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.
Highlights
Anti-angiogenic therapy has shown promising but insufficient efficacy on gliomas
vasculogenic mimicry (VM) describes the ability of aggressive tumor cells to form extracellular matrix (ECM)–rich, vasculogeniclike networks to complement the endothelial-cell-dependent vasculature[11,12,13,14,15,16]
We observed that patients with VM-positive gliomas survived a shorter period of time than those with VM-negative gliomas[19], similar to the results reported for other aggressive tumors[20,21,22,23]
Summary
Angiogenesis and vasculogenesis are widely accepted processes of tumor vascularization, for endotheliumdependent vessels. In both processes, tumor vascular endothelial cells develop from host cells located in normal tissues around the tumor or from endothelial progenitor cells. VM is completely different from angiogenesis and vasculogenesis, in another word, the blood supply to tumors is proposed to involve three types: tumor-cell-lined vessels, mosaic vessels, and endothelium-dependent vessels[26]. A study suggest that VM channels—the tumor-cell-lined vessels— could be the main source of blood supply in the early stage of tumor growth[11]. Endothelium-dependent vessels could replace VM channels via a transitional step as mosaic vessels to become the dominant blood supply pattern at the late stage of tumor growth[25]. The angiogenesis capacity of GSCs has been demonstrated; the detailed relationship of GSCs and the phenomenon VM in glioma is still unclear
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