Hutch News

Testosterone gene variant may boost inherited prostate risk

April 18, 2002

A variant of a gene required for testosterone production may put men with family history of prostate cancer at greatly increased risk of developing the disease themselves.

Dr. Janet Stanford and Public Health Sciences Division colleagues examined the association of prostate cancer risk with a particular variant (A2) of a gene known as CYP17. The study was the first population-based analysis of the link between this gene and prostate-cancer risk.

The group found that white men with a close relative who had prostate cancer and who harbor two copies of the A2 variant of the CYP17 gene were more than 19 times as likely to develop prostate cancer as men without a family history who have two copies of the A1 allele.

In addition, obese men (with a body-mass index of 30 or greater) who possess two copies of the A2 variant had more than a three-fold increased risk of developing prostate cancer relative to thinner counterparts who have the A1/A1 genotype.

Stanford said that the A2 variant did not confer an overall increase in the relative risk of prostate cancer, but was limited to these specific subgroups of the population.

"This genotype may have an independent effect in men with a first-degree family history of prostate cancer or may interact with another unidentified gene that markedly increases risk in this subgroup of men," she said. "These results need to be confirmed in larger case-control studies before any recommendations can be made about screening."

The researchers determined the CYP17 genotype of 590 prostate cancer cases aged 40 to 64 who were diagnosed between 1993 and 1996. Genotyping was also performed on an age-matched group of 538 men without cancer for comparison.

Stanford and colleagues are involved in large-scale studies to identify and characterize genes involved in hereditary, familial and sporadic prostate cancer. Once such genes are isolated, it will be feasible to determine the specific mutations and genetic variants that presdispose to this common and complex disease.

Other study investigators were Dr. Ziding Feng, Elizabeth Noonan, Lori Iwasaki, and Suzanne Kolb of PHS and Dr. Elaine Ostrander of the Clinical Research and Human Biology divisions.

The findings were published in the March edition of Cancer Epidemiology, Biomarkers & Prevention.

 

 

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