Dataset Information

Coffee consumption, genetic susceptibility and bladder cancer risk.

ABSTRACT: OBJECTIVE:We evaluated the bladder cancer risk associated with coffee consumption in a case-control study in Spain and examined the gene-environment interactions for genetic variants of caffeine-metabolizing enzymes. METHODS:The analyses included 1,136 incident cases with urothelial carcinoma of the urinary bladder and 1,138 controls. Odds ratios (OR) and 95% confidence intervals (CI) were adjusted for area, age, gender, amount of cigarette smoking, and years since quitting among former smokers. RESULTS:The OR (95% CI) for ever consumed coffee was 1.25 (0.95-1.64). For consumers of 1, 2, 3, and 4 or more cups/day relative to never drinkers, OR were, respectively, 1.24 (0.92-1.66), 1.11 (95% CI 0.82-1.51), 1.57 (1.13-2.19), and 1.27 (0.88-1.81). Coffee consumption was higher in smokers compared to never smokers. The OR for drinking at least 4 cups/day was 1.13 (0.61-2.09) in current smokers, 1.57 (0.86-2.90) in former smokers, and 1.23 (0.55-2.76) in never smokers. Gene-coffee interactions evaluated in NAT2, CYP1A2, and CYP2E1-02 and CYP1A1 were not identified after adjusting for multiple testing. CONCLUSION:We observed a modest increased bladder cancer risk among coffee drinkers that may, in part, be explained by residual confounding by smoking. The findings from the gene-coffee interactions need replication in further studies.

SUBMITTER: Villanueva CM

PROVIDER: S-EPMC2912840 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature

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Coffee consumption, genetic susceptibility and bladder cancer risk.

Villanueva Cristina M CM Silverman Debra T DT Murta-Nascimento Cristiane C Malats Núria N Garcia-Closas Montserrat M Castro Francesc F Tardon Adonina A Garcia-Closas Reina R Serra Consol C Carrato Alfredo A Rothman Nathaniel N Real Francisco X FX Dosemeci Mustafa M Kogevinas Manolis M

Cancer causes & control : CCC 20080917 1

<h4>Objective</h4>We evaluated the bladder cancer risk associated with coffee consumption in a case-control study in Spain and examined the gene-environment interactions for genetic variants of caffeine-metabolizing enzymes.<h4>Methods</h4>The analyses included 1,136 incident cases with urothelial carcinoma of the urinary bladder and 1,138 controls. Odds ratios (OR) and 95% confidence intervals (CI) were adjusted for area, age, gender, amount of cigarette smoking, and years since quitting among ...[more]

PMID: 18798002

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Project description:BACKGROUND:Clinical, pathologic, and molecular evidence indicate that bladder cancer is heterogeneous with pathologic/molecular features that define distinct subphenotypes with different prognoses. It is conceivable that specific patterns of genetic susceptibility are associated with particular subphenotypes. OBJECTIVE:To examine evidence for the contribution of germline genetic variation to bladder cancer heterogeneity. DESIGN, SETTING, AND PARTICIPANTS:The Spanish Bladder Cancer/EPICURO Study is a case-control study based in 18 hospitals located in five areas in Spain. Cases were patients with a newly diagnosed, histologically confirmed, urothelial cell carcinoma of the bladder from 1998 to 2001. Case diagnoses were reviewed and uniformly classified by pathologists following the World Health Organisation/International Society of Urological Pathology 1999 criteria. Controls were hospital-matched patients (n=1149). MEASUREMENTS:A total of 1526 candidate variants in 423 candidate genes were analysed. Three distinct subphenotypes were defined according to stage and grade: low-grade nonmuscle invasive (n=586), high-grade nonmuscle invasive (n=219), and muscle invasive (n=246). The association between each variant and subphenotype was assessed by polytomous risk models adjusting for potential confounders. Heterogeneity in genetic susceptibility among subphenotypes was also tested. RESULTS AND LIMITATIONS:Two established bladder cancer susceptibility genotypes, NAT2 slow-acetylation and GSTM1-null, exhibited similar associations among the subphenotypes, as did VEGF-rs25648, which was previously identified in our study. Other variants conferred risks for specific tumour subphenotypes such as PMS2-rs6463524 and CD4-rs3213427 (respective heterogeneity p values of 0.006 and 0.004), which were associated with muscle-invasive tumours (per-allele odds ratios [95% confidence interval] of 0.56 [0.41-0.77] and 0.71 [0.57-0.88], respectively) but not with non-muscle-invasive tumours. Heterogeneity p values were not robust in multiple testing according to their false-discovery rate. CONCLUSIONS:These exploratory analyses suggest that genetic susceptibility loci might be related to the molecular/pathologic diversity of bladder cancer. Validation through large-scale replication studies and the study of additional genes and single nucleotide polymorphisms are required.

Project description:AimsTo evaluate the utility of coffee-related genetic variants as proxies for coffee consumption in Mendelian randomization studies, by examining their association with non-alcoholic beverage consumption (including subtypes of coffee and tea) and a range of socio-demographic and life-style factors.DesignObservational study of the association of genetic risk scores for coffee consumption with different types of non-alcoholic beverage consumption.SettingUK general population.ParticipantsIndividuals of European ancestry aged 40-73 years from the UK Biobank between 2006 and 2010 (n = 114 316).MeasurementsGenetic risk scores were constructed using two, four and eight independent single nucleotide polymorphisms (SNPs) identified in genome-wide association studies (GWAS) of coffee consumption. Drinks were self-reported in a baseline questionnaire (all participants) and in detailed 24 dietary recall questionnaires in a subset (n = 48 692).FindingsGenetic risk scores explained up to 0.38, 0.19 and 0.76% of the variance in coffee, tea and combined coffee and tea consumption, respectively. Genetic risk scores demonstrated positive associations with both caffeinated and decaffeinated coffee and tea consumption, and with most subtypes of coffee consumption, but only with standard tea consumption. There was no clear evidence for positive associations with most other non-alcoholic beverages, but higher genetic risk for coffee consumption was associated with lower daily water consumption. The genetic risk scores were associated with increased alcohol consumption, but not consistently with other socio-demographic and life-style factors.ConclusionsCoffee-related genetic risk scores could be used as instruments for combined coffee and tea consumption in Mendelian randomization studies. However, associations observed with alcohol consumption require further investigation to determine whether these are due to causal effects of coffee and tea consumption or biological pleiotropy.

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Coffee consumption, genetic susceptibility and bladder cancer risk.

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Coffee consumption, genetic susceptibility and bladder cancer risk.

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