title: Blood vessels are regulators of growth, diagnostic markers and therapeutic targets in prostate cancer.
abstract: The vasculature plays an important role in the normal and malignant prostate. Under basal conditions both glandular epithelial and stromal prostate cells produce an abundance of blood flow and angiogenesis regulating substances and the expression of these is generally increased in prostate tumors. The proportion of proliferating endothelial cells is high in the normal prostate compared to other tissues in the body. After castration effects on the vasculature, such as decreased blood flow and vascular regression, precede effects on the glandular compartment. Correspondingly, hormone induced prostate growth is characterized by early effects on the vasculature such as increased blood flow and endothelial cell proliferation, thus indicating that the vasculature may be involved in the androgenic regulation of the prostate. Prostatic intraepithelial neoplasia (PIN) and prostate cancer are associated with increased vascular density and in experimental models prostate cancer growth is apparently angiogenesis-dependent since tumor growth and progression can be inhibited by antiangiogenic treatment. Moreover, vascular density has been related to prognosis in prostate cancer patients. A better understanding of the pathways regulating angiogenesis in the normal prostate and how these pathways change during malignant transformation can hopefully lead to better prognostic markers and therapies for the large group of patients with prostate cancer. The purpose of this review is therefore to summarize the current knowledge on the role and regulation of the vasculature in the prostate and its potential clinical applications.
authors.affiliation: Department of Medical Biosciences, Pathology, Umeå University, Sweden. ingela.franck.lissbrant@pathol.umu.se
authors.forename: I F
authors.initials: IF
authors.lastname: Lissbrant
authors.forename: E
authors.initials: E
authors.lastname: Lissbrant
authors.forename: J E
authors.initials: JE
authors.lastname: Damber
authors.forename: A
authors.initials: A
authors.lastname: Bergh
mesh_terms: D006801:Humans; D008297:Male; D009389:Neovascularization, Pathologic; D018919:Neovascularization, Physiologic; D011467:Prostate / Q000098:blood supply; D011471:Prostatic Neoplasms / Q000098:blood supply* / Q000473:pathology* / Q000628:therapy