ArticleOncotarget2016
The Mbd4 DNA glycosylase protects mice from inflammation-driven colon cancer and tissue injury.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Toll-like receptors in health and disease.MedComm · 2024Review
- Article
- Base Excision Repair: Mechanisms and Impact in Biology, Disease, and Medicine.International journal of molecular sciences · 2023Review
- DNA damage, inflammation and aging: Insights from mice.Frontiers in aging · 2022Review
- The base excision repair process: comparison between higher and lower eukaryotes.Cellular and molecular life sciences : CMLS · 2021Review
- Base excision repair causes age-dependent accumulation of single-stranded DNA breaks that contribute to Parkinson disease pathology.Cell reports · 2021Article
- Analysis of mutations in tumor and normal adjacent tissue via fluorescence detection.Environmental and molecular mutagenesis · 2021Article
- Inflammation-induced DNA damage, mutations and cancer.DNA repair · 2019Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Much of the global cancer burden is associated with longstanding inflammation accompanied by release of DNA-damaging reactive oxygen and nitrogen species. Here, we report that the Mbd4 DNA glycosylase is protective in the azoxymethane/dextran sodium sulfate (AOM/DSS) mouse model of inflammation-driven colon cancer. Mbd4 excises T and U from T:G and U:G mismatches caused by deamination of 5-methylcytosine and cytosine. Since the rate of deamination is higher in inflamed tissues, we investigated the role of Mbd4 in inflammation-driven tumorigenesis. In the AOM/DSS assay, Mbd4-/- mice displayed more severe clinical symptoms, decreased survival, and a greater tumor burden than wild-type (WT) controls. The increased tumor burden in Mbd4-/- mice did not arise from impairment of AOM-induced apoptosis in the intestinal crypt. Histopathological analysis indicated that the colonic epithelium of Mbd4-/- mice is more vulnerable than WT to DSS-induced tissue damage. We investigated the role of the Mbd4-/- immune system in AOM/DSS-mediated carcinogenesis by repeating the assay on WT and Mbd4-/- mice transplanted with WT bone marrow. Mbd4-/- mice with WT bone marrow behaved similarly to Mbd4-/- mice. Together, our results indicate that the colonic epithelium of Mbd4-/- mice is more vulnerable to DSS-induced injury, which exacerbates inflammation-driven tissue injury and cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.