ReviewCancer science2012
Inflammation-mediated genomic instability: roles of activation-induced cytidine deaminase in carcinogenesis.
Review in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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
64 citing papers in PubMed, 91 citations in OpenAlex.
- Copper homeostasis dysregulation promotes malignant transformation of renal tubular epithelial cells via the ROS/NF-κB/AID signaling axis.Translational andrology and urology · 2026Article
- Apoptosis-driven chromosomal rearrangements in cancer: CAD cleavage, nuclear architecture, and microhomology-mediated end joining.Oncogenesis · 2026Review
- Rethinking gastric carcinogenesis: a multiscale ecological model of risk beyondFrontiers in microbiology · 2026Review
- The Role of Nuclear APOBEC Enzymes in Neoplastic Progression of Ulcerative Colitis.Clinical and experimental gastroenterology · 2026Article
- Chromosomal Instability and Periodontal Disease in Idiopathic Infertility: Evidence of a Possible Association.Biology · 2025Article
- Linear ubiquitination of p31Cell & bioscience · 2025Article
- The Role of Inflammation in Cancer: Mechanisms of Tumor Initiation, Progression, and Metastasis.Cells · 2025Review
- A Landscape of Cancer Initiation and Cancer Stem Cells.Cancers · 2025Article
- A Fungicide, Fludioxonil, Formed the Polyploid Giant Cancer Cells and Induced Metastasis and Stemness in MDA-MB-231 Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2024Article
- Extrachromosomal Circular DNA: An Emerging Potential Biomarker for Inflammatory Bowel Diseases?Genes · 2024Review
- AID-induced CXCL12 upregulation enhances castration-resistant prostate cancer cell metastasis by stabilizing β-catenin expression.iScience · 2023Article
- Article
- Chronic inflammation and the hallmarks of aging.Molecular metabolism · 2023Review
- Review
- [Diabetes mellitus and the female reproductive system tumors].Problemy endokrinologii · 2023Article
- Inflammatory cytokine-enriched microenvironment plays key roles in the development of breast cancers.Cancer science · 2023Review
- TiSA: TimeSeriesAnalysis-a pipeline for the analysis of longitudinal transcriptomics data.NAR genomics and bioinformatics · 2023Article
- Role of the mechanisms for antibody repertoire diversification in monoclonal light chain deposition disorders: when a friend becomes foe.Frontiers in immunology · 2023Review
- Does IFITM3 link inflammation to tumorigenesis?BMB reports · 2022Review
- The Therapeutic Efficacy ofPlants (Basel, Switzerland) · 2022Review
4 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation is a strong risk factor for the development of cancer. Many previous studies have demonstrated that a transcriptional factor, nuclear factor (NF)-κB, plays an important role in the association between inflammation and cancer development, particularly tumor promotion and tumor progression. Although it is well recognized that cancer develops via stepwise accumulation of genetic aberrations, the mechanisms underlying the generation of these genetic alterations in normal epithelial cells under inflammatory conditions are not known. We recently demonstrated that pathogenic bacterial or viral factors and the subsequent inflammatory reactions lead to the aberrant expression of a DNA mutator enzyme, activation-induced cytidine deaminase (AID), in various epithelial cells via NF-κB activation, which causes the accumulation of genetic alterations in tumor-related genes. AID activation is widely observed in gastrointestinal tissues with cancer-associated inflammation, such as chronic viral hepatitis, Helicobacter pylori-related gastritis, Barrett's esophagus and inflammatory bowel disease. Furthermore, a deficiency of endogenous AID expression reduces both accumulation of somatic mutations in tumor-related genes and tumor incidence in a mouse model of inflammation-associated cancer development. These findings strongly suggest that AID plays an integral role in inflammation-associated carcinogenesis and is therefore a potential target molecule for the prevention and treatment of cancers.
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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.