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Angiogenesis in malignant gliomas
Author(s) -
Plate Karl H.,
Risau Werner
Publication year - 1995
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440150313
Subject(s) - angiogenesis , glioma , biology , cancer research , paracrine signalling , vascular endothelial growth factor , receptor tyrosine kinase , tumor progression , downregulation and upregulation , vascular endothelial growth factor a , kinase insert domain receptor , neovascularization , receptor , signal transduction , microbiology and biotechnology , cancer , vegf receptors , gene , genetics , biochemistry
One event that accompanies glioma progression is the upregulation of angiogenesis. Low‐grade gliomas are moderately vascularized tumors whereas high‐grade gliomas show prominent microvascular proliferations and areas of high vascular density. To analyze the molecular mechanisms underlying glioma angiogenesis, we studied the expression of vascular endothelial growth factor (VEGF) and its tyrosine kinase receptors VEGFR‐1 and VEGFR‐2 during normal brain development and glioma‐induced angiogenesis. Our results suggest a paracrine control of angiogenesis and endothelial cell proliferation that is tightly regulated and transient in the embryonic brain, switched off in the normal adult brain, and turned on in tumor cells (VEGF) and the host vasculature (VEGFR‐1 and −2) during tumor progression. It is unknown how VEGF and VEGF receptors are upregulated during glioma angiogenesis, but there is recent evidence that VEGF as well as endogenous inhibitors of angiogenesis could be under control of the tumor suppressor genes p53 and VHL. © 1995 Wiley‐Liss, Inc.