Angiogenesis of prostate cancer and antiangiogenic therapy.
Tumor-associated angiogenesis refers to the growth of new vessels toward and within the tumor. Several studies have revealed that increasing intratumoral microvessel density, a major of tumor-associated angiogenesis, correlates with greater aggressiveness of prostate cancer. Angiogenesis consists of multiple, sequential, and interdependent steps dependent on the local balance of proangiogenic and antiangiogenic molecules Many proangiogenic and antiangiogenic molecules have been demonstrated to regulate growth and metastasis of prostate cancer. As tumor-associated angiogenesis is a crucial step in the process of prostate cancer development, inhibition of tumor neovascularization, and/or destruction of tumor vasculature (antiangiogenic therapy) may maintain the tumors in a dormant state or, perhaps in combination with cytotoxic therapies, potentiate shrinkage of tumors. Recently, therapeutic agents targeting the receptors of proangiogenic molecules and their signal transduction cascade have been developed. In this article, the role of angiogenic molecules in prostate cancer biology, and the application of angiogenesis inhibition to therapeutics for prostate cancer are reviewed.
D042501:Angiogenic Proteins / Q000037:antagonists & inhibitors* / Q000502:physiology; D015195:Drug Design; D043169:Endostatins / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007372:Interferons / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D009389:Neovascularization, Pathologic; D011471:Prostatic Neoplasms / Q000098:blood supply* / Q000188:drug therapy* / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects
D042501:Angiogenic Proteins; D043169:Endostatins; D007372:Interferons