ReviewCancer immunology, immunotherapy : CII2012
Activation-induced cytidine deaminase (AID) linking immunity, chronic inflammation, and cancer.
Review in Cancer immunology, immunotherapy : CII, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Apoptosis-driven chromosomal rearrangements in cancer: CAD cleavage, nuclear architecture, and microhomology-mediated end joining.Oncogenesis · 2026Review
- Chronic inflammation drives epididymal tertiary lymphoid structure formation and autoimmune fertility disorders in mice.Nature communications · 2025Article
- Molecular profiling of cell-free DNA from classic Hodgkin lymphoma patients identifies potential prognostic clusters and corresponds with disease dynamics.Annals of hematology · 2025Article
- Somatic mutations in autoinflammatory and autoimmune disease.Nature reviews. Rheumatology · 2024Review
- Chronic inflammation and the hallmarks of aging.Molecular metabolism · 2023Review
- Role of the mechanisms for antibody repertoire diversification in monoclonal light chain deposition disorders: when a friend becomes foe.Frontiers in immunology · 2023Review
- Synthesis and Biological Evaluation of PEGylated MWOMolecules (Basel, Switzerland) · 2022Article
- Singularity and Commonality in Response to SARS-CoV-2 in Lung and Colon Cell Models.International journal of molecular sciences · 2022Article
- Article
- Inflammation accelerates BCR-ABL1+ B-ALL development through upregulation of AID.Blood advances · 2022Article
- Review
- World Trade Center dust exposure promotes cancer in PTEN-deficient mouse prostates.Cancer research communications · 2022Article
- The other side of the coin: IgE deficiency, a susceptibility factor for malignancy occurrence.The World Allergy Organization journal · 2021Review
- AID and APOBECs as Multifaceted Intrinsic Virus-Restricting Factors: Emerging Concepts in the Light of COVID-19.Frontiers in immunology · 2021Article
- Article
- Onset of deaminase APOBEC3B induction in response to DNA double-strand breaks.Biochemistry and biophysics reports · 2018Article
- Oxaliplatin-induced changes in microbiota, TLR4+ cells and enhanced HMGB1 expression in the murine colon.PloS one · 2018Article
- Failure of ocular photodynamic therapy for secondary choroidal metastasis: a case report and literature review.Oncotarget · 2017Article
- Review
- Subversion of host genome integrity by bacterial pathogens.Nature reviews. Molecular cell biology · 2016Review
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 2 institutions in 1 country.
Funding
Abstract
Activation-induced cytidine deaminase (AID) is critically involved in class switch recombination and somatic hypermutation of Ig loci resulting in diversification of antibodies repertoire and production of high-affinity antibodies and as such represents a physiological tool to introduce DNA alterations. These processes take place within germinal centers of secondary lymphoid organs. Under physiological conditions, AID is expressed predominantly in activated B lymphocytes. Because of the mutagenic and recombinogenic potential of AID, its expression and activity is tightly regulated on different levels to minimize the risk of unwanted DNA damage. However, chronic inflammation and, probably, combination of other not-yet-identified factors are able to create a microenvironment sufficient for triggering an aberrant AID expression in B cells and, importantly, in non-B-cell background. Under these circumstances, AID may target also non-Ig genes, including cancer-related genes as oncogenes, tumor suppressor genes, and genomic stability genes, and modulate both genetic and epigenetic information. Despite ongoing progress, the complete understanding of fundamental aspects is still lacking as (1) what are the crucial factors triggering an aberrant AID expression/activity including the impact of Th2-driven inflammation and (2) to what extent may aberrant AID in human non-B cells lead to abnormal cell state associated with an increased rate of genomic alterations as point mutations, small insertions or deletions, and/or recurrent chromosomal translocations during solid tumor development and progression.
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Identifiers
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.