According to an article recently published in the British Journal of Cancer, there does not appear to be an association between the presence of viruses in the prostate and the risk for subsequent prostate cancer among men.
Along with skin cancer, prostate cancer is the most commonly diagnosed form of cancer among males in the United States. The prostate is a walnut-sized gland that is located between the bladder and the rectum. It is responsible for forming a part of semen.
Due to the prevalence of prostate cancer, researchers continue to evaluate potential associations between genetic and environmental factors and the risk of prostate cancer. The goal is that by determining risk factors, individuals at high risk may be identified and screened more aggressively.
Recent research has indicated that infection with viruses may be linked to the development of certain cancers. This focus of research continues into various types of cancer.
Researchers from Sweden recently conducted a clinical study to evaluate potential links between infection of prostates with viruses and the subsequent risk of prostate cancer. This study included 201 samples of prostate tissue from men who had benign prostate hyperplasia (non-cancerous condition of the prostate). These men eventually developed prostate cancer. Samples from these prostate tissues were compared to 201 samples of prostate tissue from men who did not develop prostate cancer. The prostate tissue samples were evaluated for the presence of common viruses.
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There were no differences in the prevalence of the following viruses among prostate tissue samples from men who had developed prostate cancer compared to those who did not develop prostate cancer: adenovirus, herpesvirus, papilloma virus, polyoma virus, and Candida albicans DNA.
The researchers concluded that the presence of viruses in the prostate does not appear to be linked to an increased risk of developing prostate cancer.
Reference: Bergh J, Marklund I, Gustavsson C, et al. No Link Between Viral Findings in the Prostate and Subsequent Cancer Development. British Journal of Cancer. 2007;96, 137-139.
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