부산대학교 도서관

Simple Summary: Glioblastomas are resistant to treatments targeting angiogenic blood vessel development. It is possible that glioblastoma cells are forming vessel-like structures, called vasculogenic mimicry (VM), and contributing to treatment resistance through this process. We aimed to quantify VM in primary and recurrent glioblastoma and to determine whether VM vessels express the pathological vessel marker prostate-specific membrane antigen (PSMA). We found that only a small proportion of vessels in glioblastoma were VM, and that these vessels did not express PSMA. However, the expression of PSMA was decreased in recurrent compared to primary tumours, as was the total vessel density. The potential of VM as a treatment target and its contribution to treatment resistance in glioblastoma require further investigation. 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. [ABSTRACT FROM AUTHOR]