Angiogenesis is required for sustained neoplastic growth (3). The sprouting of new vessels from the pre-existing vasculature supplies a proliferating mass of hypoxic tumor cells with oxygen and nutrients. Glioblastoma multiforme is one such tumor, characterized by extensive vascular growth and remodeling. A permissive microenvironment coupled with tissue hypoxia, which promotes elaboration of the angiopoietins and vascular endothelial growth factor (VEGF), is implicated in tumor neovascularization. Angiopoietins seem to stimulate recruitment of bone marrow¡Vderived endothelial precursor cells, and VEGF induces myeloproliferation and increases circulating levels of endothelial progenitor cells (2) and also contributes to neo-angiogenesis. The receptor to which VEGF binds, Flk-1 (the mouse variant of the human KDR), is expressed on endothelial cells and helps trigger vascular proliferation when activated.