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Departments of Cancer Biology and Epidemiology and Prevention, Wake Forest University Health Sciences, Winston-Salem, North Carolina
Requests for reprints: Gary G. Schwartz, Departments of Cancer Biology and Epidemiology and Prevention, Wake Forest University Health Sciences, Winston-Salem, NC 27157. Phone: 336-716-7446; Fax: 336-716-5687. E-mail: gschwart{at}wfubmc.edu
Bony metastases from prostate cancer are a significant cause of morbidity and mortality. These metastases are predominantly blastic (bone-forming) and commonly cause increased serum levels of parathyroid hormone (PTH) as calcium ions are transferred from serum into blastic bone. The epidemiologic and clinical significance of secondary hyperparathyroidism in advanced prostate cancer have not been widely appreciated. Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone. Thus, blastic metastases appear to induce a "vicious cycle" in which PTH resorbs normal bone to support the growth of blastic bone. Recognition of the potential role of PTH in the progression of skeletal metastases suggests novel opportunities for prostate cancer secondary prevention. In particular, we propose that suppressing serum PTH in advanced prostate cancer may reduce morbidity by decreasing fractures and pain caused by bone resorption and may reduce mortality by retarding the progression of metastatic disease. (Cancer Epidemiol Biomarkers Prev 2008;17(3):478–83)
This article has been cited by other articles:
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H. G. Skinner and G. G. Schwartz A Prospective Study of Total and Ionized Serum Calcium and Fatal Prostate Cancer Cancer Epidemiol. Biomarkers Prev., February 1, 2009; 18(2): 575 - 578. [Abstract] [Full Text] [PDF] |
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H. G. Skinner and G. G. Schwartz Serum Calcium and Incident and Fatal Prostate Cancer in the National Health and Nutrition Examination Survey Cancer Epidemiol. Biomarkers Prev., September 1, 2008; 17(9): 2302 - 2305. [Abstract] [Full Text] [PDF] |
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