RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
DNA-PK 抑制维持小细胞肺癌的抗肿瘤固有免疫应答
英文原题：DNA-PK inhibition sustains the antitumor innate immune response in small cell lung cancer.
查看英文原题
DNA-PK inhibition sustains the antitumor innate immune response in small cell lung cancer.
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中文摘要
小细胞肺癌（SCLC）是一种高度侵袭性的肺癌，治疗选择有限。患者通常对初始的化疗-免疫治疗反应良好，但很快复发，因此需要新的策略来增强免疫反应性。近期研究探索将DNA损伤疗法与免疫治疗联合，以激活STING通路并改善抗肿瘤免疫反应。在化疗后加入DNA损伤修复（DDR）抑制剂，如DNA-PKcs抑制剂，已在SCLC模型中显示出激活先天免疫传感器以及增强CD8+ T细胞和NK细胞通路的潜力。这种方法可能重塑肿瘤微环境并维持抗肿瘤免疫反应，为SCLC治疗提供一种维持治疗策略。
展开英文摘要原文
Small cell lung cancer (SCLC) is a highly aggressive form of lung cancer with limited treatment options. Patients often respond well to initial chemo-immunotherapy but relapse quickly, necessitating new strategies to enhance immune responsiveness. Recent research explores combining DNA-damaging therapies with immunotherapy to activate the STING pathway and improve the antitumor immune response.
The addition of DNA Damage Repair (DDR) inhibitors, such as DNA-PKcs inhibitors, after chemotherapy has shown promise in activating innate immune sensors and enhancing CD8 + T cell and NK cell pathways in SCLC models. This approach could potentially reshape the tumor microenvironment and sustain an antitumor immune response, offering a maintenance strategy for SCLC treatment.
论文信息
- 作者
- De Rosa C、Morgillo F、Amato L、Iommelli F、De Rosa V、Tirino V、Papaccio F、Tuccillo C
- 单位
- Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80131 Naples, Italy.Italy
- 期刊
- iScience2025 Mar 21
- 原文标识
- PubMed 40034862 · DOI 10.1016/j.isci.2025.111943
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