Xu and his team, in collaboration with researchers at Johns Hopkins University, looked at variations in a gene that controls the body's response to carcinogens in the environment as well as hormones natural to the body. They found men with prostate cancer often had a different version of the gene than men who were not affected by the disease.
Scientists believe their findings may hold important clues in understanding what environmental factors may trigger the development of prostate cancer.
"Previous research suggests prostate cancer arises in certain individuals due to a combination of genetic and environmental factors," said Xu. "Our study suggests that the genetic make-up of some men leaves them more susceptible to potential carcinogens in the environment or hormones in the body that could trigger the disease."
The researchers analyzed a gene called CYPIBI, which is thought to play an important role in the development of cancer.
CYPIBI normally plays a dual role in the body and therefore has been suggested to both cause and prevent cancer. It helps the body eliminate environmental chemicals that can cause cancer but also can activate some hormones, turning them into cancer-causing agents.
Tiny variations in the gene may alter its function, say the researchers, with some increasing the cancer-causing effects of the gene and others enhancing its ability to prevent cancer.
The team looked separately at 13 variations in CYPIBI and clusters of these variations, called polymorphisms, commonly found in Caucasian male populations. They found that one cluster of variations was more common in men with prostate cancer who had no family history of the disease, while another combination appeared more frequently in men who did not have the disease.
The study suggests men with a particular gene variant have an increased risk of prostate cancer. "It's an exciting finding because we know the gene interacts with certain cancer-causing chemicals," said Xu. "Studying this more closely will bring us closer to finding out what factors in the environment or within the body may trigger the disease."
This information will help scientists better understand how changes in the gene alter its dual functions in the body, and allow them to identify people at high risk and advise them on ways to prevent the disease.
Media Contacts: Jonnie Rohrer, 336-716-6972, Karen Richardson or Robert Conn, 336-716-4587.
Journal
British Journal of Cancer