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The Vascular Microenvironment in Glioblastoma: A Comprehensive Review.胶质母细胞瘤中的血管微环境:综述
Biomedicines. 2022 May 31;10(6):1285. doi: 10.3390/biomedicines10061285.
2
P4HA1 Regulates CD31 COL6A1 in the Transition of Glioblastoma Stem-Like Cells to Tumor Endothelioid Cells.P4HA1在胶质母细胞瘤干细胞向肿瘤内皮样细胞转变过程中调控CD31和COL6A1。
Front Oncol. 2022 Apr 13;12:836511. doi: 10.3389/fonc.2022.836511. eCollection 2022.
3
Vascular Co-Option and Other Alternative Modalities of Growth of Tumor Vasculature in Glioblastoma.胶质母细胞瘤中肿瘤血管生成的血管共选及其他替代模式
Front Oncol. 2022 Mar 30;12:874554. doi: 10.3389/fonc.2022.874554. eCollection 2022.
4
Enhanced anti-angiogenetic effect of transferrin receptor-mediated delivery of VEGF-trap in a glioblastoma mouse model.转铁蛋白受体介导的 VEGF 陷阱递呈在胶质母细胞瘤小鼠模型中的增强抗血管生成作用。
MAbs. 2022 Jan-Dec;14(1):2057269. doi: 10.1080/19420862.2022.2057269.
5
Impact of Regorafenib on Endothelial Transdifferentiation of Glioblastoma Stem-like Cells.瑞戈非尼对胶质母细胞瘤干细胞样细胞内皮转分化的影响。
Cancers (Basel). 2022 Mar 18;14(6):1551. doi: 10.3390/cancers14061551.
6
Targeting Non-coding RNA for Glioblastoma Therapy: The Challenge of Overcomes the Blood-Brain Barrier.靶向非编码RNA治疗胶质母细胞瘤:克服血脑屏障的挑战
Front Med Technol. 2021 Aug 10;3:678593. doi: 10.3389/fmedt.2021.678593. eCollection 2021.
7
N6-Isopentenyladenosine Hinders the Vasculogenic Mimicry in Human Glioblastoma Cells through Src-120 Catenin Pathway Modulation and RhoA Activity Inhibition.N6-异戊烯基腺苷通过调节 Src-120 连接蛋白通路和抑制 RhoA 活性来抑制人胶质母细胞瘤细胞的血管生成拟态。
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Netrin-1 in Glioblastoma Neovascularization: The New Partner in Crime?神经轴突导向因子 1 在胶质母细胞瘤血管生成中的作用:新的犯罪伙伴?
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SUMOylation of IGF2BP2 promotes vasculogenic mimicry of glioma via regulating OIP5-AS1/miR-495-3p axis.SUMOylation 修饰 IGF2BP2 通过调控 OIP5-AS1/miR-495-3p 轴促进胶质瘤血管生成拟态。
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10
Elesclomol-induced increase of mitochondrial reactive oxygen species impairs glioblastoma stem-like cell survival and tumor growth.埃斯克洛莫尔诱导的线粒体活性氧增加损害胶质母细胞瘤干细胞样细胞的存活和肿瘤生长。
J Exp Clin Cancer Res. 2021 Jul 12;40(1):228. doi: 10.1186/s13046-021-02031-4.

胶质母细胞瘤特异性血管生成策略:对抗血管生成治疗耐药性的影响

Glioblastoma-Specific Strategies of Vascularization: Implications in Anti-Angiogenic Therapy Resistance.

作者信息

Buccarelli Mariachiara, Castellani Giorgia, Ricci-Vitiani Lucia

机构信息

Department of Oncology and Molecular Medicine, Istituto Superiore di Sanità, Viale Regina Elena, 299, 00161 Rome, Italy.

Department of Neurosurgery, Fondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del S. Cuore, Largo A. Gemelli, 8, 00168 Rome, Italy.

出版信息

J Pers Med. 2022 Oct 1;12(10):1625. doi: 10.3390/jpm12101625.

DOI:10.3390/jpm12101625
PMID:36294763
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9604754/
Abstract

Angiogenesis has long been implicated as a crucial process in GBM growth and progression. GBM can adopt several strategies to build up its abundant and aberrant vasculature. Targeting GBM angiogenesis has gained more and more attention in anti-cancer therapy, and many strategies have been developed to interfere with this hallmark. However, recent findings reveal that the effects of anti-angiogenic treatments are temporally limited and that tumors become refractory to therapy and more aggressive. In this review, we summarize the GBM-associated neovascularization processes and their implication in drug resistance mechanisms underlying the transient efficacy of current anti-angiogenic therapies. Moreover, we describe potential strategies and perspectives to overcome the mechanisms adopted by GBM to develop resistance to anti-angiogenic therapy as new potential therapeutic approaches.

摘要

长期以来,血管生成一直被认为是胶质母细胞瘤(GBM)生长和进展的关键过程。GBM可采用多种策略来构建其丰富且异常的脉管系统。在抗癌治疗中,靶向GBM血管生成已受到越来越多的关注,并且已经开发出许多策略来干扰这一特征。然而,最近的研究结果表明,抗血管生成治疗的效果在时间上是有限的,肿瘤会对治疗产生耐药性并变得更具侵袭性。在本综述中,我们总结了与GBM相关的新生血管形成过程及其在当前抗血管生成疗法短暂疗效背后的耐药机制中的作用。此外,我们描述了作为新的潜在治疗方法来克服GBM对抗血管生成治疗产生耐药性所采用机制的潜在策略和前景。