RNA methylation of CD47 mediates tumor immunosuppression in EGFR-TKI resistant NSCLC.

• Tác giả: Zhanghai He, Jialu Liang, Huayue Lin, Jiawen Wang, Kefeng Wang, Wei Zhang
• Ngôn ngữ: eng
• Ký hiệu phân loại: 363.3498 Other aspects of public safety
• Thông tin xuất bản: England : British journal of cancer , 2025
• Bộ sưu tập: NCBI
• ID: 721587

Tóm tắt

BACKGROUND: Although immune checkpoint inhibitors (ICIs) have been successfully utilized in patients with non-small cell lung cancer (NSCLC), EGFR-mutated patients didn't benefit from ICIs. The underlying mechanisms for the poor efficacy of this subgroup remain unclear. METHODS: CD8 RESULTS: We found that EGFR-TKI resistance promoted a more immunosuppressive tumor microenvironment and inhibited anti-tumor functions of CD8 CONCLUSIONS: Collectively, our findings reveal the possible underlying mechanism for poor immune response of ICIs in EGFR-TKI resistant NSCLC and provide preclinical evidence that targeted therapy combined with innate immune checkpoint blockade may provide synergistic effects in NSCLC treatment.