Common virus may play a role in prostate cancer

August 19, 2004

A common virus found in the urinary tract may play a role in the development of prostate cancer, University of Michigan Medical School researchers say.

A common virus found in the urinary tract may play a role in the development of prostate cancer, University of Michigan Medical School researchers say.

Investigator Michael J. Imperiale, PhD, and colleagues have found DNA and proteins from the BK virus in prostate tissue with abnormal cell changes. They believe these atrophic lesions can be the first step in a series of progressive cell changes leading to prostate cancer.

"Other studies have detected DNA from the BK virus in prostate cancer cells, but this study is the first to pinpoint the location of the viral protein expression to one precursor state in the development of prostate cancer, and to a specific location within the prostate cells," said Dr. Imperiale.

"We are not saying that BK virus causes prostate cancer, but our results do suggest that the virus plays a role in the transition from normal to uncontrolled growth of prostate cells."

The BK virus resides in the kidneys without causing harm. In individuals with depressed immune systems, especially those who have received a kidney transplant, the virus has been known to cause kidney and bladder disease.

In their study, the Michigan scientists examined 21 samples of prostate tissue from men who underwent prostatectomy for cancer. Seventy-one percent of the prostate samples were found to contain gene segments from the BK virus.

T antigen (TAg) protein from the BK virus was present in 43% of the tissue samples, but only in atrophic lesions. TAg was not expressed in normal cells or cancerous cells.

The researchers' working hypothesis is that the BK virus infects epithelial cells in the prostate and transforms them into atrophic lesions through TAg expression. This produces an area of uncontrolled cell growth, which if circumstances are right, can eventually develop into prostate cancer.

The original paper was published in the online edition of Oncogene (July 19, 2004).