Abstract

Approximately 3.6% of cancers worldwide derive from chronic alcohol drinking, including those of the upper aerodigestive tract, the liver, the colorectum and the breast. Although the mechanisms for alcohol-associated carcinogenesis are not completely understood, most recent research has focused on acetaldehyde, the first and most toxic ethanol metabolite, as a cancer-causing agent. Ethanol may also stimulate carcinogenesis by inhibiting DNA methylation and by interacting with retinoid metabolism. Alcohol-related carcinogenesis may interact with other factors such as smoking, diet and comorbidities, and depends on genetic susceptibility.

Author affiliations

1. Department of Medicine and Laboratory of Alcohol Research, Liver Disease and Nutrition, Salem Medical Centre, University of Heidelberg, Heidelberg, Germany.
2. Department of Clinical Pharmacology, University of Berne, Berne, Switzerland.

Correspondence to: Helmut K. Seitz¹ Email: helmut_karl.seitz@urz.uni-heidelberg.de