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28 February 2005
Risk Of Prostate Cancer May Be Inherited
by George Atkinson

A study by Mount Sinai School of Medicine researchers, published in the journal Cancer Research, suggests a single gene variant may increase a man's risk of prostate cancer by 50%.

In a previous study, Mount Sinai researchers found that a gene, known as KLF6, fails to function properly in at least 50 to 60 percent of all prostate cancer patients. This was the first single gene shown to be responsible for the majority of cases of this disease. KLF6 functions as a tumor suppressor gene. When KLF6 fails to function properly cell growth goes unchecked and cancer may result. It has since been discovered that KLF6 defects are implicated in a number of other human cancers, including colorectal cancer, lung cancer and liver cancer.

The findings of the earlier study led the researchers to ask whether or not mutations in this gene that are present from birth might increase an individuals susceptibility to prostate cancer. Researcher John Martignetti and colleagues addressed this question by analyzing differences in the KLF6 gene in blood samples from men registered at three major cancer centers. Blood samples were divided into three groups based on the individuals from which they were taken - those with prostate cancer who had a family history of prostate cancer, those with prostate cancer and no family history of the disease, and those without prostate cancer.

Around 17 percent of the patients with a family history of the disease and 15 percent of patients with no such history carried at lease one copy a single KLF6 variant, but only 11 percent of the men without prostate cancer had a copy. The significant difference in prevalence of the variant among these three groups indicates that individuals with this particular gene variant face an approximately 50 percent increased risk for developing prostate cancer. The variant of the gene produces a an altered version of the KLF6 protein. Rather than entering the cell nucleus to suppress cell growth as the KLF6 protein usually does, this altered version remains in the cytoplasm, where it has the opposite effect, thus increasing cell growth and potentially leading to the development of caner.

"Our findings highlight a completely novel and previously unexplored pathway for the development of prostate cancer," said Martignetti. "Ultimately, we plan to investigate the potential of this gene as a diagnostic tool, an indicator of a patients risk for prostate cancer, and as a potential target for new treatments," he concluded.




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