Article

Body mass index and incidence of localized and advanced prostate cancer—A dose-response meta-analysis of prospective studies

Nutritional Epidemiology Unit, Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Annals of Oncology (Impact Factor: 7.04). 01/2012; 23(7):1665-71. DOI: 10.1093/annonc/mdr603
Source: PubMed

ABSTRACT

The relationship between obesity and risk of prostate cancer (PCa) is unclear; however, etiologic heterogeneity by subtype of PCa (localized, advanced) related to obesity was suggested. Therefore, we conducted a dose-response meta-analysis of prospective studies to assess the association between body mass index (BMI) and risk of localized and advanced PCa.
Relevant prospective studies were identified by a search of Medline and Embase databases to 03 October 2011. Twelve studies on localized PCa (1,033,009 men, 19,130 cases) and 13 on advanced PCa (1,080,790 men, 7067 cases) were identified. We carried out a dose-response meta-analysis using random-effects model.
For localized PCa, we observed an inverse linear relationship with BMI [Ptrend<0.001, relative risk (RR): 0.94 (95% confidence interval, 95% CI, 0.91-0.97) for every 5 kg/m2 increase]; there was no evidence of heterogeneity (Pheterogeneity=0.27). For advanced PCa, we observed a linear direct relationship with BMI (Ptrend=0.001, RR: 1.09 (95% CI 1.02-1.16) for every 5 kg/m2 increase); there was weak evidence of heterogeneity (Pheterogeneity=0.08). Omitting one study that contributed substantially to the heterogeneity yielded a pooled RR of 1.07 (95% CI 1.01-1.13) for every 5 kg/m2 increase (Pheterogeneity=0.26).
The quantitative summary of the accumulated evidence indicates that obesity may have a dual effect on PCa-a decreased risk for localized PCa and an increased risk for advanced PCa.

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Available from: Andrea Discacciati, Jun 30, 2015
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    • "Body mass index (BMI), smoking, and alcohol consumption are PCa-related environmental factors that affect the risk of this disease. A meta-analysis of prospective studies indicated that obesity may have a dual effect on the risk of PCa: a decreased risk for localized PCa and an increased risk for advanced PCa[10]. Smoking cessation can reduce the risk of developing PCa[11]. "
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    ABSTRACT: Prostate cancer (PCa) is a multifactorial disease involving complex genetic and environmental factors interactions. Gene-gene and gene-environment interactions associated with PCa in Chinese men are less studied. We explored the association between 36 SNPs and PCa in 574 subjects from northern China. Body mass index (BMI), smoking, and alcohol consumption were determined through self-administered questionnaires in 134 PCa patients. Then gene-gene and gene-environment interactions among the PCa-associated SNPs were analyzed using the generalized multifactor dimensionality reduction (GMDR) and logistic regression methods. Allelic and genotypic association analyses showed that six variants were associated with PCa and the cumulative effect suggested men who carried any combination of 1, 2, or ≥3 risk genotypes had a gradually increased PCa risk (odds ratios (ORs) = 1.79-4.41). GMDR analysis identified the best gene-gene interaction model with scores of 10 for both the cross-validation consistency and sign tests. For gene-environment interactions, rs6983561 CC and rs16901966 GG in individuals with a BMI ≥ 28 had ORs of 7.66 (p = 0.032) and 5.33 (p = 0.046), respectively. rs7679673 CC + CA and rs12653946 TT in individuals that smoked had ORs of 2.77 (p = 0.007) and 3.11 (p = 0.024), respectively. rs7679673 CC in individuals that consumed alcohol had an OR of 4.37 (p = 0.041). These results suggest that polymorphisms, either individually or by interacting with other genes or environmental factors, contribute to an increased risk of PCa.
    Preview · Article · Jan 2016 · International Journal of Environmental Research and Public Health
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    • "In 2008 there were 903,500 estimated new cases and 258,400 estimated deaths worldwide, resulting as the sixth cause of death by cancer in men [1]. Despite extensive research effort, no modifiable risk factors have been consistently identified for PC, except perhaps smoking [2], obesity [3] and a sedentary lifestyle [4]. "
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    ABSTRACT: Prostate cancer (PC) is the second most incident cancer and the sixth cause of death by cancer in men worldwide. Despite extensive research efforts, no modifiable risk factors have been consistently identified for PC risk. A number of studies have focused on possible relationships between sexually transmitted infections (STIs) and PC. We performed a meta-analysis to explore the association between infection caused by Neisseria gonorrheae, Treponema pallidum, Chlamydia trachomatis, Trichomonas vaginalis, Ureaplasma urealyticum, Mycoplasma hominis, Herpes Simplex Virus types 1 and 2, Human Herpes Virus 8 and Cytomegalovirus, and PC. We conducted a comprehensive, systematic bibliographic search of medical literature to identify relevant studies. We calculated summary relative risk (SRR) and 95% confidence intervals (CI) for the association between each STI and PC through random effect models. Subgroup, meta-regression and sensitivity analyses were carried out to detect between-study heterogeneity and bias. We included 47 studies published between 1971 and 2011. Men who reported having ever had any STI in lifetime had an increased PC (SRR 1.49, 95% CI 1.19-1.92). We found a significantly increased PC risk in men having had gonorrhoea (SRR 1.20, 95% CI 1.05-1.37). No other single STI was significantly associated with PC. Due to high incidence of both STIs and PC worldwide, prevention of STIs may help preventing a considerable number of PC cases.
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    • "and positively associated with advanced prostate cancer risk (1.07, 95% CI 1.01-1.13) [43]. "
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    ABSTRACT: Background Although a previous meta-analysis reported no association between metabolic syndrome (MetS) and prostate cancer risk, a number of studies suggest that MetS may be associated with the aggressiveness and progression of prostate cancer. However, these results have been inconsistent. This systematic review and meta-analysis investigated the nature of this association. Methods We systematically searched MEDLINE, EMBASE and bibliographies of retrieved studies up to January 2013 using the keywords “metabolic syndrome” and “prostate cancer”. We assessed relative risks (RRs) of the prostate cancer, several parameters of prostate cancer aggressiveness and progression associated with MetS using 95% confidence intervals (95% CIs). Results The literature search produced 547 hits from which 19 papers were extracted for the meta-analysis. In cancer-free population with and without MetS, the combined adjusted RR (95% CI) of prostate cancer risk and prostate cancer-specific mortality in longitudinal cohort studies is 0.96 (0.85 ~ 1.09) and 1.12 (1.02 ~ 1.23) respectively. In the prostate cancer patients with and without MetS, the combined unadjusted OR (95% CI) of high grade Gleason prostate cancer is 1.44 (1.20 ~ 1.72), the OR of advanced prostate cancer is 1.37 (1.12 ~ 1.68) and the OR of biochemical recurrence is 2.06 (1.43 ~ 2.96). Conclusions The overall analyses revealed no association between MetS and prostate cancer risk, although men with MetS appear more likely to have high-grade prostate cancer and more advanced disease, were at greater risk of progression after radical prostatectomy and were more likely to suffer prostate cancer-specific death. Further primary studies with adjustment for appropriate confounders and larger, prospective, multicenter investigations are required.
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