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Uterine, prostate cancers may be linked on genetic level

Issue: May 25, 2011

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By conducting a genome-wide association study for uterine cancer, scientists have discovered a genetic region that reduces the risk for the disease, according to data published in Nature Genetics.

In men, the HNF1B gene is located in the same region and has been previously linked to a reduced risk for prostate cancer but a higher risk for type 2 diabetes.

"This study is the first to highlight a potential link between womb cancer in women and prostate cancer in men, providing new insight into the underlying genes and mechanisms that lead to the development of both diseases," Douglas Easton, PhD, director of the genetic epidemiology unit at Cancer Research UK, University of Cambridge, said in a press release.

Easton and colleagues conducted a genotype association study among 1,265 patients with endometrial cancer and 5,190 controls, and they compared genotype frequencies for 519,655 single nucleotide polymorphisms. According to the press release, women with the protective "version" of the gene are on average 15% to 18% less likely to develop uterine cancer, whereas men with the same version are 21% less likely to develop prostate cancer. It has also been linked to a 10% to 14% greater risk for type 2 diabetes.

"Understanding how these influence a person's risk of developing cancer is a crucial step in being able to identify high-risk groups who may benefit from closer monitoring or measures to reduce their risk of developing the disease," Easton said.

Forty-seven SNPs showed evidence of being associated with endometrial cancer; the researchers genotyped these in 3,957 patients with uterine cancer and 6,886 controls. Three SNPs were significantly linked to a decreased risk for uterine cancer, all of which overlapped with the HNF1B gene on chromosome 17.

The study was funded by Cancer Research UK, the National Health and Medical Research Council in Australia and the Wellcome Trust.

For more information:

• Spurdle AB. Nat Genet. 2011;doi:10.1038/ng.812

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