CD81 通过阻断 CD274/PD-L1 的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸
CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Dissecting the aberrant vasculature of glioblastoma: mechanisms and therapeutic targets.
Dissecting the aberrant vasculature of glioblastoma: mechanisms and therapeutic targets.
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胶质母细胞瘤(GBM)是一种高度侵袭性且几乎无法治愈的中枢神经系统肿瘤。GBM微环境被大量异常且异质的血管所浸润,形成独特的混乱且不规则的血管网络。这些异常血管不仅破坏了氧气和营养物质的输送,还在GBM的恶性侵袭、免疫逃逸和治疗耐药中发挥关键作用。在这篇综述中,我们全面讨论了GBM血管系统与正常血脑屏障相比的形态和功能改变,重点强调异常血管形成的细胞和分子机制及其对肿瘤进展的贡献。此外,我们提供了GBM当前血管靶向治疗的最新概述,并探索了潜在的未来临床治疗方向。
Glioblastoma (GBM) is a highly aggressive and almost incurable tumor of the central nervous system. The GBM microenvironment is infiltrated by numerous abnormal and heterogeneous blood vessels, forming a unique chaotic and irregular vascular network. These aberrant vessels not only disrupt the delivery of oxygen and nutrients but also play critical roles in the malignant invasion, immune evasion, and therapeutic resistance of GBM.
In this review, we comprehensively discuss the morphological and functional alterations of the GBM vasculature compared with the normal blood-brain barrier, emphasizing the cellular and molecular mechanisms underlying abnormal vessel formation and their contributions to tumor progression.
Furthermore, we provide an updated overview of current vascular-targeted therapies for GBM and explore potential future clinical therapeutic directions.
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