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Glioblastoma stem cells: Molecular characteristics and therapeutic implications.胶质母细胞瘤干细胞:分子特征与治疗意义
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Engagement of cellular prion protein with the co-chaperone Hsp70/90 organizing protein regulates the proliferation of glioblastoma stem-like cells.细胞朊蛋白与伴侣蛋白组织蛋白Hsp70/90的结合调节胶质母细胞瘤干细胞样细胞的增殖。
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High expression of RFX4 is associated with tumor progression and poor prognosis in patients with glioblastoma.RFX4 的高表达与胶质母细胞瘤患者的肿瘤进展和不良预后相关。
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Combining HDAC and MEK Inhibitors with Radiation against Glioblastoma-Derived Spheres.联合 HDAC 和 MEK 抑制剂与放射治疗胶质母细胞瘤球体。
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Matrix Hyaluronic Acid and Hypoxia Influence a CD133 Subset of Patient-Derived Glioblastoma Cells.基质透明质酸和缺氧影响患者来源的胶质母细胞瘤细胞中的 CD133 亚群。
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本文引用的文献

1
Tissue resident stem cells: till death do us part.组织驻留干细胞:至死不渝。
Biogerontology. 2013 Dec;14(6):573-90. doi: 10.1007/s10522-013-9469-9. Epub 2013 Oct 2.
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Adult neural stem cells: plastic or restricted neuronal fates?成体神经干细胞:可塑性还是受限的神经元命运?
Development. 2013 Aug;140(16):3303-9. doi: 10.1242/dev.093096.
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Investigating the link between molecular subtypes of glioblastoma, epithelial-mesenchymal transition, and CD133 cell surface protein.研究胶质母细胞瘤的分子亚型、上皮-间充质转化和 CD133 细胞表面蛋白之间的联系。
PLoS One. 2013 May 29;8(5):e64169. doi: 10.1371/journal.pone.0064169. Print 2013.
4
Glioblastoma stem cells generate vascular pericytes to support vessel function and tumor growth.胶质母细胞瘤干细胞生成血管周细胞以支持血管功能和肿瘤生长。
Cell. 2013 Mar 28;153(1):139-52. doi: 10.1016/j.cell.2013.02.021.
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Wnt activation promotes neuronal differentiation of glioblastoma.Wnt 激活促进神经胶质瘤的神经元分化。
Cell Death Dis. 2013 Feb 21;4(2):e500. doi: 10.1038/cddis.2013.32.
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CD133 is essential for glioblastoma stem cell maintenance.CD133 对于神经胶质瘤干细胞的维持至关重要。
Stem Cells. 2013 May;31(5):857-69. doi: 10.1002/stem.1317.
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Mechanisms of glioma-associated neovascularization.胶质瘤相关血管新生的机制。
Am J Pathol. 2012 Oct;181(4):1126-41. doi: 10.1016/j.ajpath.2012.06.030. Epub 2012 Aug 2.
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A restricted cell population propagates glioblastoma growth after chemotherapy.化疗后,受限制的细胞群体促进胶质母细胞瘤生长。
Nature. 2012 Aug 23;488(7412):522-6. doi: 10.1038/nature11287.
9
LGR5 is a marker of poor prognosis in glioblastoma and is required for survival of brain cancer stem-like cells.LGR5 是胶质母细胞瘤预后不良的标志物,并且是脑肿瘤类干细胞存活所必需的。
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10
Resistance of glioblastoma-initiating cells to radiation mediated by the tumor microenvironment can be abolished by inhibiting transforming growth factor-β.肿瘤微环境介导的脑胶质瘤起始细胞对辐射的抵抗作用可以通过抑制转化生长因子-β来消除。
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胶质母细胞瘤干细胞:分子特征与治疗意义

Glioblastoma stem cells: Molecular characteristics and therapeutic implications.

作者信息

Bayin Nermin Sumru, Modrek Aram Sandaldjian, Placantonakis Dimitris George

机构信息

Nermin Sumru Bayin, Aram Sandaldjian Modrek, Dimitris George Placantonakis, Department of Neurosurgery, New York University School of Medicine, New York, NY 10016, United States.

出版信息

World J Stem Cells. 2014 Apr 26;6(2):230-8. doi: 10.4252/wjsc.v6.i2.230.

DOI:10.4252/wjsc.v6.i2.230
PMID:24772249
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3999780/
Abstract

Glioblastoma Multiforme (GBM) is a grade IV astrocytoma, with a median survival of 14.6 mo. Within GBM, stem-like cells, namely glioblastoma stem cells (GSCs), have the ability to self-renew, differentiate into distinct lineages within the tumor and initiate tumor xenografts in immunocompromised animal models. More importantly, GSCs utilize cell-autonomous and tumor microenvironment-mediated mechanisms to overcome current therapeutic approaches. They are, therefore, very important therapeutic targets. Although the functional criteria defining GSCs are well defined, their molecular characteristics, the mechanisms whereby they establish the cellular hierarchy within tumors, and their contribution to tumor heterogeneity are not well understood. This review is aimed at summarizing current findings about GSCs and their therapeutic importance from a molecular and cellular point of view. A better characterization of GSCs is crucial for designing effective GSC-targeted therapies.

摘要

多形性胶质母细胞瘤(GBM)是一种IV级星形细胞瘤,中位生存期为14.6个月。在GBM中,干细胞样细胞,即胶质母细胞瘤干细胞(GSCs),具有自我更新能力,可在肿瘤内分化为不同谱系,并在免疫缺陷动物模型中引发肿瘤异种移植。更重要的是,GSCs利用细胞自主和肿瘤微环境介导的机制来克服当前的治疗方法。因此,它们是非常重要的治疗靶点。尽管定义GSCs的功能标准已明确,但它们分子特征、在肿瘤内建立细胞层次结构的机制以及它们对肿瘤异质性的贡献仍未得到充分了解。本综述旨在从分子和细胞角度总结关于GSCs及其治疗重要性的当前研究结果。更好地表征GSCs对于设计有效的GSC靶向治疗至关重要。