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Alcohol consumption and distinct molecular pathways to colorectal cancer

Author: Bongaerts, B.W.C. · Goeij, A.F.P.M. de · Vogel, S. de · Brandt, P.A. van den · Goldbohm, R.A. · Weijenberg, M.P.
Type:article
Date:2007
Institution: TNO Kwaliteit van Leven
Source:British Journal of Nutrition, 3, 97, 430-434
Identifier: 239854
doi: doi:10.1017/S0007114507381336
Keywords: Health · Food and Chemical Risk Analysis · Alcohol · Cohort study · Colorectal cancer · Genetics · The Netherlands · APC protein · K ras protein · protein MLH1 · protein p53 · adult · aged · alcohol consumption · article · cancer risk · chromosomal instability · cohort analysis · colorectal cancer · confidence interval · controlled study · female · gene mutation · gene overexpression · human · human experiment · human tissue · incidence · male · microsatellite instability · Netherlands · normal human · nutritional assessment · protein expression · questionnaire · risk assessment · risk factor · statistical significance · tumor classification · clinical trial · colorectal tumor · drinking behavior · epidemiology · genetic predisposition · genetics · middle aged · multicenter study · mutation · tumor suppressor gene · Aged · Alcohol Drinking · Chromosomal Instability · Colorectal Neoplasms · Epidemiologic Methods · Female · Genes, APC · Genetic Predisposition to Disease · Humans · Male · Microsatellite Instability · Middle Aged · Mutation · Netherlands

Abstract

High alcohol consumption is related to colorectal cancer (CRC). Our objective was to study associations between alcohol consumption and risk of CRC according to characteristics of aetiological pathways: the chromosomal instability (CIN) and the microsatellite instability (MIN) pathway. We classified CIN+ tumours (tumours with either a truncating APC mutation, an activating K-ras mutation or overexpression of p53), MIN+ tumours (tumours lacking hMLH1 expression) and CIN-/MIN- tumours (tumours without these defects). In the Netherlands Cohort Study on diet and cancer, 120 852 men and women, aged 55-69 years, completed a questionnaire on risk factors for cancer at baseline (1986). Case-cohort analyses were conducted using 573 CRC cases with complete data after 7.3 years of follow-up, excluding the first 2.3 years. Adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) were estimated. Compared with abstaining, alcohol consumption of ≥30 g/d was positively associated with the risk of CRC irrespective of genetic or molecular aberrations present, although statistical significance was not reached (RR 1.35 (95% CI 0.9-2.0) for the CIN+ tumours, RR 1.59 (95% CI 0.4-5.8) for the MIN+ tumours and RR 1.15 (95% CI 0.5-2.7) for the CIN-/MIN- tumours). Beer, wine and liquor consumption were, independent of their alcoholic content, not consistently associated with the risk of CRC within the defined subgroups. In conclusion, our results indicate that a daily alcohol consumption of ≥ 30 g is associated with an increase in risk of CRC, independent of the presence or absence of the studied characteristics of different aetiological pathways.