ArticleInternational journal of biological sciences2013
Mismatch repair deficient mice show susceptibility to oxidative stress-induced intestinal carcinogenesis.
Article in International journal of biological sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
- A common food mutagen promotes intestinal carcinogenesis by multiple mechanisms in mouse models of Lynch syndrome.NAR cancer · 2025Article
- Oxidative stress accelerates repeat sequence instability and base substitutions promoting gastrointestinal driver mutations in MSH2 deficient mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Article
- Platinum chemotherapeutic-induced oxidative stress affects the transcriptional response of DNA repair genes in murine mesenchymal stem cells.American journal of stem cells · 2025Article
- Article
- Characteristic mutations induced in the small intestine of Msh2-knockout gpt delta mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021Article
- Resveratrol and its Related Polyphenols Contribute to the Maintenance of Genome Stability.Scientific reports · 2020Article
- MLH1 deficiency leads to deregulated mitochondrial metabolism.Cell death & disease · 2019Article
- Hidden Markov models lead to higher resolution maps of mutation signature activity in cancer.Genome medicine · 2019Article
- Mutant Frequency is not Increased in Mice Orally Exposed to Sodium Dichromate.Food safety (Tokyo, Japan) · 2019Article
- Effects of Nrf2 silencing on oxidative stress-associated intestinal carcinogenesis in mice.Cancer medicine · 2016Article
- Oregano Essential Oil Induces SOD1 and GSH Expression through Nrf2 Activation and Alleviates Hydrogen Peroxide-Induced Oxidative Damage in IPEC-J2 Cells.Oxidative medicine and cellular longevity · 2016Article
- Review
- DNA mismatch repair and oxidative DNA damage: implications for cancer biology and treatment.Cancers · 2014Review
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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
We have previously established an experimental system for oxidative DNA damage-induced tumorigenesis in the small intestine of mice. To elucidate the roles of mismatch repair genes in the tumor suppression, we performed oxidative DNA damage-induced tumorigenesis experiments using Msh2-deficient mice. Oral administration of 0.2% Potassium Bromate, KBrO3, effectively induced epithelial tumors in the small intestines of Msh2-deficient mice. We observed a 22.5-fold increase in tumor formation in the small intestines of Msh2-deficient mice compared with the wild type mice. These results indicate that mismatch repair is involved in the suppression of oxidative stress-induced intestinal tumorigenesis in mice. A mutation analysis of the Ctnnb1 gene of the tumors revealed predominant occurrences of G:C to A:T transitions. The TUNEL analysis showed a decreased number of TUNEL-positive cells in the crypts of small intestines from the Msh2-deficient mice compared with the wild type mice after treatment of KBrO3. These results suggest that the mismatch repair system may simultaneously function in both avoiding mutagenesis and inducing cell death to suppress the tumorigenesis induced by oxidative stress in the small intestine of mice.
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