Table C-7Summary of results from combination study (animal, cell line) on colorectal cancer

StudyMechanism ExaminedExperimental ModelAmount and Duration of Ethanol and/or Acetaldehyde ExposureUse of CarcinogenResultsConclusions as Reported by Study Authors
Pannequin et al. 2007141Accumulation of phosphatidylethanol resulting in a signal change in intestinal cell proliferationMice, Caco-2Animal study:
2 mol/L (10%) ethanol for 4 months.

Cell line study:
10 mmol/L of ethanol or 0.5 mmol/L of acetaldehyde once daily for 48 hours.
NoneChronic exposure to low doses of ethanol (10 mmol/L) induces an increase of maximal intestinal cell density.The disruption of cellular signals might facilitate the stimulatory role of ethanol metabolites such as acetaldehyde on the proliferation of cells within intestinal crypts, thereby participating in the well-established cocarcinogenic role of alcohol consumption in the colon.

From: Appendix C, Evidence Tables

Cover of Alcohol Consumption and Cancer Risk
Alcohol Consumption and Cancer Risk: Understanding Possible Causal Mechanisms for Breast and Colorectal Cancers.
Evidence Reports/Technology Assessments, No. 197.
Oyesanmi O, Snyder D, Sullivan N, et al.

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