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:Tumor immune microenvironment in non-small cell lung cancer progression.
Tumor immune microenvironment in non-small cell lung cancer progression.
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。
非小细胞肺癌(NSCLC)是肺部恶性肿瘤中最常见的类型,尽管手术、靶向治疗和免疫治疗取得了进展,它仍然是癌症相关死亡的主要原因。越来越多的证据表明,肿瘤免疫微环境(TIME)是疾病进展、免疫逃逸和治疗耐药的关键决定因素。本综述综合了当前关于固有免疫和适应性免疫细胞群体——包括肿瘤相关巨噬细胞、中性粒细胞、树突状细胞、肥大细胞、髓源性抑制细胞、NK 细胞、T细胞和B细胞——在塑造肿瘤动态中作用的认识。特别强调了这些免疫亚群在TIME中的表型可塑性和功能重编程。我们进一步讨论了免疫细胞异质性对免疫治疗应答和耐药的意义。通过突出肿瘤细胞与免疫景观之间的相互作用,本综述强调了基于TIME的策略在优化患者分层和推进NSCLC联合免疫治疗方面的潜力。
Non-small cell lung cancer (NSCLC), the most prevalent form of lung malignancy, remains a leading cause of cancer-related mortality despite advances in surgery, targeted therapy, and immunotherapy. A growing body of evidence implicates the tumor immune microenvironment (TIME) as a critical determinant of disease progression, immune evasion, and therapeutic resistance.
This review synthesizes current insights into the roles of innate and adaptive immune populations-including tumor-associated macrophages, neutrophils, dendritic cells, mast cells, myeloid-derived suppressor cells, natural killer cells, T cells, and B cells-in shaping tumor dynamics. Special emphasis is placed on the phenotypic plasticity and functional reprogramming of these immune subsets within the TIME.
We further discuss the implications of immune cell heterogeneity for immunotherapy response and resistance. By highlighting the interplay between tumor cells and the immune landscape, this review underscores the potential for TIME-informed strategies to optimize patient stratification and advance combinatorial immunotherapeutic approaches in NSCLC.
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。