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利用神经发育来治疗胶质母细胞瘤。

Taking advantage of neural development to treat glioblastoma.

作者信息

Zhang Zhiyuan, Lin Chia-Ching John

机构信息

Department of Neurosurgery, Nanjing Jinling Hospital, School of Medicine, Nanjing University, Jiangsu Province, China; Center for Cell and Gene Therapy, Baylor College of Medicine, One Baylor Plaza, Houston, TX, USA.

出版信息

Eur J Neurosci. 2014 Sep;40(6):2859-66. doi: 10.1111/ejn.12655. Epub 2014 Jun 25.

DOI:10.1111/ejn.12655
PMID:24964151
Abstract

Glioblastoma (GBM) is by far the most common and most malignant primary adult brain tumor (World Health Organization grade IV), containing a fraction of stem-like cells that are highly tumorigenic and multipotent. Recent research has revealed that GBM stem-like cells play important roles in GBM pathogenesis. GBM is thought to arise from genetic anomalies in glial development. Over the past decade, a wide range of studies have shown that several signaling pathways involved in neural development, including basic helix-loop-helix, Wnt-β-catenin, bone morphogenetic proteins-Smads, epidermal growth factor-epidermal growth factor receptor, and Notch, play important roles in GBM pathogenesis. In this review, we highlight the significance of these pathways in the context of developing treatments for GBM. Extrapolating knowledge and concepts from neural development will have significant implications for designing better strategies with which to treat GBM.

摘要

胶质母细胞瘤(GBM)是目前最常见且最具侵袭性的原发性成人大脑肿瘤(世界卫生组织IV级),其中含有一部分具有高度致瘤性和多能性的干细胞样细胞。最近的研究表明,GBM干细胞样细胞在GBM发病机制中起着重要作用。GBM被认为起源于神经胶质发育过程中的基因异常。在过去十年中,大量研究表明,包括碱性螺旋-环-螺旋、Wnt-β-连环蛋白、骨形态发生蛋白-Smads、表皮生长因子-表皮生长因子受体和Notch在内的几种参与神经发育的信号通路,在GBM发病机制中发挥着重要作用。在本综述中,我们强调这些通路在GBM治疗发展背景下的重要性。从神经发育中推断知识和概念将对设计更好的GBM治疗策略产生重大影响。

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1
Taking advantage of neural development to treat glioblastoma.利用神经发育来治疗胶质母细胞瘤。
Eur J Neurosci. 2014 Sep;40(6):2859-66. doi: 10.1111/ejn.12655. Epub 2014 Jun 25.
2
New aspects of glioblastoma multiforme revealed by similarities between neural and glioblastoma stem cells.胶质母细胞瘤多形性通过神经和胶质母细胞瘤干细胞之间的相似性揭示的新方面。
Cell Biol Toxicol. 2018 Dec;34(6):425-440. doi: 10.1007/s10565-017-9420-y. Epub 2018 Jan 31.
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MicroRNAs as regulators of neural stem cell-related pathways in glioblastoma multiforme.微小 RNA 作为多形性胶质母细胞瘤中神经干细胞相关途径的调节因子。
Mol Neurobiol. 2011 Dec;44(3):235-49. doi: 10.1007/s12035-011-8196-y. Epub 2011 Jul 5.
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Neural stem cells, the subventricular zone and radiotherapy: implications for treating glioblastoma.神经干细胞、脑室下区与放射治疗:对胶质母细胞瘤治疗的启示
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Glioblastoma tumor initiating cells: therapeutic strategies targeting apoptosis and microRNA pathways.胶质母细胞瘤肿瘤起始细胞:靶向细胞凋亡和 microRNA 通路的治疗策略。
Curr Mol Med. 2013 Mar;13(3):352-7.
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Developmental signaling pathways in brain tumor-derived stem-like cells.脑肿瘤来源的干细胞样细胞中的发育信号通路。
Dev Dyn. 2007 Dec;236(12):3297-308. doi: 10.1002/dvdy.21381.
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[Progress in the study of brain tumor stem cells as treatment targets].[脑肿瘤干细胞作为治疗靶点的研究进展]
Brain Nerve. 2009 Jul;61(7):781-9.
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Combination of a ptgs2 inhibitor and an epidermal growth factor receptor-signaling inhibitor prevents tumorigenesis of oligodendrocyte lineage-derived glioma-initiating cells.PTGS2 抑制剂与表皮生长因子受体信号抑制剂的联合应用可预防少突胶质细胞源性胶质瘤起始细胞的肿瘤发生。
Stem Cells. 2011 Apr;29(4):590-9. doi: 10.1002/stem.618.
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EGFR targeted inhibition resistance: compensatory activation of ERBB family members in glioblastoma cancer stem-like cells promotes proliferation.表皮生长因子受体(EGFR)靶向抑制耐药性:胶质母细胞瘤癌干细胞样细胞中ERBB家族成员的代偿性激活促进增殖。
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Molecular advances of brain tumors in radiation oncology.放射肿瘤学中脑肿瘤的分子进展
Semin Radiat Oncol. 2009 Jul;19(3):171-8. doi: 10.1016/j.semradonc.2009.02.005.

引用本文的文献

1
Role of miR-223/paired box 6 signaling in temozolomide chemoresistance in glioblastoma multiforme cells.微小RNA-223/配对盒6信号通路在多形性胶质母细胞瘤细胞对替莫唑胺化疗耐药中的作用
Mol Med Rep. 2017 Feb;15(2):597-604. doi: 10.3892/mmr.2016.6078. Epub 2016 Dec 27.
2
Podocalyxin promotes glioblastoma multiforme cell invasion and proliferation via β-catenin signaling.足细胞外蛋白通过β-连环蛋白信号通路促进多形性胶质母细胞瘤细胞的侵袭和增殖。
PLoS One. 2014 Oct 28;9(10):e111343. doi: 10.1371/journal.pone.0111343. eCollection 2014.