Growth factor receptors and angiogenesis play major roles in the oncogenesis of 
gliomas. Over the last several years, several noncytotoxic molecular targeted 
therapies have been developed against growth factor receptors and tumor 
angiogenesis. In gliomas, two main anti-growth factor receptor strategies have 
been evaluated in phase I/II clinical trials: (a) small molecule tyrosine kinase 
inhibitors (TKIs) and (b) monoclonal antibodies that target growth factors or 
growth factor receptors other than vascular endothelial growth factor (VEGF). Up 
to now, few glioma patients have responded to small TKIs (0%-14%) or monoclonal 
antibodies (three case reports) delivered as a single agent. Greater doses, 
combined therapies, as well as the identification of molecular biomarkers 
predictive of response and resistance are important in order to optimize drug 
delivery and improve efficacy. Antiangiogenic therapies are promising for the 
treatment of gliomas. Thalidomide and metronomic chemotherapy were the first 
antiangiogenic strategies evaluated, but they have shown only modest activity. 
Recent studies of bevacizumab, an anti-VEGF antibody, and irinotecan, a 
topoisomerase I inhibitor, have demonstrated a high response rate, suggesting 
that targeted antiangiogenic therapies may play a significant role in the 
management of high-grade gliomas in the future. However, the toxicity profiles 
of these agents are not fully defined and the radiological evaluation of 
possible tumor response is challenging. Clinical evaluation of several VEGF 
receptor TKIs is currently ongoing; one of these inhibitors, cediranib, has 
already demonstrated interesting activity as a single agent. The integrin 
inhibitor cilengitide represents another promising strategy.