Cancer Causes & Control

, Volume 10, Issue 5, pp 369–377

Alcohol dehydrogenase 3 genotype modification of the associationof alcohol consumption with breast cancer risk

Authors

  • Jo L. Freudenheim
    • Department of Social and Preventive Medicine
  • Christine B. Ambrosone
    • Division of Molecular EpidemiologyNational Center for Toxicological Research
  • Kirsten B. Moysich
    • Roswell Park Cancer Institute, Cancer Epidemiology and Prevention
  • John E. Vena
    • Department of Social and Preventive Medicine
  • Saxon Graham
    • Department of Social and Preventive Medicine
  • James R. Marshall
    • Arizona Cancer Center
  • Paola Muti
    • Department of Social and Preventive Medicine
  • Rosemary Laughlin
    • Department of Social and Preventive Medicine
  • Takuma Nemoto
    • Department of SurgeryState University of New York
  • Lea C. Harty
    • Division of Cancer Epidemiology and Genetics
  • G. Adam Crits
    • Laboratory of Human CarcinogenesisNational Cancer Institute
  • Arthur W.K. Chan
    • Research Institute on Addictions
  • Peter G. Shields
    • Laboratory of Human CarcinogenesisNational Cancer Institute
Article

DOI: 10.1023/A:1008950717205

Cite this article as:
Freudenheim, J.L., Ambrosone, C.B., Moysich, K.B. et al. Cancer Causes Control (1999) 10: 369. doi:10.1023/A:1008950717205

Abstract

Objectives: Because alcohol dehydrogenase 3 (ADH3) is rate-limiting in alcohol oxidation and is polymorphic, we examined ADH3 genotype in relation to alcohol intake and breast cancer risk.

Methods: We conducted a case–control study among Caucasian women aged 40–85 with incident, pathologically confirmed breast cancer and controls, frequency-matched on age and county. Queries included alcohol intake in the past 20 years. Genomic DNA was genotyped for the exon VIII ADH polymorphism by PCR followed by restriction enzyme digestion. Computation of odds ratios (OR) and 95% confidence intervals (CI) was by unconditional logistic regression.

Results: We found increased risk among pre- (OR 2.3, 95%, CI 1.2–4.3) but not postmenopausal women (OR 1.1, 95% CI 0.7–1.7) associated with ADH31-1 compared to ADH31-2 and ADH32-2 genotypes. Risk was increased for premenopausal women with the ADH31-1 genotype and alcohol intake above the median (OR 3.6, 95% CI 1.5–8.8) compared to lighter drinkers with the ADH32-2 or ADH31-2 genotypes. ORs were close to null for premenopausal women in other drinking and genotype groups and for postmenopausal women categorized by genotype and alcohol consumption.

Conclusion: Among premenopausal women there may be a group more genetically susceptible to an alcohol consumption effect on breast cancer risk.

alcoholalcohol dehydrogenasebreast neoplasmsepidemiologygenetic polymorphisms
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Copyright information

© Kluwer Academic Publishers 1999