Vascular endothelial growth factor (VEGF) is a hypoxia-inducible angio
genesis and vascular permeability factor which is expressed in high am
ounts in perinecrotic palisading cells in human glioblastomas. In vitr
o 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 approach
es to inhibit tumor angiogenesis and edema formation in glioblastoma p
atients will concentrate on the disruption of VEGF/VEGF receptor Signa
l transduction pathway in vivo.