Next Article in Journal
Precision Immuno-Oncology: Prospects of Individualized Immunotherapy for Pancreatic Cancer
Next Article in Special Issue
Liver Transplantation for Alcoholic Liver Disease and Hepatocellular Carcinoma
Previous Article in Journal
Electrotransfer of Different Control Plasmids Elicits Different Antitumor Effectiveness in B16.F10 Melanoma
Previous Article in Special Issue
Alcohol-Derived Acetaldehyde Exposure in the Oral Cavity
Article Menu
Issue 2 (February) cover image

Export Article

Open AccessFeature PaperReview

Colorectal Cancer and Alcohol Consumption—Populations to Molecules

Division of Digestive Diseases, Hepatology, and Nutrition, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612, USA
Author to whom correspondence should be addressed.
Cancers 2018, 10(2), 38;
Received: 19 December 2017 / Revised: 22 January 2018 / Accepted: 24 January 2018 / Published: 30 January 2018
(This article belongs to the Special Issue Alcohol and Cancer)
PDF [1425 KB, uploaded 30 January 2018]


Colorectal cancer (CRC) is a major cause of morbidity and mortality, being the third most common cancer diagnosed in both men and women in the world. Several environmental and habitual factors have been associated with the CRC risk. Alcohol intake, a common and rising habit of modern society, is one of the major risk factors for development of CRC. Here, we will summarize the evidence linking alcohol with colon carcinogenesis and possible underlying mechanisms. Some epidemiologic studies suggest that even moderate drinking increases the CRC risk. Metabolism of alcohol involves ethanol conversion to its metabolites that could exert carcinogenic effects in the colon. Production of ethanol metabolites can be affected by the colon microbiota, another recently recognized mediating factor to colon carcinogenesis. The generation of acetaldehyde and alcohol’s other metabolites leads to activation of cancer promoting cascades, such as DNA-adduct formation, oxidative stress and lipid peroxidation, epigenetic alterations, epithelial barrier dysfunction, and immune modulatory effects. Not only does alcohol induce its toxic effect through carcinogenic metabolites, but alcoholics themselves are predisposed to a poor diet, low in folate and fiber, and circadian disruption, which could further augment alcohol-induced colon carcinogenesis. View Full-Text
Keywords: alcohol; CRC; polyposis; metabolism; epigenetics; immunity alcohol; CRC; polyposis; metabolism; epigenetics; immunity

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Rossi, M.; Jahanzaib Anwar, M.; Usman, A.; Keshavarzian, A.; Bishehsari, F. Colorectal Cancer and Alcohol Consumption—Populations to Molecules. Cancers 2018, 10, 38.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cancers EISSN 2072-6694 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top