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Deficiencies in Mouse Myh and Ogg1 Result in Tumor Predisposition and G to T Mutations in Codon 12 of the K-Ras Oncogene in Lung Tumors
Abstract
Oxidative DNA damage is unavoidably and continuously generated by oxidant byproducts of normal cellular metabolism. The DNA damage repair genes, mutY and mutM, prevent G to T mutations caused by reactive oxygen species in Escherichia coli, but it has remained debatable whether deficiencies in their mammalian counterparts, Myh and Ogg1, are directly involved in tumorigenesis. Here, we demonstrate that deficiencies in Myh and Ogg1 predispose 65.7% of mice to tumors, predominantly lung and ovarian tumors, and lymphomas. Remarkably, subsequent analyses identified G to T mutations in 75% of the lung tumors at an activating hot spot, codon 12, of the K-ras oncogene, but none in their adjacent normal tissues. Moreover, malignant lung tumors were increased with combined heterozygosity of Msh2, a mismatch repair gene involved in oxidative DNA damage repair as well. Thus, oxidative DNA damage appears to play a causal role in tumorigenesis, and codon 12 of K-ras is likely to be an important downstream target in lung tumorigenesis. The multiple oxidative repair genes are required to prevent mutagenesis and tumor formation. The mice described here provide a valuable model for studying the mechanisms of oxidative DNA damage in tumorigenesis and investigating preventive or therapeutic approaches.
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“The ogg1 or ogg1/mth1 knock-out mice have 20-fold higher levels of 8-oxoguanine in mtDNA (de Souza-Pinto et al., 2001) and half the life expectancy relative to wild-type (WT) mice (Xie et al., 2004), but no increase in mtDNA mutations (Halsne et al., 2012).”
From Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases (2017) · cites this paper as Xie et al., 2004
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Metadata
- Authors
- Xie, Y., Yang, H., Cunanan, C., Okamoto, K., Shibata, D., Pan, J., Barnes, D. E., Lindahl, T., McIlhatton, M., Fishel, R., & Miller, J. H.
- Affiliations
- University of California, Los Angeles (US)
- University of Southern California (US)
- Cancer Research UK (GB)
- Thomas Jefferson University (US)
- Venue
- Cancer Research
- Published
- 2004-05-01
- Volume
- 64
- Issue
- 9
- Pages
- 3096-3102
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2137854060
- Cited by
- 291
- References
- 38
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 7 · 2023: 4 · 2022: 8 · 2021: 15 · 2020: 10 · 2019: 16 · 2018: 11 · 2017: 10 · 2016: 11 · 2015: 11 · 2014: 14 · 2013: 15 · 2012: 17
- FWCI
- 7.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca085952-04)
- National Cancer Institute (CA 85952)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- MUTYH, OGG1, oxidative DNA damage, lung cancer, cancer susceptibility, MutY, formamidopyrimidine-DNA glycosylase, MSH2, DNA mismatch repair, oxidative DNA damage repair, mutagenesis, lymphoma, ovarian neoplasms, reactive oxygen species, mouse model
- MeSH terms
- Animals, Codon, DNA Damage, DNA-Binding Proteins, Female, Humans, Lung Neoplasms, Lymphoma, Male, Mice, Inbred C57BL, Ovarian Neoplasms, Oxidation-Reduction, Proto-Oncogene Proteins, Genes, ras, Point Mutation, Mice, Knockout, Genetic Predisposition to Disease, DNA Glycosylases, Mice, MutS Homolog 2 Protein
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