This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Vessella, R. L. Articles by Corey, E. Search for Related Content PubMed PubMed Citation Articles by Vessella, R. L. Articles by Corey, E.

Targeting Factors Involved in Bone Remodeling as Treatment Strategies in Prostate Cancer Bone Metastasis

Authors' Affiliations: ¹ Department of Urology, University of Washington Medical Center and Puget Sound Veterans Administration Health Care System and ² Department of Urology, University of Washington Medical Center, Seattle, Washington

Requests for reprints: Robert L. Vessella, Department of Urology, Box 356510, University of Washington Medical Center, 1959 Northeast Pacific Street, Seattle, WA 98195. E-mail: vessella{at}u.washington.edu.

Prostate cancer is the most commonly diagnosed cancer in men within the western world and the third leading cause of cancer-related deaths. Even if the cancer is considered localized to the prostate, there is a 15% to 20% incidence of subsequent metastatic disease. Prostate cancer has a very high proclivity for metastasizing to bone, with 90% of men with advanced disease having skeletal lesions. The prostate cancer metastases are characteristically osteoblastic, with extensive new bone deposition, unlike other tumors that metastasize to bone and cause an osteolytic response reflective of bone degradation. There are a considerable number of studies relating to inhibition of the osteoblastic response, including interference with endothelin-1, bone morphogenetic proteins, and Wnt signaling pathways. Within the past few years, several studies showed that increased osteolytic activity also occurs in the background of the prostate cancer skeletal metastases. Because growth factors are being released from the bone matrix during degradation, it suggests that inhibition of osteolysis might be effective in slowing tumor growth. Several strategies are being developed and applied to affect directly the osteolytic events, including use of bisphosphonates and targeting the critical biological regulators of osteoclastogenesis, receptor activator of nuclear factor-B and receptor activator of nuclear factor-B ligand. This review focuses on several of the clinical and preclinical strategies to inhibit the growth of prostate cancer cells in bone and to alleviate the multitude of associated skeletal-related events.

This article has been cited by other articles:

				A. Angelucci, S. Garofalo, S. Speca, A. Bovadilla, G. L. Gravina, P. Muzi, C. Vicentini, and M. Bologna Arachidonic acid modulates the crosstalk between prostate carcinoma and bone stromal cells Endocr. Relat. Cancer, March 1, 2008; 15(1): 91 - 100. [Abstract] [Full Text] [PDF]

				E.-L. Alarmo, T. Korhonen, T. Kuukasjarvi, H. Huhtala, K. Holli, and A. Kallioniemi Bone morphogenetic protein 7 expression associates with bone metastasis in breast carcinomas Ann. Onc., February 1, 2008; 19(2): 308 - 314. [Abstract] [Full Text] [PDF]