Angiogenesis is required for invasive tumor growth and metastasis and 
constitutes an important point in the control of cancer progression. Its 
inhibition may be a valuable new approach to cancer therapy. Avascular tumors 
are severely restricted in their growth potential because of the lack of a blood 
supply. For tumors to develop in size and metastatic potential they must make an 
"angiogenic switch" through perturbing the local balance of proangiogenic and 
antiangiogenic factors. Frequently, tumors overexpress proangiogenic factors, 
such as vascular endothelial growth factor, allowing them to make this 
angiogenic switch. Two strategies used in the development of antiangiogenic 
agents involve the inhibition of proangiogenic factors (eg, anti-vascular 
endothelial growth factor monoclonal antibodies) as well as therapy with 
endogenous inhibitors of angiogenesis, such as endostatin and angiostatin. 
Therapy with endogenous angiogenic inhibitors such as endostatin and angiostatin 
may reverse the angiogenic switch preventing growth of tumor vasculature. 
Preclinical studies have shown that endostatin effectively inhibits tumor growth 
and shrinks existing tumor blood vessels. Phase 1 clinical trials of endostatin 
and angiostatin are ongoing, and preliminary results show minimal toxicities.