ArticleThe Journal of clinical investigation2012
DNA repair is indispensable for survival after acute inflammation.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Molecular regulation of DNA damage and repair in female infertility: a systematic review.Reproductive biology and endocrinology : RB&E · 2024Pooled it
- Predictive Analysis and Validation of Critical Missense SNPs of theInternational journal of molecular sciences · 2025Review
- Comprehensive whole-genome sequencing reveals origins of mutational signatures associated with aging, mismatch repair deficiency and temozolomide chemotherapy.Nucleic acids research · 2025Article
- MFAP2, upregulated by m1A methylation, promotes colorectal cancer invasiveness via CLK3.Cancer medicine · 2023Article
- DNA Alkylation Damage by Nitrosamines and Relevant DNA Repair Pathways.International journal of molecular sciences · 2023Review
- Clinical significance of ALKBH4 expression in non-small cell lung cancer.Translational cancer research · 2022Article
- Association between the genetic variants of base excision repair pathway genes and allergic rhinitis susceptibility in Chinese children.The World Allergy Organization journal · 2022Article
- DNA damage, inflammation and aging: Insights from mice.Frontiers in aging · 2022Review
- Tumor-Associated Inflammation: The Tumor-Promoting Immunity in the Early Stages of Tumorigenesis.Journal of immunology research · 2022Review
- Excision of mutagenic replication-blocking lesions suppresses cancer but promotes cytotoxicity and lethality in nitrosamine-exposed mice.Cell reports · 2021Article
- Article
- DNA alkylation lesion repair: outcomes and implications in cancer chemotherapy.Journal of Zhejiang University. Science. B · 2021Review
- Genetic and Epigenetic Impact of Chronic Inflammation on Colon Mucosa Cells.Frontiers in genetics · 2021Article
- Human ALKBH6 Is Required for Maintenance of Genomic Stability and Promoting Cell Survival During Exposure of Alkylating Agents in Pancreatic Cancer.Frontiers in genetics · 2021Article
- Multi-substrate selectivity based on key loops and non-homologous domains: new insight into ALKBH family.Cellular and molecular life sciences : CMLS · 2021Review
- Recognition of 1,The Journal of biological chemistry · 2020Article
- OGG1 deficiency alters the intestinal microbiome and increases intestinal inflammation in a mouse model.PloS one · 2020Article
- Inflammation-induced DNA damage, mutations and cancer.DNA repair · 2019Review
- N(6)-Methyladenine in eukaryotes.Cellular and molecular life sciences : CMLS · 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
11 authors at 3 institutions in 2 countries.
Funding
Abstract
More than 15% of cancer deaths worldwide are associated with underlying infections or inflammatory conditions, therefore understanding how inflammation contributes to cancer etiology is important for both cancer prevention and treatment. Inflamed tissues are known to harbor elevated etheno-base (ε-base) DNA lesions induced by the lipid peroxidation that is stimulated by reactive oxygen and nitrogen species (RONS) released from activated neutrophils and macrophages. Inflammation contributes to carcinogenesis in part via RONS-induced cytotoxic and mutagenic DNA lesions, including ε-base lesions. The mouse alkyl adenine DNA glycosylase (AAG, also known as MPG) recognizes such base lesions, thus protecting against inflammation-associated colon cancer. Two other DNA repair enzymes are known to repair ε-base lesions, namely ALKBH2 and ALKBH3; thus, we sought to determine whether these DNA dioxygenase enzymes could protect against chronic inflammation-mediated colon carcinogenesis. Using established chemically induced colitis and colon cancer models in mice, we show here that ALKBH2 and ALKBH3 provide cancer protection similar to that of the DNA glycosylase AAG. Moreover, Alkbh2 and Alkbh3 each display apparent epistasis with Aag. Surprisingly, deficiency in all 3 DNA repair enzymes confers a massively synergistic phenotype, such that animals lacking all 3 DNA repair enzymes cannot survive even a single bout of chemically induced colitis.
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What OpenQuestion holds
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.