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Cancer

Estrogen Affects Prostate Cancer Risk

April 30, 2010 By Namita Nayyar (Editor in chief)

Estrogen Affects Prostate Cancer Risk

Reported April 26, 2010

(Ivanhoe Newswire) — A high level of one type of estrogen in a man’s body might increase his risk of developing prostate cancer. At the same time, high levels of another kind — the kind that fuels breast cancer — might offer a protective benefit against prostate cancer.

The health of the prostate has long been considered dependent on the level of the male hormones, collectively known as androgens. Researchers now recognize, however, that estrogens and their metabolites also play a role in the prostate’s normal growth as well as in prostate cancer.

“The aim of our study was to evaluate the use of estrogen metabolites as a marker for prostate cancer risk,” senior author Ourania Kosti, Ph.D., at Georgetown Lombardi Comprehensive Cancer Center, was quoted as saying.

The researchers measured estrogens and their metabolites in urine collected from 77 men with prostate cancer, 77 healthy controls and 37 men who underwent biopsy but were diagnosed cancer-free.

 

 

The relative amounts of the 15 estrogens and estrogen metabolites in the urine of men with prostate cancer were similar to those of non-cancer patients with the exception of the estrogen metabolite 4-OHE1. Kosti explained, “This particular estrogen metabolite appeared to be more abundant among men diagnosed with prostate cancer.”

Kosti said her team also observed that the estrogen metabolites considered ‘harmful’ estrogens in breast cancer (16-KE2 and 17-epiE3) are secreted in higher amounts among men without prostate cancer and in lower amounts in those with prostate cancer.

“This suggests that these particular estrogens may have a protective role against prostate cancer development,” Kosti explained. “It is possible that different tissues respond to estrogens different ways, therefore the potential role of 16-KE2 and 17-epiE3 in prostate cancer prevention and management should be further explored.”

SOURCE: Presented at the American Association of Cancer Research (AACR) Annual Meeting, April 18, 2010

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