a tumor suppressor gene, its protein product must be in the cells nucleus, explains Imperiale. TAg apparently sequesters p53 protein in the cells cytoplasm, preventing it from entering the nucleus and giving the signal for the cell to stop dividing and die.
Imperiales 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.
If hes right, prostate cancer may have something in common with cervical cancer, which is caused by a different virus the human papillomavirus.
Papillomavirus makes proteins with the same function as T antigen, Imperiale says. They induce cell growth and inactivate the p53 gene, preventing it from killing abnormal cells. So, its a logical possibility that a similar mechanism occurs in at least some cases of prostate cancer, but much additional research will be needed before we can know for sure.
The U-M study was funded by a grant from the U.S. Armys Medical Research and Material Command, Department of Defense.