Vasculogenic mimicry: a novel target for glioma therapy.
Vasculogenic mimicry: a novel target for glioma therapy.
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DOI：
10.5732/cjc.012.10292
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发表时间：
2014-02
影响因子：
--
通讯作者：
Chen ZP
中科院分区：
文献类型：
--
作者：
Chen YS;Chen ZP
抗血管生成治疗已显示出有希望的，但对神经胶质瘤的疗效不足。最近的研究表明，血管生成拟态（VM），或形成非内皮，肿瘤细胞内衬微血管通道，发生在侵袭性肿瘤，包括胶质瘤。也有证据表明内皮衬里的脉管系统和VM通道之间存在生理联系。肿瘤细胞凭借其高可塑性，自身可以形成血管样结构，其可以起到血液供应网络的作用。我们以前对胶质瘤的研究表明，VM阳性肿瘤中的微血管密度低于VM阴性肿瘤。因此，VM可能作为一种补充，以确保肿瘤的血液供应，特别是在区域与微血管密度较低。VM阳性胶质瘤患者的生存时间短于VM阴性胶质瘤患者。虽然VM的详细分子机制尚未完全了解，但胶质瘤干细胞可能发挥关键作用，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。在未来，胶质瘤的成功治疗应该涉及靶向VM和血管生成。本文就胶质瘤VM的研究进展及面临的挑战作一综述。
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.
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影响因子：
3.6
作者：
Hess, AR;Seftor, EA;Hendrix, MJC
通讯作者：
Hendrix, MJC
DOI：
10.1007/s10555-007-9094-7
发表时间：
2007-12
期刊：
Cancer metastasis reviews
影响因子：
--
作者：
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通讯作者：
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158.5
作者：
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通讯作者：
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影响因子：
4.2
作者：
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影响因子：
3.9
作者：
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通讯作者：
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