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肿瘤干细胞启动肿瘤血管生成。

Cancer stem cells switch on tumor neovascularization.

机构信息

Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.

出版信息

Curr Mol Med. 2011 Feb;11(1):69-75. doi: 10.2174/156652411794474383.

DOI:10.2174/156652411794474383
PMID:21189116
Abstract

Recent studies on cancer stem cells (CSCs), a special subpopulation of tumor cells, promote our understanding of tumorigenesis, neovascularization, invasion, drug resistance and tumor recurrence, which establishes new concepts for cancer diagnosis and treatment. Therefore, the biological features and behaviors of CSCs have become an exciting frontier of cancer research. CSCs initiate tumor neovascularization and promote invasion with yet to be defined mechanisms. In this review, we provide evidence for the role of CSCs in tumor vascularization and discuss the potential mechanisms and therapeutic significance based on the interaction between CSCs and their vascular niches.

摘要

最近关于癌症干细胞(CSCs)的研究,肿瘤细胞的一个特殊亚群,促进了我们对肿瘤发生、血管生成、侵袭、耐药和肿瘤复发的理解,为癌症的诊断和治疗建立了新的概念。因此,CSCs 的生物学特征和行为已成为癌症研究的一个令人兴奋的前沿领域。CSCs 通过尚未确定的机制启动肿瘤血管生成并促进侵袭。在这篇综述中,我们提供了 CSCs 在肿瘤血管生成中的作用的证据,并根据 CSCs 与其血管龛之间的相互作用讨论了潜在的机制和治疗意义。

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Cancer stem cells switch on tumor neovascularization.肿瘤干细胞启动肿瘤血管生成。
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2
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Vascular endothelial growth factor receptor 2 (VEGFR-2) plays a key role in vasculogenic mimicry formation, neovascularization and tumor initiation by Glioma stem-like cells.血管内皮生长因子受体 2(VEGFR-2)在血管生成拟态形成、Glioma 干细胞样细胞的新生血管形成和肿瘤起始中发挥关键作用。
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