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在肺腺癌发育过程中对免疫微环境和基因组的研究

Qingyi Wang^1,2, Bin Xie², Jingyue Sun^1,2

¹Department of Pathology, School of Basic Medicine, Central South University, Changsha, Hunan, 410078, China.

Journal of Cancer

|February 19, 2024

概括

随着肺腺癌 (LUAD) 从早期阶段 (AIS,MIA) 发展为侵袭性癌症,免疫细胞透,但变得枯竭. 像EGFR和LRP1B这样的驱动基因突变会影响这种瘤微环境,可能促进瘤生长和免疫逃脱.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
遗传学遗传学是一个

背景情况:

在位腺癌 (AIS) 和微侵袭性腺癌 (MIA) 之前的侵袭性肺腺癌 (LUAD).
关于免疫编辑模式和驱动基因参与LUAD瘤微环境 (TME) 的理解有限.
阐明TME在LUAD开发中的监管作用至关重要.

研究的目的:

调查免疫细胞透,分子突变和AIS,MIA和LUAD中的致癌途径.
了解驱动基因改变如何在LUAD进展过程中塑造TME.
描述免疫格局及其与 LUAD 中遗传突变的关联.

主要方法:

对145个手术切除的肺结节 (28 AIS,52 MIA,65 LUAD) 的分析.
免疫标志物 (CD3,CD4,CD8,CD68,PD-L1) 的免疫组织化学 (IHC).
针对基因组数据和瘤突变负担的下一代测序 (NGS).

主要成果:

与AIS/MIA相比,LUAD显示免疫细胞透,TMB和通路激活的增加.
在LUAD中,EGFR共变与较高的CD4/CD8比率和CD68透相关.
LRP1B突变与更高的TMB和PD-L1表达有关.
与进展相关的突变 (PAMs) 与淋巴细胞分化和T细胞枯竭有关.
过渡到LUAD将TME转移到PD-L1+/CD8+表型,表明了适应性抵抗.

结论:

瘤透免疫细胞随着LUAD入侵而积累,但进展到免疫衰竭和逃逸.
EGFR和LRP1B突变可能会创建一个支持瘤生长的免疫利基.
在LUAD中的PAMs可能通过诱导T细胞耗尽来加速进展.

关键词:

免疫编辑免疫编辑侵袭前的腺癌瘤瘤免疫类型的定型透到瘤中的淋巴细胞

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