ABSTRACT
Angiogenesis is defined by Merriam Webster dictionary as ‘‘the formation and differentiation of new blood vessels.’’ The British surgeon John Hunter was the first to describe this phenomenon, detailing vascular networks formed within a healing wound (1). Hertig (2) first used ‘‘angiogenesis’’ in describing the formation of blood vessels to bring oxygen and nutrients to the developing placenta. In 1971, Folkman (3,4) used this same term to describe the production of vasculature to support a tumor’s growth. Without angiogenesis, tumorigenesis, tumor invasion, and metastasis would not occur (5,6). In order for a tumor to grow past 0.5mm3, the limit of diffusion to provide adequate oxygenation and nutrients, vascularization must occur (7). Gimbrone et al. (8) showed that blocking angiogenesis caused tumor cells to become dormant. Although this dormancy was due to mechanical isolation of the implanted tumor cells into avascular areas, improved understanding of tumor biology and drug design has brought forth compounds that target the production or receptor binding of these proangiogenic stimulators. With this chapter, we will review the tumor biology of angiogenesis and examine therapeutic uses of anti-angiogenesis in the context of treating prostate cancer.
