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STK11/LKB1-缺陷的表型而不是突变降低了免疫疗法的有效性,并代表NSCLC中STING/I型干扰素/CD8+T细胞功能障碍

Anlin Li¹, Yuanyuan Wang¹, Zhixin Yu²

¹Department of Medical Oncology, Sun Yat-sen University Cancer Center, Guangzhou, People's Republic of China; State Key Laboratory of Oncology in South People's Republic of China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, People's Republic of China.

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

|July 26, 2023

概括

在非小细胞肺癌 (NSCLC) 中,STK11表型,而不是突变,更好地预测对免疫检查点抑制剂的反应. 缺乏STK11的瘤表现不佳,这表明潜在的免疫抑制和T细胞功能障碍.

科学领域:

在瘤学瘤学.
免疫治疗是一种免疫疗法.
遗传学是一个遗传学.

背景情况:

关于STK11/LKB1突变和免疫检查点抑制剂 (ICB) 在非小细胞肺癌 (NSCLC) 疗效方面存在相互矛盾的数据.
瘤可以在没有突变的情况下损害STK11/LKB1功能,从而使治疗反应预测复杂化.

研究的目的:

为了调查STK11表型,而不是突变状态,更好地分层ICB结果在NSCLC.
为STK11表型 (缺陷与精通) 开发基于转录学的分类器.

主要方法:

开发了一种基于转录学的STK11表型分类器 (STK11缺陷[-def]或-熟练[-prof]).
分析了来自三个随机NSCLC试验 (ORIENT-11,OAK,POPLAR) 和癌症基因组图谱-NSCLC队列的数据.

主要成果:

STK11突变状态没有影响ICB结果.
与化疗相比,STK11缺乏的瘤显示ICB的生存效益丧失或逆转.
STK11野生型/缺陷瘤的ICB结果比STK11突变型/熟练型瘤更差.
STK11缺乏与干扰的STING/INTERFERON-I信号和CD8+T细胞功能障碍有关,独立于PD-L1表达.

结论:

STK11表型准确地识别了ICB耐火性NSCLC,并反映了免疫抑制.
现型分类可以完善NSCLC分层算法用于临床研究.
这种方法有助于基础和翻译研究确定NSCLC的治疗点.

关键词:

CD8 ((+) T 细胞国际货币基金组织-I 免疫检查点抑制剂免疫检查点抑制剂一个LKB1一个LKB1 刺痛是一种刺痛.在STK11中,STK11就是STK11.

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