Vasculogenic Mimicry Occurs at Low Levels in Primary and Recurrent Glioblastoma

Vasculogenic mimicry (VM), the ability of tumour cells to form functional microvasculature without an endothelial lining, may contribute to anti-angiogenic treatment resistance in glioblastoma. We aimed to assess the extent of VM formation in primary and recurrent glioblastomas and to determine whether VM vessels also express prostate-specific membrane antigen (PSMA), a pathological vessel marker. Formalin-fixed paraffin-embedded tissue from 35 matched pairs of primary and recurrent glioblastoma was immunohistochemically labelled for PSMA and CD34 and stained with periodic acid-Schiff (PAS). Vascular structures were categorised as endothelial vessels (CD34+/PAS+) or VM (CD34-/PAS+). Most blood vessels in both primary and recurrent tumours were endothelial vessels, and these significantly decreased in recurrent tumours (p < 0.001). PSMA was expressed by endothelial vessels, and its expression was also decreased in recurrent tumours (p = 0.027). VM was observed in 42.86% of primary tumours and 28.57% of recurrent tumours. VM accounted for only a small proportion of the tumour vasculature and VM density did not differ between primary and recurrent tumours (p = 0.266). The functional contribution of VM and its potential as a treatment target in glioblastoma require further investigation.