At this point, the tumor releases angiogenic factors and may attract mononuclear cells that also release such factors. The tumor neovascular system is qualitatively defective because the vessels have no pericytes and little or no muscularity. The system is also quantitatively deficient, and thus, most solid tumors are hypoxic. Finally, the fenestration of the vessels allows tumor cells to enter the vascular system, facilitating hematogenous metastases. Indeed, in clinical studies, the degree of neovascularization correlates negatively with prognosis.
Angiogenesis is under precise, dynamic, and complex homeostatic control.
Indeed, homeostasis of angiogenesis, with its array of promoters and inhibitors, has been likened to the coagulation-anticoagulation mechanism. Alterations in angiogenesis control are important not only for tumor growth but also for the pathogenesis of specific conditions, such as diabetic retinopathy and rheumatoid arthritis. Many of the factors that play a role in angiogenesis have been identified. Systemic administration of recombinant FGF in vivo increases vascularization of experimental tumors, and a monoclonal antiserum to basic FGF inhibits this vascularization. Furthermore, FGF receptors are prominent in vascular endothelium.