ABSTRACT
Most solid tumors arise as small nodal growths and utilize preexisting surrounding local vasculature to acquire oxygen and nutrients. As tumors continue to grow, they outsize the available blood supply and become dormant, potentially remaining so for years. Further expansion is believed to require acquisition of a proangiogenic phenotype, referred to as the “angiogenic switch” (1). The hypothesis that tumors are angiogenesis-dependent was put forth by Folkman (2) over 30 years ago. Although at first greeted with some skepticism, a large body of evidence now supports this idea, including recent genetic experiments (3).
