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Urinary estrogen metabolites and prostate cancer : a case-control study and meta-analysis

By Maddalena Barba, Ph.D. Li Yang, Holger J. Schünemann, Francesca Sperati, Sara Grioni, Saverio Stranges, Kim C. Westerlind, Giovanni Blandino, M. (Michele) Gallucci, Rossella Lauria, Luca Malorni and Paola Muti

Abstract

Objective: To investigate prostate cancer (Pca) risk in relation to estrogen metabolism, expressed as urinary 2-hydroxyestrone (2-OHE1), 16α-hydroxyestrone (16α-OHE1) and 2-OHE1 to 16α-OHE1 ratio. \ud 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, 16αOHE1 and 2-OHE1 to 16α-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. \ud 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 16α-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 16α-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 16α-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 16α-OHE1 ratio (third vs. first tertile: OR 0.53, 95% CI 0.31-0.90). \ud 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

Topics: RC0254, QP
Publisher: BioMed Central Ltd.
Year: 2009
OAI identifier: oai:wrap.warwick.ac.uk:2653

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  1. (2000). Berrino F: Estrogen metabolism and risk of breast cancer: a prospective study of the 2:16alpha-hydroxyestrone ratio in premenopausal and postmenopausal women. Epidemiology doi
  2. (1992). Bradlow HL: Induction by estrogen metabolite 16α-OHE1 of genotoxic damage and aberrant proliferation in mouse mammary epithelial cells. doi
  3. (1997). Bradlow HL: Urinary estrogen metabolites and breast cancer: a case-control study. Cancer Epidemiol Biomarkers Prev
  4. (2002). Bradlow L: Urinary estrogen metabolites and prostate cancer: a case-control study in the United States. Cancer Causes Control doi
  5. (2006). Coltman CA: Assessing prostate cancer risk: results from the Prostate Cancer Prevention Trial. doi
  6. (1998). Coney A: Functional role of estrogen metabolism in target cells: reviews and perspectives. Carcinogenesis doi
  7. (2007). Delle Fave G: Meta-analysis: the use of non-steroidal anti-inflammatory drugs and pancreatic cancer risk for different exposure categories. Aliment Pharmaco Ther doi
  8. (1996). Does prostate cancer start at puberty? Clin Lab Anal doi
  9. (2009). EG: Novel Biomarker for Risk of Prostate Cancer: results from a case-control study. Prostate doi
  10. (1995). Epidemiologic characteristics of prostate cancer. doi
  11. (1998). Estrogenic and antiestrogenic activities of alpha- and 2-hydroxyestrone of 17beta-estradiol in MCF-7 and T47D human breast cancer cells. doi
  12. (2006). Estrogens and Mechanisms of Prostate Cancer Progression. doi
  13. Global Cancer Statistics, doi
  14. (2001). Hormones and prostate cancer: what's next? Epidemiol Rev doi
  15. (2004). Hovay K: Drinking pattern and risk of non-fatal myocardial infarction: a population-based casecontrol study. Addiction doi
  16. (1995). Induction at high incidence of ductal prostate adenocarcinomas in NBL/Cr and SpragueDawley Hsd:SD rats treated with a combination of testosterone and estradiol-17β or diethylbestrol. Carcinogenesis doi
  17. (2005). JR: Urinary estrogen metabolites, prostate specific antigen, and body mass index among African-American men in South Carolina. Cancer Detect Prev doi
  18. (1997). MC: A pilot study of urinary estrogen metabolites (16alpha-OHE1 and 2-OHE1) in postmenopausal women with and without breast cancer. Environ Health Perspect doi
  19. (1999). MP: Multifunctional aspects of the action of indol-3-carbinol as an antitumor agent. Ann NY Acad Sci doi
  20. (2008). 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 doi
  21. (2002). Quantifying heterogeneity in a meta-analysis. Stat Med doi
  22. (2001). Regulation of cell cycle and cyclins by16alpha-hydroxyestrone in MCF-7 breast cancer cells.
  23. (2007). Roj Y: Prostatic intraepithelial neoplasia: recent evidence. Arch Pathol Lab Med
  24. (2001). RT: Tissue-selective effects of continuous release of 2-hydrohyestrone and 16α-hydroxyestrone on bone, uterus and mammary gland in ovariectorized growing rats.
  25. (2008). Schünemann HJ: Anticoagulation for the initial treatment of venous thromboembolism in patients with cancer: a systematic review. Cancer doi
  26. (2008). Schünemann HJ: Low-molecular-weight heparin vs unfractionated heparin for perioperative thromboprophylaxis in patients with cancer: a systematic review and meta-analysis. Arch Intern Med doi
  27. (2008). Schünemann HJ: Low-molecular-weight heparins are superior to vitamin K antagonists for the long term treatment of venous thromboembolism in patients with cancer: a cochrane systematic review. doi
  28. (1998). Sepkovic DW, Kuller LH: Do urinary oestrogen metabolites predict breast cancer? Guernsey III cohort follow-up. doi
  29. (1993). Serum pituitary and sex steroid hormone levels in the etiology of prostatic cancer--a population-based case-control study. doi
  30. (1996). Sex hormone-induction and dietary modulation of prostatic adenocarcinoma (PA) in animal models. Urol Oncol doi
  31. (1996). Stampfer MJ: Prospective study of sex hormone levels and risk of prostate cancer. doi
  32. (1993). Telang NT: Experimental down-regulation of intermediate biomarkers of carcinogenesis in mouse mammary epithelial cells. Breast Cancer Res Treat doi
  33. (1993). Telang NT: Upregulation of estradiol C16α-hydroxylation in human breast tissue: a potential biomarker of breast caner risk. doi
  34. (2000). The role of steroid hormones in prostate cancerogenesis. doi
  35. (1997). Trichopoulos D: Serum steroids in relation to prostate cancer risk in a case-control study (Greece). Cancer Causes Control doi

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