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基于的新辅助化疗可调节STING/IFN通路的表达,并促进TILs在NSCLC中的透

Huan Gao¹, Xiaoni Zhang², Mengdi Ren¹

¹Department of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Frontiers in oncology

|March 1, 2024

概括

新辅助化疗 (NACT) 激活STING/IFN通路,并在非小细胞肺癌 (NSCLC) 中增强瘤透淋巴细胞 (TIL). TILs和ypN阶段的变化是患者生存的关键预测因素.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
癌症研究癌症研究

背景情况:

非小细胞肺癌 (NSCLC) 仍然是全球癌症死亡的主要原因.
基于的新辅助化疗 (NACT) 是NSCLC的标准治疗方式.
了解NACT的免疫调节作用对于优化治疗策略至关重要.

研究的目的:

研究基于的NACT对NSCLC的STING/IFN通路和瘤透淋巴细胞 (TILs) 的影响.
为了确定影响NACT后患者生存的临床病理因素.
探索免疫标志物与治疗反应之间的关系.

主要方法:

对68名接受NACT和手术的NSCLC患者的回顾性分析.
免疫组织化学和免疫光学评估STING,PD-L1,IFN-β蛋白水平和CD3+/CD8+TIL透.
免疫标记,临床病理特征和生存结果 (DFS和OS) 的相关性分析.

主要成果:

NACT显著增加了STING,IFN-β和PD-L1的表达,以及CD3+/CD8+TIL透.
ypTNM阶段,ypN阶段,CD3+TIL变化和PD-L1水平与无病生存时间 (DFS) 相相关.
CD3+ TIL 变化和 ypN 阶段是 DFS 和整体存活 (OS) 的独立预后因素.

结论:

NACT刺激STING/IFN-β通路,增强TIL透,并上调PD-L1,支持其与免疫治疗的结合.
在NACT后增加的CD3+TIL和有利的ypN分期 (ypN0-1) 与改善的DFS有关.
在NACT后,患有ypN0和CD3+TIL增加的患者表现出更好的OS益处.

关键词:

国际货币基金组织 IFN IFN 在 PDL1 中,PDL1 是 PDL1.刺痛是一种刺痛.新辅助性化疗是一种新辅助性化疗.非小细胞肺癌的肺癌.瘤透到T淋巴细胞中

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