[Study Progression on Non-small Cell Lung Cancer with EGFR Mutation Treated by Immune Checkpoint Inhibitors]

Zhongguo Fei Ai Za Zhi. 2018 Aug 20;21(8):641-648. doi: 10.3779/j.issn.1009-3419.2018.08.11.
[Article in Chinese]

Abstract

In recent years, epidermal growth factor receptor tyrosine kinase inhibitors have been recommended by many guidelines as first-line drugs for advanced non-small cell lung cancer (NSCLC) with EGFR gene mutations and no resistance. However, with the prolongation of medication time, most appear acquired resistance. In recent years, breakthroughs in inhibitors of programmed death-1 (PD-1) and its ligand (PD1 ligand, PD-L1) have rapidly changed the therapeutic model of NSCLC. Recent studies have shown that the efficacy of immune checkpoint inhibitors in EGFR-mutant NSCLC patients is not satisfactory, which might be caused by low PD-L1 expression, inhibitory immune microenvironment and low tumor mutation load. This review will elaborate the immune microenvironment of NSCLC patients with EGFR mutation, the latest study progression of immune checkpoint inhibitors and its combined with TKI, expecting to bring new hopes for the treatment of EGFR-mutant NSCLC patients. .

【中文题目:免疫检查点抑制剂治疗EGFR突变非小细胞 肺癌的研究进展】 【中文摘要:近年来,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)已被多项指南推荐作为表皮生长因子受体(epidermal growth factor receptor, EGFR)基因敏感突变且不存在耐药的晚期非小细胞肺癌(non-small cell lung cancer, NSCLC)的一线治疗药物,但随着用药时间的延长,大多数患者出现获得性耐药。近几年,针对免疫检查点程序死亡受体(programmed death-1, PD-1)及其配体(PD-1 ligand, PD-L1)的抑制剂取得突破性进展,迅速改变着NSCLC的治疗模式。而近期研究显示,EGFR突变NSCLC患者免疫检查点抑制剂疗效尚不理想,可能机制主要包括PD-L1低表达、抑制性免疫微环境及低肿瘤突变负荷等。通过对EGFR突变NSCLC患者免疫微环境的变化情况,免疫检查点抑制剂及其与TKI联合应用的研究进展的系列分析,有望为EGFR突变NSCLC患者的治疗带来新希望。 】 【中文关键词:免疫检查点抑制剂;肺肿瘤;表皮生长因子受体基因突变;程序性死亡配体-1】.

Keywords: EGFR mutation; Immune checkpoint inhibitors; Lung neoplasms; PD-L1.

Publication types

  • Review

MeSH terms

  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / immunology
  • ErbB Receptors / genetics*
  • Humans
  • Immune System / drug effects*
  • Immune System / immunology
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / immunology
  • Molecular Targeted Therapy / methods*
  • Mutation*

Substances

  • ErbB Receptors