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Prostate cancer risk unaffected by steroid hormone gene variation

Genetic variations in a specific gene involved in the production of steroid hormones such as testosterone do not appear to influence the development of prostate cancer in men in the United States and Europe.

That finding resulted from the first substantive effort by the large, international Breast and Prostate Cancer Cohort Consortium (the BPC3), which includes five researchers from the Keck School of Medicine. Their results were published online in the peer-reviewed, open-access Public Library of Science journal, PLoS Genetics.

Participants in the BPC3 come from a variety of institutions including Harvard School of Public Health, the University of Cambridge, the National Cancer Institute, the Broad Institute at Harvard and the Massachusetts Institute of Technology, the Keck School of Medicine and many others. Keck School participants in this study included these researchers: Christopher A. Haiman, assistant professor of preventive medicine; Brian E. Henderson, dean of the Keck School and the Kenneth T. Norris Jr. Chair in Cancer Prevention; Malcolm C. Pike, professor of preventive medicine; Wendy V. Setiawan, research associate in preventive medicine; and Daniel O. Stram, professor of preventive medicine.

The consortium was created to assess how variations in genes that play a role in steroid hormone production might—or might not—influence the development of breast and prostate cancer. They chose as their first major project a gene called HSD17B1.

The group began by mapping the gene, which plays a role in producing both estrogen and testosterone, and identifying the areas of variation (called single-nucleotide polymorphisms, or SNPs) within it.

They then identified these variations in 8,290 prostate cancer patients and 9,367 people who were matched by age and ethnicity, but did not have prostate cancer.

In the final analysis, none of the SNPs identified were found to be significantly more common in the prostate cancer patients than the controls.

There was, however, a “significant inverse association” between one SNP and prostate cancer in Latinos and Japanese Americans—in other words, having that SNP reduced their likelihood of prostate cancer—that was not found in the other groups studied (African Americans, Native Hawaiians and whites).

However, the researchers indicated that the smaller numbers of Latinos and Japanese Americans in the study may make results unreliable.

Overall, the researchers wrote, “The absence of an association between HSD17B1 variants and risk of prostate cancer suggests that we can rule out large or moderate associations between common HSD17B1 variants and risk of prostate cancer among U.S. and European whites.”

Nonetheless, they added, it remains to be determined whether variants in other genes in steroidal hormone pathways play a more important role or if the combined effects of several genes within these pathways have a larger impact. The BPC3 plans to investigate these questions by comprehensively measuring variation in more than 30 genes involves in the steroidal hormone pathway and their associated receptors.

Kraft P, Pharoah P, Chanock SJ, Albanes D, Kolonel LN, et. al. (2005) “Genetic variation in the HSD17B1 gene and risk of prostate cancer. PLoS Genetics 1(5): e68.

Prostate cancer risk unaffected by steroid hormone gene variation

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