ArticleDisease models & mechanisms2023
Acetaldehyde and defective mismatch repair increase colonic tumours in a Lynch syndrome model with Aldh1b1 inactivation.
Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Mitochondrial vulnerability to aldehydic load and the role mitochondrial aldehyde dehydrogenases.Pharmacological research · 2026Review
- Aldehyde Detoxification in Cancer: Metabolic Guardians of the Genome.Biomolecules · 2026Review
- Common human ALDH1B1 and ALDH2 variants increase neuroinflammatory response to a single ethanol dose in mice.Science advances · 2026Article
- Reactive carbonyl species in health and chronic disease: from methylglyoxal to an integrative network of metabolic regulation.Cardiovascular diabetology · 2026Review
- Recent updates and future perspectives about ALDH1B1 as a potential anticancer target: a review.Journal of cancer research and clinical oncology · 2025Review
- Article
- Multiple DNA repair pathways prevent acetaldehyde-induced mutagenesis in yeast.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
ALDH1B1 expressed in the intestinal epithelium metabolises acetaldehyde to acetate, protecting against acetaldehyde-induced DNA damage. MSH2 is a key component of the DNA mismatch repair (MMR) pathway involved in Lynch syndrome (LS)-associated colorectal cancers. Here, we show that defective MMR (dMMR) interacts with acetaldehyde, in a gene/environment interaction, enhancing dMMR-driven colonic tumour formation in a LS murine model of Msh2 conditional inactivation (Lgr5-CreER; Msh2flox/-, or Msh2-LS) combined with Aldh1b1 inactivation. Conditional (Aldh1b1flox/flox) or constitutive (Aldh1b1-/-) Aldh1b1 knockout alleles combined with the conditional Msh2flox/- intestinal knockout mouse model of LS (Msh2-LS) received either ethanol, which is metabolised to acetaldehyde, or water. We demonstrated that 41.7% of ethanol-treated Aldh1b1flox/flox Msh2-LS mice and 66.7% of Aldh1b1-/- Msh2-LS mice developed colonic epithelial hyperproliferation and adenoma formation, in 4.5 and 6 months, respectively, significantly greater than 0% in water-treated control mice. Significantly higher numbers of dMMR colonic crypt foci precursors and increased plasma acetaldehyde levels were observed in ethanol-treated Aldh1b1flox/flox Msh2-LS and Aldh1b1-/- Msh2-LS mice compared with those in water-treated controls. Hence, ALDH1B1 loss increases acetaldehyde levels and DNA damage that interacts with dMMR to accelerate colonic, but not small intestinal, tumour formation.
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