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Meta-Analysis
. 2009 Oct 8;28(1):135.
doi: 10.1186/1756-9966-28-135.

Urinary Estrogen Metabolites and Prostate Cancer: A Case-Control Study and Meta-Analysis

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Free PMC article
Meta-Analysis

Urinary Estrogen Metabolites and Prostate Cancer: A Case-Control Study and Meta-Analysis

Maddalena Barba et al. J Exp Clin Cancer Res. .
Free PMC article

Abstract

Objective: To investigate prostate cancer (Pca) risk in relation to estrogen metabolism, expressed as urinary 2-hydroxyestrone (2-OHE1), 16alpha-hydroxyestrone (16alpha-OHE1) and 2-OHE1 to 16alpha-OHE1 ratio.

Methods: We conducted a case-control study within the Western New York Health Cohort Study (WNYHCS) from 1996 to 2001. From January 2003 through September 2004, we completed the re-call and follow-up of 1092 cohort participants. Cases (n = 26) and controls (n = 110) were matched on age, race and recruitment period according to a 1:4 ratio. We used the unconditional logistic regression to compute crude and adjusted odds ratios (OR) and 95% confident interval (CI) of Pca in relation to 2-OHE1, 16alphaOHE1 and 2-OHE1 to 16alpha-OHE1 by tertiles of urine concentrations (stored in a biorepository for an average of 4 years). We identified age, race, education and body mass index as covariates. We also conducted a systematic review of the literature which revealed no additional studies, but we pooled the results from this study with those from a previously conducted case-control study using the DerSimonian-Laird random effects method.

Results: We observed a non-significant risk reduction in the highest tertile of 2-OHE1 (OR 0.72, 95% CI 0.25-2.10). Conversely, the odds in the highest tertile of 16alpha-OHE1 showed a non-significant risk increase (OR 1.76 95% CI 0.62-4.98). There was a suggestion of reduced Pca risk for men in the highest tertile of 2-OHE1 to 16alpha-OHE1 ratio (OR 0.56, 95% CI 0.19-1.68). The pooled estimates confirmed the association between an increased Pca risk and higher urinary levels of 16alpha-OHE1 (third vs. first tertile: OR 1.82, 95% CI 1.09-3.05) and the protective effect of a higher 2-OHE 1 to 16alpha-OHE1 ratio (third vs. first tertile: OR 0.53, 95% CI 0.31-0.90).

Conclusion: Our study and the pooled results provide evidence for a differential role of the estrogen hydroxylation pathway in Pca development and encourage further study.

Figures

Figure 1
Figure 1
Pooled estimates of Prostate Cancer Risk in relation to Estrogen Metabolites.

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References

    1. Parkin DM, Bray F, Ferlay J, Pisani P. Global Cancer Statistics, 2002. CA Cancer J Clin. 2005;55:74–108. doi: 10.3322/canjclin.55.2.74. - DOI - PubMed
    1. Giovannucci E. Epidemiologic characteristics of prostate cancer. Cancer. 1995;(75):1766–77. doi: 10.1002/1097-0142(19950401)75:7+<1766::AID-CNCR2820751604>3.0.CO;2-T. - DOI
    1. Bosland MC. The role of steroid hormones in prostate cancerogenesis. J Natl Cancer Inst Momogr. 2000;27:39–66. - PubMed
    1. Diamandis EP, Yu H. Does prostate cancer start at puberty? Clin Lab Anal. 1996;10(6):468–9. doi: 10.1002/(SICI)1098-2825(1996)10:6<468::AID-JCLA27>3.0.CO;2-U. - DOI - PubMed
    1. Barba M, Terrenato I, Schünemann H, Fuhrman B, Sperati F, Teter B, Gallucci M, D'Amato A, Muti P. Indicators of Sexual and Somatic Development and Adolescent Body Size in Relation to Prostate Cancer Risk: Results from a Case-control Study. Urology. 2008;72(1):183–7. doi: 10.1016/j.urology.2007.09.065. - DOI - PubMed
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