CEBP  Translational Cancer Medicine 2008: Cancer Clinical Trials and Personalized Medicine
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Cancer Epidemiology Biomarkers & Prevention Vol. 15, 2056-2062, November 2006
© 2006 American Association for Cancer Research


Review

A Meta-analysis of Diabetes Mellitus and the Risk of Prostate Cancer

Jocelyn S. Kasper1,2 and Edward Giovannucci1,2,3

Departments of 1 Nutrition and 2 Epidemiology, Harvard School of Public Health; and 3 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts

Requests for reprints: Edward Giovannucci, Department of Nutrition, Harvard School of Public Health, Boston, MA 02115. Phone: 617-432-4648; Fax: 617-432-2345. E-mail: egiovann{at}hsph.harvard.edu

Background: Studies investigating the association between diabetes mellitus and prostate cancer have reported inconsistent findings. We examined this association by conducting a detailed meta-analysis of the studies published on the subject.

Methods: MEDLINE and EMBASE databases and bibliographies of retrieved articles were searched. Studies investigating the relationship between diabetes mellitus and prostate cancer were included in the meta-analysis. Potential sources of heterogeneity between studies were explored and publication bias was evaluated. Pooled relative risk (RR) was calculated using the random-effects model. Numerous relevant subgroup analyses were also done.

Results: We included 19 studies, published between 1971 and 2005, in the meta-analysis and found an inverse association between diabetes mellitus and prostate cancer [RR, 0.84, 95% confidence interval (CI), 0.76-0.93, P for heterogeneity ≤ 0.01]. For cohort studies alone, the RR was 0.81 (95% CI, 0.71-0.92, P for heterogeneity ≤ 0.01) and for case-control studies alone, the RR was 0.89 (95% CI, 0.72-1.11, P for heterogeneity = 0.02). The significant heterogeneity was mitigated in some of the subgroup analyses. For studies conducted before prostate-specific antigen screening was introduced as a common procedure, the RR was 0.94 (95% CI, 0.85-1.03, P for heterogeneity = 0.15), and for studies conducted after this time, the RR was 0.73 (95% CI, 0.64-0.83, P for heterogeneity = 0.10). For studies that adjusted for three or more potential confounders, the RR was 0.74 (95% CI, 0.65-0.85, P for heterogeneity = 0.06) and for studies that adjusted for less than three potential confounders, the RR was 0.93 (95% CI, 0.86-1.02, P for heterogeneity = 0.18).

Conclusion: This study suggests an inverse relationship between diabetes and prostate cancer. Potential biological mechanisms underlying this association, as well as possible biases, are discussed. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2056–62)




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Cell Growth & Differentiation
Copyright © 2006 by the American Association for Cancer Research.