ArticleNature communications2020
Limiting oxidative DNA damage reduces microbe-induced colitis-associated colorectal cancer.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 3 of them syntheses that pooled it.
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
71 citing papers in PubMed, 3 syntheses or guidelines pooled it, 105 citations in OpenAlex.
- IBD-related inflammatory memory and colorectal cancer: epigenetic mechanisms and microbiome interventions.Frontiers in immunology · 2026Pooled it
- Gut microbiota and gastrointestinal tumors: insights from a bibliometric analysis.Frontiers in microbiology · 2025Pooled it
- Preventing Colitis-Associated Colon Cancer With Antioxidants: A Systematic Review.Cellular and molecular gastroenterology and hepatology · 2021Pooled it
- Gut microbiota and diet in colorectal cancer: Converging determinants of carcinogenesis.Gut microbes · 2026Review
- Nitric Oxide in the Intestinal Stem Cell Niche: A Spatial Model of Nitrosative Stress and Clonal Evolution in Colitis-Associated Colorectal Cancer.Digestive diseases and sciences · 2026Review
- Apurinic/apyrimidinic endonuclease 1 prevents oxidative DNA damage in intestinal epithelial cells induced by genotoxic Escherichia coli NC101.Redox biology · 2026Article
- Stromal BMP signalling maintains stem cell genome integrity and prevents gastric cancer initiation.Cell death & disease · 2026Article
- Article
- Analysis of intratumoural bacteria: Opportunities and challenges for cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- The gut microbiome as a biomarker and modifiable risk factor in Lynch Syndrome.Familial cancer · 2026Review
- Molecular mechanisms of bacteria-mediated cancer immunotherapy: from intratumoral microbiota to engineered therapeutics.Frontiers in immunology · 2026Review
- Tumor-Promoting Gut Microbes in Colorectal Cancer: Mechanisms and Translational Perspectives.International journal of medical sciences · 2026Review
- Microbiota-miR-101 interactions in obesity-associated colorectal cancer: from barrier dysfunction to precision therapeutic strategies.Frontiers in pharmacology · 2026Review
- Microbiome dysbiosis and its modulation in cancer development, prevention and therapy.Frontiers in oncology · 2026Review
- Gegen Qinlian Decoction, a classic traditional Chinese medicine formula: a potential therapeutic strategy for ulcerative colitis and colorectal cancer.Frontiers in pharmacology · 2026Review
- A common food mutagen promotes intestinal carcinogenesis by multiple mechanisms in mouse models of Lynch syndrome.NAR cancer · 2025Article
- Article
- Cancer microbiota: a focus on tumor-resident bacteria.EMBO reports · 2025Review
- Dietary fibre counters the oncogenic potential of colibactin-producing Escherichia coli in colorectal cancer.Nature microbiology · 2025Article
- Mitochondrial defects and metabolic vulnerabilities in Lynch syndrome-associated MSH2-deficient endometrial cancer.JCI insight · 2025Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Inflammatory bowel disease patients have a greatly increased risk of developing colitis-associated colon cancer (CAC); however, the basis for inflammation-induced genetic damage requisite for neoplasia is unclear. Using three models of CAC, we find that sustained inflammation triggers 8-oxoguanine DNA lesions. Strikingly, antioxidants or iNOS inhibitors reduce 8-oxoguanine and polyps in CAC models. Because the mismatch repair (MMR) system repairs 8-oxoguanine and is frequently defective in colorectal cancer (CRC), we test whether 8-oxoguanine mediates oncogenesis in a Lynch syndrome (MMR-deficient) model. We show that microbiota generates an accumulation of 8-oxoguanine lesions in MMR-deficient colons. Accordingly, we find that 8-oxoguanine is elevated in neoplastic tissue of Lynch syndrome patients compared to matched untransformed tissue or non-Lynch syndrome neoplastic tissue. While antioxidants reduce 8-oxoguanine, they do not reduce CRC in Lynch syndrome models. Hence, microbe-induced oxidative/nitrosative DNA damage play causative roles in inflammatory CRC models, but not in Lynch syndrome models.
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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 OpenQuestion graph.