Print Email Facebook Twitter Alcohol consumption and mutations or promoter hypermethylation of the von Hippel-Lindau gene in renal cell carcinoma Title Alcohol consumption and mutations or promoter hypermethylation of the von Hippel-Lindau gene in renal cell carcinoma Author Schouten, L.J. van Dijk, B.A.C. Oosterwijk, E. van Engeland, M. van de Hulsbergen-Kaa, C.A. Kiemeney, L.A.L.M. Goldbohm, R.A. Kester, A. de Vogel, S. Schalken, J.A. van den Brandt, P.A. TNO Kwaliteit van Leven Publication year 2008 Abstract Alcohol consumption has been associated with a decreased risk for renal cell cancer in several studies. We investigated whether alcohol is associated with (epi)genetic changes of the von Hippel-Lindau (VHL) gene in renal cell cancer. The Netherlands Cohort Study (NLCS) on Diet and Cancer started in 1986 (n = 120,852) and uses the case-cohort method. After 11.3 years of follow-up, 314 renal cell cancer cases and 4,511 subcohort members were available for analysis. DNA was isolated from paraffin-embedded tumor tissue from 235 cases. VHL mutations were analyzed by sequencing, whereas VHL promoter methylation was analyzed using methylation-specific PCR. In multivariate analysis, hazard ratios of renal cell cancer for cohort members who consumed up to 5, 15, 30, and ≥30 g of alcohol per day were 0.72, 0.64, 0.81, and 0.69, respectively, compared with nondrinkers [95% confidence interval(95% CI) for the ≥30 category, 0.44-1.07; P for trend, 0.17]. Alcohol intake from beer, wine, and liquor was associated with decreased risks for renal cell cancer, although not statistically significant. Hazard ratios were not different for clear-cell renal cell cancer with and without VHL mutations, except for alcohol from beer, which was associated with an increased risk for clear-cell renal cell cancer without VHL mutations (hazard ratio for ≥5 g of alcohol from beer compared with nondrinkers, 2.74; 95% CI, 1.35-5.57). Alcohol was associated with a decreased risk for clear-cell renal cell cancer without VHL gene promoter methylation (hazard ratio for >15 g compared with nondrinkers, 0.58; 95% CI, 0.34-0.99). In this study, a not statistically significant inverse association was observed between alcohol and renal cell cancer. There was no statistical significant heterogeneity by VHL mutation or methylation status. Copyright © 2008 American Association for Cancer Research. Subject HealthAdultAlcohol consumptionCancer riskClear cell carcinomaControlled studyDisease associationDNA determinationEpigeneticsGene mutationKidney carcinomaMajor clinical studyRisk assessmentTumor geneVon Hippel Lindau geneAgedAlcohol DrinkingCarcinoma, Renal CellCase-Control StudiesCpG IslandsDNA MethylationFemaleHumansKidney NeoplasmsMaleMiddle AgedMutationProportional Hazards ModelsProspective StudiesQuestionnairesRisk FactorsVon Hippel-Lindau Tumor Suppressor Protein To reference this document use: http://resolver.tudelft.nl/uuid:0446fd0e-c17c-472a-b8bb-0486a6167c26 DOI https://doi.org/10.1158/1055-9965.epi-08-0321 TNO identifier 241157 ISSN 1055-9965 Source Cancer Epidemiology Biomarkers and Prevention, 17 (12), 3543-3550 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.