The UGT2B17 gene deletion polymorphism and risk of prostate cancer. A case-control study in Caucasians. Other Scholarly Work

Gallagher, Carla J, Kadlubar, Fred F, Muscat, Joshua E et al. (2007). The UGT2B17 gene deletion polymorphism and risk of prostate cancer. A case-control study in Caucasians. . 31(4), 310-315. 10.1016/j.cdp.2007.07.005

cited authors

  • Gallagher, Carla J; Kadlubar, Fred F; Muscat, Joshua E; Ambrosone, Christine B; Lang, Nicholas P; Lazarus, Philip

fiu authors

abstract

  • Background

    UDP-glucuronosyltransferase (UGT) 2B17 is a phase II metabolizing enzyme that mediates the glucuronidation of C(19) steroids. A deletion polymorphism in the UGT2B17 gene is associated with a substantial reduction in glucuronidation activity in vitro.

    Methods

    We examined the association between the UGT2B17 deletion polymorphism and the risk of incident prostate cancer in a population-based study from central Arkansas that included 411 Caucasian cases and 397 Caucasian controls. We developed a novel high-throughput procedure that uses real-time PCR and allelic discrimination for genotyping analysis.

    Results

    The prevalence of the UGT2B17 deletion [(0/0)] was 12% in the controls, which was consistent with previous population estimates and with Hardy Weinberg equilibrium. There was no association between the UGT2B17 deletion polymorphism and prostate cancer risk in unconditional logistic regression analysis. Compared to the wild-type group (+/+), the adjusted odds ratio (OR) was 0.89 (95% CI=0.55-1.45) for the homozygous deletion (0/0), and the OR was 0.99 (95% CI=0.73-1.35) for the heterozygote group (+/0).

    Conclusion

    These findings show that the UGT2B17 deletion polymorphism is not associated with prostate cancer risk in Caucasians.

publication date

  • January 1, 2007

keywords

  • Aged
  • Case-Control Studies
  • Gene Deletion
  • Glucuronosyltransferase
  • Humans
  • Male
  • Middle Aged
  • Minor Histocompatibility Antigens
  • Odds Ratio
  • Polymerase Chain Reaction
  • Polymorphism, Genetic
  • Prostatic Neoplasms
  • Risk
  • Whites

Digital Object Identifier (DOI)

Medium

  • Print

start page

  • 310

end page

  • 315

volume

  • 31

issue

  • 4