New genetic variant linked to onset of prostate cancer identified

London, Sept 2 : Scientists from Wake Forest University School of Medicine have identified a new variant in the gene HNF1B, responsible for developing prostate cancer.

The research team has reported the discovery of a second independent site within the HNF1B gene on chromosome 17 (17q12), thus increasing the number of genetic variants that may contribute to risk of developing the disease.

Jianfeng Xu, M.D., Dr. Ph.H, senior researcher on the study and a professor of epidemiology and cancer biology and Director of the Center for Cancer Genomics then compared the newly discovered site with the site discovered earlier in the same gene and said, "these data strongly suggest that the two sites are genetically independent.

"We found another genetic variant associated with prostate cancer risk," Nature Genetics quoted Xu, as saying.

"The more genetic variants we discover, the better off we are. As we find more of these, it improves our ability to predict prostate cancer risk," Xu added.

In the study what the researchers called a "fine-mapping study" two groups were studied, one called CAPS, from Sweden, that had 2,899 prostate cancer cases and 1,722 control participants, and the Johns Hopkins study that had 1,527 prostate cancer patients and 482 control participants.

They identified two separate clusters of prostate-cancer-associated SNPs (single nucleotide polymorphisms), one in a region previously identified and one in a new region.

To understand, whether the genetic variants were linked to prostate cancer the team analysed the same locations in five other large studies of prostate cancer patients.

The analysis showed that prostate cancer risk was higher among men who had the genetic variants.

Previous studies have also shown that a man with four of the five already discovered variants has a 400 percent increased risk of developing prostate cancer compared to men with none of the variants.

he findings appear in current on-line version of Nature Genetics.

ANI