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Review
. 2001 Mar;158(3):789-96.
doi: 10.1016/S0002-9440(10)64025-4.

Glomeruloid microvascular proliferation orchestrated by VPF/VEGF: a new world of angiogenesis research

D J Brat  1 , E G Van Meir
Affiliations
Review

Glomeruloid microvascular proliferation orchestrated by VPF/VEGF: a new world of angiogenesis research

D J Brat et al. Am J Pathol. 2001 Mar.
No abstract available

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Figures

Figure 1.
Figure 1.
Glomeruloid vascular proliferation in a glioblastoma multiforme (arrow). Newly sprouted vessels arranged in tufted aggregates resemble renal glomeruli. Adjacent vessels demonstrate other morphological forms of microvascular hyperplasia in glioblastoma.
Figure 2.
Figure 2.
Schematic diagram showing the histopathological progression of infiltrating astrocytoma (WHO grade II, left) to glioblastoma multiforme (WHO grade IV, right). In grade II infiltrating astrocytomas, individual tumor cells are scattered within the central nervous system neuropil. Blood vessel architecture and density are similar to normal brain white matter (far left). Neoplastic cells become more numerous and atypical, and show occasional mitotic figures in anaplastic astrocytoma (WHO grade III). In glioblastoma multiforme, microvascular hyperplasia, including glomeruloid vascular proliferation (open arrow), and necrosis with pseudopalisading (black arrows) are seen. Glomeruloid vascular proliferation is often noted in zones surrounding pseudopalisading necrosis. Illustration by Bill Winn.
Figure 3.
Figure 3.
Proposed model for the evolution of vascular changes during astrocytoma progression to glioblastoma multiforme. In early stages of tumorigenesis (left), low grade infiltrating astrocytoma cells co-opt existing small capillaries. As neoplastic cells proliferate to form a more cellular neoplasm (middle), endothelial cells resist co-option by releasing Ang-2, which acts in an autocrine fashion to cause endothelial apoptosis and vascular regression in the absence of VPF/VEGF. Astrocytoma cells in the immediate vicinity of degenerated, co-opted vessels begin to die, initiating the well-recognized pattern of pseudopalisading necrosis (right). Hypoxic astrocytoma cells in zones surrounding central necrosis up-regulate the expression and secretion of VPF/VEGF, which acts on nearby vessels to cause vascular hyperplasia, including glomeruloid vascular proliferation.
See this image and copyright information in PMC

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References

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