Immunotherapy for EGFR-mutant non-small cell lung cancer after EGFR-TKI acquired resistance
10.3760/cma.j.cn371439-20220719-00020
- VernacularTitle:EGFR突变型非小细胞肺癌EGFR-TKI获得性耐药后免疫治疗现状
- Author:
Bixia ZHANG
1
;
Jianghua DING
Author Information
1. 九江学院医学院，九江 332000
- Keywords:
Carcinoma, non-small-cell lung;
Immunotherapy;
Epidermal growth factor receptors;
Tyrosine kinase inhibitors
- From:
Journal of International Oncology
2023;50(2):97-101
- CountryChina
- Language:Chinese
-
Abstract:
Epidermal growth factor receptor (EGFR) -mutant advanced non-small cell lung cancer (NSCLC) was previously regarded as a cold tumor according to tumor immune microenvironment (TIME) . However, recent studies have found that EGFR-tyrosine kinase inhibitors (EGFR-TKIs) treatment can transform the host immunity from immunosuppressive to immunosupportive state, bringing new hope for immunotherapy. There are four main therapeutic strategies for patients after EGFR-TKIs acquired resistance: immunotherapy alone (Im) , immunotherapy plus chemotherapy (Im+C) , immunotherapy plus antiangiogenic drugs (Im+A) , and immunotherapy combined with antiangiogenic drugs and chemotherapy (Im+A+C) . Among them, the efficacy of Im is extremely limited, being significantly lower than that of chemotherapy alone, while there is still scarce evidence for the efficacy of Im+A with few clinical studies. The combination of Im+C and Im+A+C shows better efficacy than chemotherapy alone. Im+A+C has a superior clinical outcome to Im+C. Additionally, the EGFR L858R mutation subgroup benefits more from Im+C than the EGFR 19 del mutation subgroup. The T790M-negative subgroup has a greater benefit from Im+A+C than the T790M-positive subgroup. In general, the strategy of combining immunotherapy with chemotherapy and/or an antiangiogenic drug represents a novel and promising method for treating EGFR-mutant NSCLC after EGFR-TKI failure.
