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Neurotherapeutics. 2017 Apr;14(2):385-392. doi: 10.1007/s13311-017-0523-1.
2
Dissecting inherent intratumor heterogeneity in patient-derived glioblastoma culture models.剖析患者来源的胶质母细胞瘤培养模型中固有的肿瘤内异质性。
Neuro Oncol. 2017 Jun 1;19(6):820-832. doi: 10.1093/neuonc/now253.
3
Endogenous Neoantigen-Specific CD8 T Cells Identified in Two Glioblastoma Models Using a Cancer Immunogenomics Approach.采用癌症免疫基因组学方法在两种脑胶质瘤模型中鉴定内源性新抗原特异性 CD8 T 细胞。
Cancer Immunol Res. 2016 Dec;4(12):1007-1015. doi: 10.1158/2326-6066.CIR-16-0156. Epub 2016 Oct 31.
4
Expression of Idh1 in the Murine Subventricular Zone Stem Cell Niche Recapitulates Features of Early Gliomagenesis.异柠檬酸脱氢酶1(Idh1)在小鼠脑室下区干细胞微环境中的表达重现了早期胶质瘤发生的特征。
Cancer Cell. 2016 Oct 10;30(4):578-594. doi: 10.1016/j.ccell.2016.08.017. Epub 2016 Sep 29.
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The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary.2016 年世界卫生组织中枢神经系统肿瘤分类:概述。
Acta Neuropathol. 2016 Jun;131(6):803-20. doi: 10.1007/s00401-016-1545-1. Epub 2016 May 9.
6
Targeting CXCR4 by a selective peptide antagonist modulates tumor microenvironment and microglia reactivity in a human glioblastoma model.在人胶质母细胞瘤模型中,通过选择性肽拮抗剂靶向CXCR4可调节肿瘤微环境和小胶质细胞反应性。
J Exp Clin Cancer Res. 2016 Mar 25;35:55. doi: 10.1186/s13046-016-0326-y.
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Autocrine VEGFR1 and VEGFR2 signaling promotes survival in human glioblastoma models in vitro and in vivo.自分泌血管内皮生长因子受体1(VEGFR1)和血管内皮生长因子受体2(VEGFR2)信号传导在体外和体内的人胶质母细胞瘤模型中促进细胞存活。
Neuro Oncol. 2016 Sep;18(9):1242-52. doi: 10.1093/neuonc/now043. Epub 2016 Mar 23.
8
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Nat Commun. 2016 Feb 22;7:10743. doi: 10.1038/ncomms10743.
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mTOR inhibition decreases SOX2-SOX9 mediated glioma stem cell activity and temozolomide resistance.mTOR抑制可降低SOX2 - SOX9介导的胶质瘤干细胞活性及替莫唑胺耐药性。
Expert Opin Ther Targets. 2016;20(4):393-405. doi: 10.1517/14728222.2016.1151002.
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A Novel Mouse Model of Diffuse Intrinsic Pontine Glioma Initiated in Pax3-Expressing Cells.一种在表达Pax3的细胞中引发的弥漫性脑桥内在胶质瘤的新型小鼠模型。
Neoplasia. 2016 Jan;18(1):60-70. doi: 10.1016/j.neo.2015.12.002.

胶质母细胞瘤小鼠模型的当前趋势。

Current trends in mouse models of glioblastoma.

机构信息

Department of Tumor Pathology, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu, 501-1194, Japan.

Department of Neurosurgery, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu, 501-1194, Japan.

出版信息

J Neurooncol. 2017 Dec;135(3):423-432. doi: 10.1007/s11060-017-2626-2. Epub 2017 Oct 20.

DOI:10.1007/s11060-017-2626-2
PMID:29052807
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5700231/
Abstract

Glioblastoma is the most deadly brain tumor type and is characterized by a severe and high rate of angiogenesis, remaining an incurable disease in the majority of cases. Mechanistic understanding of glioblastoma initiation and progression is complicated by the complexity of genetic and/or environmental initiating events and lack of clarity regarding the cell or tissue of origin. To determine these mechanisms, mouse models that recapitulate the molecular and histological characteristics of glioblastoma are required. Unlike in other malignancies, viral-mediated mouse models of glioblastoma rather than chemically induced mouse models have been developed because of its sensitivity to viruses. Based on recent molecular analyses reported for human glioblastoma, this review critically evaluates genetically engineered, xenograft, allograft, viral-mediated, and chemically induced mouse models of glioblastoma. Further, we focus on the clinical value of these models by examining their contributions to studies of glioblastoma prevention, tumorigenesis, and chemoresistance.

摘要

胶质母细胞瘤是最致命的脑肿瘤类型,其特征是严重且高血管生成率,在大多数情况下仍是一种无法治愈的疾病。由于遗传和/或环境起始事件的复杂性以及对起源细胞或组织缺乏明确性,胶质母细胞瘤的发生和进展的机制理解变得复杂。为了确定这些机制,需要能够重现胶质母细胞瘤分子和组织学特征的小鼠模型。与其他恶性肿瘤不同,由于其对病毒的敏感性,已经开发出病毒介导的而非化学诱导的小鼠胶质母细胞瘤模型,而不是化学诱导的小鼠模型。基于最近报道的人类胶质母细胞瘤的分子分析,本文对基因工程、异种移植、同种异体移植、病毒介导和化学诱导的胶质母细胞瘤小鼠模型进行了批判性评估。此外,我们通过研究这些模型在胶质母细胞瘤预防、肿瘤发生和化疗耐药性研究中的贡献,关注这些模型的临床价值。