London, April 2 : Scientists have identified seven genetic risk factors that predict risk for prostate cancer.

Led by researchers at the Keck School of Medicine of the University of Southern California (USC) and Harvard Medical School, the study recognised the DNA sequences that are clustered in a single region of the human genome on chromosome 8, and which powerfully predict a person’s probability of developing prostate cancer.

“The study has identified combinations of genetic variants that predict more than a fivefold range of risk for prostate cancer,” Nature Genetics quoted senior author David Reich, assistant professor of genetics at Harvard Medical School and associate member of the Broad Institute of Harvard and MIT, as saying.

“Both high- and low-risk combinations of variants are common in human populations,” he added.

Since these risk factors are carried by some people, not everyone, the researchers believe that they may help identify those men who are more likely to contract prostate.

“Clinical testing of these genetic variants may help us identify men who should be prioritised for early prostate cancer screening and prevention efforts,” says Reich.

The researchers noted that the seven genetic variants each independently predicted risk for prostate cancer. They also observed that all these factors were of highest frequency in African Americans, and thus might contribute to the known higher rate of prostate cancer among African Americans compared with other US populations.

“The identification of these genetic variants is an important step in helping us understand the higher risk for prostate cancer in African Americans compared with other US populations and, more importantly, why some men develop prostate cancer and others do not,” says lead author Christopher Haiman, assistant professor of preventive medicine at the Keck School of Medicine of USC.

The study also produced novel biological findings, revealing that each genetic contributor to prostate cancer risk is located outside of the coding regions of genes, in regions previously designated as junk DNA.

“The discovery of multiple, independent genetic changes that are in close proximity to one another, but outside of any known gene, suggests that these results may also teach us about novel molecular mechanisms whereby DNA changes can alter risk of disease,” says Brian Henderson, dean of the Keck School of Medicine of USC. (ANI)