Cellular components of microvascular proliferation in human glial and metastatic brain neoplasms. A light microscopic and immunohistochemical study of formalin-fixed, routinely processed material.

Since the origin of cells contributing to microvascular proliferation (MVP) in glial neoplasms is unsettled, a light microscopic and immunohistochemical study for vascular smooth muscle cells and endothelial cells was performed in formalin-fixed, routinely processed brain tumor biopsy material. MVP in glial neoplasms was compared with that in intracerebral metastatic carcinomas and in intracranial granulation tissue. On the basis of the degree of hyperplasia of hypertrophic cells in the microvascular wall, MVP was subjectively divided into mild, moderate, and glomeruloid (marked) proliferation. The relative contribution of vascular smooth muscle cells and endothelial cells to different degrees of MVP was estimated immunohistochemically using antibodies against alpha-smooth muscle actin and von Willebrand factor, respectively. Glomeruloid MVP occurred in 50% of the malignant glial neoplasms. Moderate MVP was found in most malignant gliomas and in some pilocytic astrocytomas. Glomeruloid MVP was present in peritumoral glial tissue in 4 out of 15 intracerebral metastatic carcinomas, while only mild to moderate MVP was found within these tumors. In granulation tissue MVP was mild. In glomeruloid and moderate MVP vascular smooth muscle cells were more hypertrophic and more numerous than endothelial cells. The contribution of hypertrophic vascular smooth muscle cells to mild MVP was variable. MVP in glial neoplasms was generally not accompanied by a matrix of fibrous stroma but was directly embedded in glial tissue. The architecture of this MVP suggested "in situ" proliferation of microvascular cells without migration of these cells into the surrounding tissue.