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早期的免疫变化支持在CDH1-驱动的遗传扩散性胃癌发生时的标志环细胞休眠

Benjamin L Green¹, Lauren A Gamble¹, Laurence P Diggs¹

¹Surgical Oncology Program, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Molecular cancer research : MCR

|September 14, 2023

概括

在遗传性扩散性胃癌 (HDGC) 中的早期胃癌显示T细胞信号传递,而不是瘤性途径. 增加的CD4+T细胞与休眠性相关,而调节性T细胞则表明在密封环细胞 (SRC) 中免疫逃脱.

科学领域:

胃肠病学胃肠病学
在瘤学瘤学.
免疫学免疫学免疫学

背景情况:

遗传性扩散性胃癌 (HDGC) 与生殖基线CDH1变异和具有内密封环细胞 (SRCs) 的早期胃腺癌有关.
驱动SRCs在HDGC中的恶性转化和休眠的分子机制在很大程度上是未知的.
了解这些早期事件对于开发有效的癌症拦截策略至关重要.

研究的目的:

研究HDGC患者早期SRCs的分子和免疫微环境.
确定SRC启动和休眠的潜在分子驱动因素或抑制因素.
探索瘤免疫微环境在HDGC病变发生中的作用.

主要方法:

在激光捕获微切割 (LCM) SRCs和相邻的非SRC上皮质 (NEP) 上进行了全外体大批量RNA测序 (RNA-seq).
分析包括差异性基因表达 (DEG),途径丰富分析,以及针对免疫细胞解的CIBERSORTx.
免疫组织化学 (IHC) 用于确认特定免疫细胞标记物的发现 (FOXP3,CD4,HLA-DR).

主要成果:

在SRC中没有观察到癌源途径的显著上调;相反,与T细胞信号传递相关的途径被丰富.
CIBERSORTx预测,IHC证实SRC区域内的调节性T细胞 (Tregs) 和CD4+T细胞的增加.
增加的CD4+T细胞与观察到的SRC休眠相关,而Treg上调表明潜在的免疫逃生机制.

结论:

瘤免疫微环境与HDGC中的IA期胃SRC密切相关.
免疫细胞群,特别是Tregs,可能在调节SRC行为和休眠状态方面发挥重要作用.
这些发现突显了免疫导向疗法的潜力,用于在扩散型胃癌中拦截癌症.

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