 2017, 27(11): 913-916.

秦闪闪, 常建华. The resistance mechanism and coping strategy of the third-generation EGFR-TKIs in NSCLC[J]. China Oncology, 2017, 27(11): 913-916.
秦闪闪,常建华. 第三代EGFR-TKIs在非小细胞肺癌中的耐药机制及应对策略[J]. 中国癌症杂志, 2017, 27(11): 913-916. DOI： 10.19401/j.cnki.1007-3639.2017.11.013.

秦闪闪, 常建华. The resistance mechanism and coping strategy of the third-generation EGFR-TKIs in NSCLC[J]. China Oncology, 2017, 27(11): 913-916. DOI： 10.19401/j.cnki.1007-3639.2017.11.013.

摘要

表皮生长因子受体酪氨酸激酶抑制剂(epidermal growth factor receptor tyrosine kinase inhibitors，EGFR-TKIs)靶向治疗相对于传统化疗具有很大的优势，已成为晚期非小细胞肺癌EGFR敏感突变患者的一线治疗方案。然而，耐药现象不可避免地发生。EGFR第20号外显子的T790M突变是第一、二代EGFRTKIs的主要耐药机制。第三代EGFR-TKIs，如AZD9291、CO-1686等可克服T790M耐药，并在临床试验中显示出良好的治疗效果，然而，第三代EGFR-TKIs的耐药同样不可避免，该文就第三代EGFR-TKIs的耐药机制及目前的应对策略进行综述。

Abstract

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) targeted therapy has great advantages compared to conventional chemotherapies and has become the first-line treatment of EGFR sensitive mutations in patients with advanced non-small cell lung cancer. However

the development of acquired drug resistance is inevitable. EGFR T790M mutation is the main mechanism of the first and second generation EGFR-TKIs. The thirdgeneration EGFR-TKIs including AZD9291 and CO-1686 showed favorable treatment effect in clinical trials. However

resistance problems appeared soon. This review summarized the resistance mechanisms of the third-generation EGFRTKIs and the potential coping strategy.

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