ArticleCell cycle (Georgetown, Tex.)2023
The p53 DNA damage response and Fanconi anemia DNA repair pathway protect against acetaldehyde-induced replication stress in esophageal keratinocytes.
Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.PLoS computational biology · 2025Article
- Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.bioRxiv : the preprint server for biology · 2025Article
- Homologous recombination contributes to the repair of acetaldehyde-induced DNA damage.Cell cycle (Georgetown, Tex.) · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alcohol contributes to cellular accumulation of acetaldehyde, a primary metabolite of alcohol and a major human carcinogen. Acetaldehyde can form DNA adducts and induce interstrand crosslinks (ICLs) that are repaired by the Fanconi anemia DNA repair pathway (FA pathway). Individuals with deficiency in acetaldehyde detoxification or in the FA pathway have an increased risk of squamous-cell carcinomas (SCCs) including those of the esophagus. In a recent report, we described the molecular basis of acetaldehyde-induced DNA damage in esophageal keratinocytes [1]. We demonstrated that, at physiologically relevant concentrations, acetaldehyde induces DNA damage at the DNA replication fork. This resulted in replication stress, leading to activation of the ATR-Chk1-dependent cell cycle checkpoints. We also reported that the p53 DNA damage response is elevated in response to acetaldehyde and that the FA pathway limits acetaldehyde-induced genomic instability. Here, we highlight these findings and present additional results to discuss the role of the FA pathway and p53 DNA damage response in the protection against genomic instability and esophageal carcinogenesis.
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