INTRODUCTION: To provide further insight into the association between type 2 diabetes mellitus (T2DM) and the pathophysiology of prostate cancer, we conducted an updated, detailed meta-analysis of 56 published case-control and cohort studies. METHODS: MEDLINE and EMBASE were used to identify the literature published in April 2012 related to both diabetes mellitus and prostate cancer. A sensitivity analysis was performed, and potential confounding effects were investigated using a stratified meta-analysis. A cumulative meta-analysis was also carried out to evaluate the cumulative effect estimate over time. RESULTS: A total of 24 case-control and 32 cohort studies with information on a total of ~8,000,000 subjects and ~140,000 individuals with prostatic cancer showed published estimates of the association between diabetes and prostate cancer malignancy. The pooled effect estimate revealed a relative risk (RR) of 0.88 (95% CI, 0.82-0.93). Interestingly, there was an increased trend for Asians (RR = 1.72, n = 7) but not Americans (RR = 0.82, n = 28) and Europeans (RR = 0.86, n = 21) regarding the association between diabetes mellitus and prostate cancer. The sensitivity analysis, excluding any one study, did not significantly change the pooled RR. The range for the pooled RR when one study was omitted was 0.84-0.89. DISCUSSION: The findings of our meta-analysis provide strong evidence of an inverse association between diabetes and prostate cancer. CONCLUSIONS: Further research should focus on limitations in the current literature and re-assess the relationship between diabetes and prostate cancer by analyzing the two different diabetes mellitus types separately.
INTRODUCTION: To provide further insight into the association between type 2 diabetes mellitus (T2DM) and the pathophysiology of prostate cancer, we conducted an updated, detailed meta-analysis of 56 published case-control and cohort studies. METHODS: MEDLINE and EMBASE were used to identify the literature published in April 2012 related to both diabetes mellitus and prostate cancer. A sensitivity analysis was performed, and potential confounding effects were investigated using a stratified meta-analysis. A cumulative meta-analysis was also carried out to evaluate the cumulative effect estimate over time. RESULTS: A total of 24 case-control and 32 cohort studies with information on a total of ~8,000,000 subjects and ~140,000 individuals with prostatic cancer showed published estimates of the association between diabetes and prostate cancer malignancy. The pooled effect estimate revealed a relative risk (RR) of 0.88 (95% CI, 0.82-0.93). Interestingly, there was an increased trend for Asians (RR = 1.72, n = 7) but not Americans (RR = 0.82, n = 28) and Europeans (RR = 0.86, n = 21) regarding the association between diabetes mellitus and prostate cancer. The sensitivity analysis, excluding any one study, did not significantly change the pooled RR. The range for the pooled RR when one study was omitted was 0.84-0.89. DISCUSSION: The findings of our meta-analysis provide strong evidence of an inverse association between diabetes and prostate cancer. CONCLUSIONS: Further research should focus on limitations in the current literature and re-assess the relationship between diabetes and prostate cancer by analyzing the two different diabetes mellitus types separately.
Entities:
Keywords:
Age decade; annual growth rate; diabetes mellitus; evidence-based medicine; meta-analysis; prostate cancer
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