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探索弥漫性脑桥内在型胶质瘤的肿瘤微环境:免疫学见解与治疗挑战

Exploring the tumor microenvironment in diffuse intrinsic pontine glioma: immunological insights and therapeutic challenges.

作者信息

Van den Ende Bieke, Riva Matteo, De Smet Frederik, Jacobs Sandra, Hulleman Esther, Coosemans An

机构信息

Department of Oncology, KU Leuven, Leuven, Belgium.

Department of Neurosurgery, CHU UCL Namur, Yvoir, Belgium.

出版信息

J Immunother Cancer. 2025 Jun 12;13(6):e012009. doi: 10.1136/jitc-2025-012009.

DOI:10.1136/jitc-2025-012009
PMID:40514066
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12164617/
Abstract

Diffuse intrinsic pontine glioma (DIPG) is a rare and highly aggressive pediatric brain tumor with a median survival of less than 12 months. The tumor arises in the pons, making surgical resection unfeasible and limiting treatment options to palliative radiation, which offers minimal survival benefit. One of the major challenges in treating DIPG is the poorly understood tumor immune microenvironment, which has hindered the development of effective immunotherapies. DIPG tumors are considered to be immunologically cold with limited immune cell infiltration. Recent studies have begun to reveal the complex and heterogeneous immune landscape of DIPG, highlighting distinct immunological subgroups. This review aims to provide a comprehensive overview of the immune landscape of DIPG based on the latest insights, identify research gaps, and suggest potential areas for future investigation to improve treatment outcomes for patients with DIPG.

摘要

弥漫性脑桥内在型胶质瘤(DIPG)是一种罕见且侵袭性很强的儿童脑肿瘤,中位生存期不到12个月。肿瘤起源于脑桥,使得手术切除不可行,治疗选择仅限于姑息性放疗,而姑息性放疗带来的生存获益极小。治疗DIPG的主要挑战之一是对肿瘤免疫微环境了解甚少,这阻碍了有效免疫疗法的开发。DIPG肿瘤被认为是免疫冷型的,免疫细胞浸润有限。最近的研究开始揭示DIPG复杂且异质性的免疫格局,突出了不同的免疫亚组。本综述旨在基于最新见解全面概述DIPG的免疫格局,识别研究空白,并提出未来潜在的研究领域,以改善DIPG患者的治疗结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f643/12164617/1c6b232765bc/jitc-13-6-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f643/12164617/1c6b232765bc/jitc-13-6-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f643/12164617/1c6b232765bc/jitc-13-6-g001.jpg

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本文引用的文献

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Nat Med. 2025 Mar;31(3):861-868. doi: 10.1038/s41591-024-03451-3. Epub 2025 Jan 7.
2
Homeostatic microglia initially seed and activated microglia later reshape amyloid plaques in Alzheimer's Disease.稳态小胶质细胞最初播种,而活化的小胶质细胞随后重塑阿尔茨海默病中的淀粉样斑块。
Nat Commun. 2024 Dec 5;15(1):10634. doi: 10.1038/s41467-024-54779-w.
3
Author Correction: Intravenous and intracranial GD2-CAR T cells for H3K27M diffuse midline gliomas.
作者更正:用于H3K27M弥漫性中线胶质瘤的静脉内和颅内GD2嵌合抗原受体T细胞
Nature. 2024 Dec;636(8043):E6. doi: 10.1038/s41586-024-08452-3.
4
Microglia and monocyte-derived macrophages drive progression of pediatric high-grade gliomas and are transcriptionally shaped by histone mutations.小胶质细胞和单核细胞来源的巨噬细胞推动小儿高级别脑胶质瘤的进展,并通过组蛋白突变在转录水平上被塑造。
Immunity. 2024 Nov 12;57(11):2669-2687.e6. doi: 10.1016/j.immuni.2024.09.007. Epub 2024 Oct 11.
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CAF-induced physical constraints controlling T cell state and localization in solid tumours.CAF 诱导的物理约束控制实体瘤中 T 细胞的状态和定位。
Nat Rev Cancer. 2024 Oct;24(10):676-693. doi: 10.1038/s41568-024-00740-4. Epub 2024 Sep 9.
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Immune landscape of oncohistone-mutant gliomas reveals diverse myeloid populations and tumor-promoting function.免疫组化染色在原发性中枢神经系统淋巴瘤中的诊断应用
Nat Commun. 2024 Sep 5;15(1):7769. doi: 10.1038/s41467-024-52096-w.
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Front Genet. 2024 May 7;15:1349612. doi: 10.3389/fgene.2024.1349612. eCollection 2024.