Researchers Spot Genes Linked to Testicular Cancer
MONDAY, June 1 (HealthDay News) -- U.S. scientists say they've identified key gene variants tied to an increased risk of testicular cancer.
They said the findings are an important step toward understanding which men are at high risk for the disease.
"Despite being quite heritable, there really have not been any clear genetic risk factors that can account for most cases of testicular cancer. These variants are the first striking genetic risk factors found for this disease to date," Dr. Katherine L. Nathanson, an assistant professor of medicine at the University of Pennsylvania School of Medicine and a specialist in medical genetics at the Abramson Cancer Center, said in a news release.
Nathanson and colleagues found that men with two copies of the common version of the c-KIT ligand (KITLG) gene are 4.5 times more likely to develop testicular cancer than men with two copies of the less common versions of the gene.
The researchers also found that men with two copies of the common version of variants next to another gene called sprouty 4 (SPRY4) are almost 1.5 times more likely to develop testicular cancer than men with two copies of the less common version of the gene.
The study appears online in the journal Nature Genetics.
Environmental exposure has been suspected as a factor in the growing incidence of testicular cancer, which is the most common cancer among young men, the study authors note. This study shows that genes also play a major role in a man's risk of developing the disease.
"This finding is quite different than those observed in many other genome-wide association studies," Nathanson said. "In most studies, the increased risk of disease is associated with the less common variant of the gene. In this case, it is the more common variant in Caucasians that is associated with risk. If you carry two copies of the less common variant you are probably at incredibly low risk."
-- Robert Preidt
SOURCE: University of Pennsylvania School of Medicine, news release, May 31, 2009
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