ABSTRACT
Recent data suggest that tumor-associated neovascularization is a central process for the growth, invasion and metastasis of brain malignancies. Neovascularization involves multiple steps and pathways dependent on the local balance between positive and negative regulatory factors, as well as interactions between the tumor, its vasculature and the surrounding extracellular tissue matrix. When a tumor remains in its dormant state the cellular proliferation rate is balanced by the apoptotic rate; thus, it is unable to grow in size beyond a few millimeters in the absence of the acquired angiogenic phenotype. The mechanism by which tumors switch to the angiogenic phenotype has not been completely elucidated.
