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血管生成拟态:胶质瘤治疗的新靶点。

Vasculogenic mimicry: a novel target for glioma therapy.

作者信息

Chen Yin-Sheng, Chen Zhong-Ping

机构信息

Department of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong 510060, P. R. China.

出版信息

Chin J Cancer. 2014 Feb;33(2):74-9. doi: 10.5732/cjc.012.10292. Epub 2013 Jul 2.

DOI:10.5732/cjc.012.10292
PMID:23816560
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3935008/
Abstract

Anti-angiogenic therapy has shown promising but insufficient efficacy on gliomas. Recent studies suggest that vasculogenic mimicry (VM), or the formation of non-endothelial, tumor-cell-lined microvascular channels, occurs in aggressive tumors, including gliomas. There is also evidence of a physiological connection between the endothelial-lined vasculature and VM channels. Tumor cells, by virtue of their high plasticity, can form vessel-like structures themselves, which may function as blood supply networks. Our previous study on gliomas showed that microvessel density was comparably less in VM-positive tumors than in VM-negative tumors. Thus, VM may act as a complement to ensure tumor blood supply, especially in regions with less microvessel density. Patients with VM-positive gliomas survived a shorter period of time than did patients with VM-negative gliomas. Although the detailed molecular mechanisms for VM are not fully understood, glioma stem cells might play a key role, since they are involved in tumor tissue remodeling and contribute to neovascularization via transdifferentiation. In the future, successful treatment of gliomas should involve targeting both VM and angiogenesis. In this review, we summarize the progress and challenges of VM in gliomas.

摘要

抗血管生成疗法对胶质瘤显示出了有前景但尚不充分的疗效。最近的研究表明,血管生成拟态(VM),即非内皮细胞、由肿瘤细胞排列形成的微血管通道,在包括胶质瘤在内的侵袭性肿瘤中存在。也有证据表明内皮细胞衬里的脉管系统与VM通道之间存在生理联系。肿瘤细胞由于其高度可塑性,自身可以形成血管样结构,这些结构可能起到血液供应网络的作用。我们之前对胶质瘤的研究表明,VM阳性肿瘤中的微血管密度比VM阴性肿瘤中的微血管密度相对更低。因此,VM可能作为一种补充来确保肿瘤的血液供应,尤其是在微血管密度较低的区域。VM阳性胶质瘤患者的生存期比VM阴性胶质瘤患者的生存期更短。尽管VM的详细分子机制尚未完全明确,但胶质瘤干细胞可能起着关键作用,因为它们参与肿瘤组织重塑,并通过转分化促进新血管形成。未来,成功治疗胶质瘤应同时针对VM和血管生成。在这篇综述中,我们总结了胶质瘤中VM的研究进展和挑战。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ca4/3935008/129567ba007f/cjc-33-02-074-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ca4/3935008/4cf463774b97/cjc-33-02-074-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ca4/3935008/129567ba007f/cjc-33-02-074-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ca4/3935008/4cf463774b97/cjc-33-02-074-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ca4/3935008/129567ba007f/cjc-33-02-074-g002.jpg

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