Angiogenesis is the process in which new blood vessels grow by sprouting from established ones. Blood vessel growth occurs in the embryo but rarely in the adult. Exceptions arise, however, in the female reproductive system, where programmed capillary growth occurs at vanous stages of the reproductive cycle, in wound healing, when vascularization is needed to repair damaged tissue and in pathological processes such as cancer, during which vascularization is needed to provide nutrients necessary for solid tumor growth. The notion first suggested by Folkman [l] that tumor growth is angiogenesisdependent, has fueled atn intense effort to identify purify and clone angiogenesis factors-one long-range goal being to antagonize their activity in tumors. To this end, numerous angiogenesis factors have been identified and characterized in the last 10 years (reviewed in [2]). The list includes the fibroblast growth factors (FGF), vascular endothelial growth factor/vascular permeability factor (~ GF/wF), angiogenin, tumor necrosis factor-a (TNF cl), transforming growth factor-cl (TGF-CX), transforming growth factor-p (TGF $), platelet-derived endothelial cell growth factor (PD-ECGF), platelet-derived growth factor (PDGF) and interleukir-8 (IL-S).

Basic FGF (bFGF) had been considered by many to be the major angiogenesis factor because of its expression in tumor cells, its potency as both an endothelial cell rni togen in culture and as an angiogenic factor when administered irz vivo. Yet some of the properties of bFGF force us to question its suitability as a physiological or pathological regulator of angiogenesis. For example, bFGF is mitogenic for many cell types other than endothelial cells. It is not a secreted factor and, thus, it is difficult to envision it participating in paracrine mechanisms of blood vessel stimulation. Finally, there is no definitive evidence for a temporal and spatial correlation between the expression of bFGF and its receptors and angiogenesis in vivo.