| 胡嘉芮,李占林.晚期非小细胞肺癌EGFR-TKI耐药后抗血管生成联合免疫检查点抑制剂作用机制的研究进展[J].中国肿瘤,2023,32(8):617-623. |
| 晚期非小细胞肺癌EGFR-TKI耐药后抗血管生成联合免疫检查点抑制剂作用机制的研究进展 |
| Advances on Anti-Angiogenesis Combined with ICIs After EGFR-TKI Resistance in Advanced Non-Small Cell Lung Cancer |
| 投稿时间：2023-02-21 |
| DOI：10.11735/j.issn.1004-0242.2023.08.A008 |
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| 中文关键词: 非小细胞肺癌 EGFR突变 肿瘤微环境 免疫检查点抑制剂 抗血管生成治疗 |
| 英文关键词:non-small cell lung cancer EGFR mutation tumor microenvironment immune checkpoint inhibitors antiangiogenic therapy |
| 基金项目:河北省中医药管理局科研计划项目（2022423）；河北省财政厅指令性项目 |
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| 中文摘要: |
| 摘 要：非小细胞肺癌（NSCLC）是肺癌中最常见的病理类型，表皮生长因子受体（EGFR）突变是NSCLC最常见的驱动基因突变。EGFR突变促进免疫抑制性肿瘤微环境（TME），但研究发现经表皮生长因子受体-酪氨酸激酶抑制剂（EGFR-TKI）治疗后TME发生改变，这种改变可能为优化随后的免疫检查点抑制剂（ICIs）治疗提供线索。临床前研究提示抗血管生成药物可以通过促进效应细胞浸润、减少免疫抑制等改善TME免疫抑制状态，增强ICIs疗效，ICIs也可促进血管正常化，两者具有协同抗肿瘤作用。EGFR-TKI耐药机制相对复杂，在缺乏特异性耐药机制患者中，单纯化疗或单纯ICIs获益有限，抗血管生成药物联合ICIs相关临床研究提示对于晚期EGFR-TKI耐药NSCLC患者可改善预后。全文就晚期 EGFR突变NSCLC的TKI治疗对TME的影响、抗血管生成治疗联合ICIs的生物学原理、EGFR-TKI耐药后抗血管生成治疗联合ICIs相关临床研究等作一综述。 |
| 英文摘要: |
| Abstract： Non-small cell lung cancer(NSCLC) is the most common pathological type of lung cancer， and epidermal growth factor receptor(EGFR) mutation is the most common driving gene mutation in NSCLC. EGFR mutation promotes the immunosuppressive tumor microenvironment(TME)， but studies have found that TME changes after epidermal growth factor receptor-tyrosine kinase inhibitor(EGFR-TKI) treatment， which may provide clues for optimizing the subsequent treatment of immune checkpoint inhibitors(ICIs). Pre-clinical studies suggest that anti-angiogenic drugs can improve the immunosuppressive state of TME by promoting the infiltration of effector cells and reducing immunosuppression， and enhance the efficacy of ICIs. ICIs can also promote the norma-lization of blood vessels， and the two have synergistic anti-tumor effects. The drug resistance mechanism of EGFR-TKI is relatively complex. In patients without specific drug resistance mechanism， the benefits of single-drug chemotherapy or ICIs are still limited. The clinical studies of anti-angiogenesis combined with ICIs suggest that the prognosis of patients with advanced EGFR-TKI resistant NSCLC can be improved. This paper reviews the EGFR mutation of advanced NSCLC and the effects of TKI treatment on TME， the biological principle of anti-angiogenesis combined with ICIs， and the clinical research of anti-angiogenesis combined with ICIs after EGFR-TKI resistance. |
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