The vascular response to tumor infiltration in malignant gliomas. Morphometric and reconstruction study

Acta Neuropathol. 1989;77(4):369-78. doi: 10.1007/BF00687371.

Abstract

Neo-vascularization and endothelial hyperplasia have been shown to be very active in malignant gliomas. In this contribution the vascularization of the cortex infiltrated by malignant gliomas is morphometrically studied and the endothelial proliferations are immunohistochemically investigated and reconstructed by a three-dimensional computer-assisted procedure. Vessel density increases after tumor infiltration in some cases only. The diameter of vessels increases and so does the number of nuclei/vessel after the complete invasion of the cortex when vascular glomeruli develop. In completely infiltrated cortex with development of glomeruli and circumscribed necroses, vessel density is very low. No neoformation of vessels takes place before the complete infiltration of the cortex by the tumor. The hyperplastic formations, usually arranged parallel to the deep or outer cortical layers, take origin from the radially penetrating vessels from the meninges and their lateral branching. The hyperplasia deforms the vascular network, making it often inadequate to supply tumor cells. Immunohistochemically, the cells composing the hyperplastic structures are variably positive for factor VIII/RAg and, at a lesser extent, for alpha-smooth muscle actin. The poorness of the vascular network in many instances of completely infiltrated cortex is responsible for the development of circumscribed necroses.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Brain Neoplasms / blood supply*
  • Brain Neoplasms / pathology
  • Cerebral Cortex / blood supply*
  • Cerebral Cortex / pathology
  • Endothelium, Vascular / pathology
  • Factor VIII / analysis
  • Glioblastoma / blood supply*
  • Glioblastoma / pathology
  • Humans
  • Hyperplasia
  • Immunohistochemistry
  • Neoplasm Invasiveness
  • Neovascularization, Pathologic

Substances

  • Factor VIII