RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Major histocompatibility complex class I chain-related A and B molecules and their potential role in virus-associated cancers.
Major histocompatibility complex class I chain-related A and B molecules and their potential role in virus-associated cancers.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
某些病毒感染是特定癌症的重要危险因素。人类主要组织相容性复合体I类链相关基因A(MICA)和B(MICB)是位于人类白细胞抗原区域内的多态性非经典主要组织相容性复合体I类基因。这些基因的多态性与多种病毒相关癌症的易感性和预后相关。其潜在机制涉及通过破坏自然杀伤组2成员D-MICA/B轴来调节NK 细胞和CD8+ T细胞介导的细胞毒性。由此产生的MICA和MICB的可溶性形式最近作为病毒诱导恶性肿瘤和疾病严重程度的潜在预测生物标志物而受到关注。靶向该轴的治疗策略显示出相当大的前景。这篇小型综述总结了MICA和MICB的遗传学和生物学,强调了它们在病毒相关癌症发病机制中新出现的重要性。
Infections with certain viruses are strong risk factors for specific cancers. The human major histocompatibility complex class I chain-related genes A (MICA) and B (MICB) are polymorphic, non-classical major histocompatibility complex class I genes located within the human leukocyte antigen region. Polymorphisms in these genes have been associated with susceptibility and outcomes of several virus-associated cancers.
The underlying mechanisms involve modulation of natural killer cell- and CD8+ T cell-mediated cytotoxicity by disrupting the natural killer group 2-member D-MICA/B axis. The resulting soluble forms of both MICA and MICB have recently gained attention as potential predictive biomarkers for virus-induced malignancies and disease severity.
Therapeutic strategies targeting this axis show considerable promise. This minireview summarizes the genetics and biology of MICA and MICB, highlighting their emerging importance in the pathogenesis of virus-associated cancers.
在 PubMed 查看 → 出版商原文(DOI) 全文 PDF(PMC)· 可下载 治疗专题与资料阅读指南 资料来源与翻译说明 报告译文或资料问题 →
MEMBER ACCOUNT
登录成功会直接打开下一页。