Abstract
Vascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenesis and vascular permeability factor which is expressed in high amounts in perinecrotic palisading cells in human glioblastomas. In vitro VEGF gene expression is enhanced approximately ten times by hypoxia. Current evidence suggests, that hypoxia is also the driving force for VEGF gene expression in glioblastoma cells in vivo and represents the most important trigger for tumor angiogenesis and edema. Our approaches to inhibit tumor angiogenesis and edema formation in glioblastoma patients will concentrate on the disruption of VEGF/VEGF receptor signal transduction pathway in vivo.
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