Molecular Mechanisms of Alcohol-Induced Colorectal Carcinogenesis
Department of Environmental Health Sciences, Yale School of Public Health, Yale University, New Haven, CT 06520, USA
Department of Clinical Pharmacy, School of Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA
Author to whom correspondence should be addressed.
These authors contributed equally to this work and therefore should be considered as first authors.
Academic Editor: Axel H. Schönthal
Received: 19 July 2021
Revised: 25 August 2021
Accepted: 26 August 2021
Published: 31 August 2021
Alcohol consumption is a leading cause of lifestyle-induced morbidity and mortality worldwide. It is well-established that there is an association between alcohol consumption and an increased risk of colorectal cancer. Long-term alcohol consumption causes a spectrum of liver diseases, including steatosis, hepatitis, and liver cancer, and is detrimental to many other organs. In the body, alcohol can be metabolized to chemicals that exhibit biological activity, such as acetaldehyde. The intracellular accumulation of these compounds can result in suppression of antioxidant defense systems, and alterations in DNA. In addition, they can elicit changes at the tissue level, leading to reductions in nutrient absorption, inflammation, and impairment of the immune system. Together, these effects may increase the risk of cancer in a variety of organs. This review discusses the mechanisms by which alcohol may promote colorectal cancer. It is anticipated that a clearer understanding of the mechanisms by which alcohol induces cancer will facilitate the development of more effective therapeutic interventions.