单细胞转录基因分析揭示了KRAS/TP53-驱动的中性粒细胞在Luad中的重编程:多基因预后模型和RHOV的治疗向
Yinghui Ye1, Yulou Luo2, Yutian Sun3
1Department of Laboratory Medicine, Xinhua Hospital, Shenzhen, 518000, China.
Oncology research
|June 9, 2025
概括
肺腺癌 (LUAD) 中的KRAS/TP53突变改变了瘤微环境中的中性粒细胞. 一个五个基因的签名预测了生存和免疫治疗反应,以RHOV作为治疗目标.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 基因组学就是基因组学.
背景情况:
- 肺腺癌 (LUAD) 的进展与KRAS/TP53突变有关.
- 这些突变对瘤微环境 (TME) 异质性的影响,特别是中性粒细胞动态,尚不清楚.
研究的目的:
- 研究KRAS/TP53突变如何在LUAD中重编程TME.
- 为LUAD患者开发一个以中性粒细胞为中心的预后特征.
主要方法:
- 单细胞RNA测序和转录组数据分析以确定中性粒细胞亚群.
- 使用高维权基因共同表达网络分析和回归模型进行预测性签名开发.
- 通过敲击实验对RHOV (Ras同类家族成员V) 的功能验证.
主要成果:
- KRAS/TP53突变的LUAD显示中性粒细胞透率增加和特定的信号通路.
- 一个五个基因签名 (MS4A1,ANLN,FAM83A,RHOV,KRT6A) 通过总生存率有效地对患者进行了分层.
- 该签名证明了外部免疫疗法队列中治疗反应的预测能力.
结论:
- KRAS/TP53突变影响LUAD TME中性粒细胞异质性,影响预后和治疗.
- 五个基因特征和RHOV向性对LUAD风险分层和治疗具有翻译潜力.
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