Gary Schwartz Lab

In the United States, a new case of prostate cancer is diagnosed every three minutes and a man dies from prostate cancer every fifteen minutes, making prostate cancer the most common non-skin cancer and, after lung cancer, the second most fatal. What clues can epidemiology provide about the cause of prostate cancer? We have suggested that the descriptive epidemiology of prostate cancer (i.e., the increasing risk with age, Black race, and residence at northern latitudes) resembles the descriptive epidemiology of vitamin D deficiency in the elderly. Human prostate cells are known to possess specific receptors for the hormonal form of vitamin D, 1,25(OH)2 D. We have shown that when human prostate cancer cells are exposed to 1,25(OH)2 D, 1,25(OH)2 D promotes their differentiation and inhibits their proliferation, invasive-ness, and metastasis. These findings have led to human clinical trials of 1,25(OH)2 D and 1,25(OH)2 D analogues as differentiation therapy for prostate cancer. We have recently demonstrated that prostate cells synthesize 1,25(OH)2 D from its prohormonal precursor, 25-Hydroxyvitamin D – an ability previously believed to be exclusive to kidney cells and keratinocytes. This autocrine synthesis of 1,25(OH)2 D opens new possibilities for prostate cancer prevention and therapy, because until it is bioactivated by prostate cells, 25-Hydroxyvitamin D is inactive and can be administered more safely than 1,25(OH)2 D.

Gary Schwartz Lab Figure 1


Synthesis of 1,25(OH)2 D. The kidney is the “classic” source of 1,25(OH)2 D. However, our recent findings have established that the prostate also synthesizes 1,25(OH)2 D from the prohormone, 25-OH-D. These findings suggest that 25-OH-D may be an effective therapy for prostate cancer because it is converted into the active hormone by prostatic cells.

More recently, we have shown that elements of the vitamin D endocrine system other than vitamin D appear to be biologically active in men with or at risk for prostate cancer.  For example, the observations that men with advanced prostate cancer commonly have elevated parathyroid hormone (PTH) and that PTH promotes the profession and metastasis of prostate cancer cells led us to a clinical trial of PTH suppression (using a vitamin D analogue) in men with metastatic androgen-insensitive prostrate cancer.  Finally, we have shown that men with elevated serum calcium within the normal range are approximately 3 times more likely to die from prostate cancer than are men whose serum calcium levels are lower.  These findings raise the possibility that serum calcium is a prospective biomarker of fatal prostate cancer, a finding that has large implications for prostate cancer screening and early detection.

Gary Schwartz Lab Figure 2

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