Trial reportEuropean journal of immunology2014
AID induces intraclonal diversity and genomic damage in CD86(+) chronic lymphocytic leukemia cells.
Trial report in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 24 citations in OpenAlex.
- Ibrutinib therapy downregulates AID enzyme and proliferative fractions in chronic lymphocytic leukemia.Blood · 2019Trial
- CD86, the double agent: Significance of CD86 expression in B-cell malignancies.International journal of cancer · 2025Review
- Ibrutinib enhances the bias of T cell responses towards staphylococcal superantigens sustaining inflammation in chronic lymphocytic leukaemia.Frontiers in immunology · 2025Article
- B Cell Chronic Lymphocytic Leukemia Development in Mice with Chronic Lung Exposure to Coccidioides Fungal Arthroconidia.ImmunoHorizons · 2023Article
- Revealing a Phenotypical Appearance of Ibrutinib Resistance in Patients With Chronic Lymphocytic Leukaemia by Flow Cytometry.Pathology oncology research : POR · 2022Article
- Structure-Based Design of First-Generation Small Molecule Inhibitors Targeting the Catalytic Pockets of AID, APOBEC3A, and APOBEC3B.ACS pharmacology & translational science · 2021Article
- AID Contributes to Accelerated Disease Progression in the TCL1 Mouse Transplant Model for CLL.Cancers · 2021Article
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- Identification and Validation of CYBB, CD86, and C3AR1 as the Key Genes Related to Macrophage Infiltration of Gastric Cancer.Frontiers in molecular biosciences · 2021Article
- Immunoglobulin somatic hypermutation has clinical impact in DLBCL and potential implications for immune checkpoint blockade and neoantigen-based immunotherapies.Journal for immunotherapy of cancer · 2019Article
- The Effect of CD86 Expression on the Proliferation and the Survival of CLL Cells.Pathology oncology research : POR · 2019Article
- Activation-induced deaminase and its splice variants associate with trisomy 12 in chronic lymphocytic leukemia.Annals of hematology · 2019Article
- Article
- Whole-genome sequencing reveals activation-induced cytidine deaminase signatures during indolent chronic lymphocytic leukaemia evolution.Nature communications · 2015Article
- AIDing cancer treatment: Reducing AID activity via HSP90 inhibition.European journal of immunology · 2015Article
- HSP90 inhibitors decrease AID levels and activity in mice and in human cells.European journal of immunology · 2015Article
- Evolving Concepts: Immunity in Oncology from Targets to Treatments.Journal of oncology · 2015Review
- AID/APOBEC deaminases and cancer.Oncoscience · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The activation-induced cytidine deaminase (AID) mediates somatic hypermutation and class switch recombination of the Ig genes by directly deaminating cytosines to uracils. As AID causes a substantial amount of off-target mutations, its activity has been associated with lymphomagenesis and clonal evolution of B-cell malignancies. Although it has been shown that AID is expressed in B-cell chronic lymphocytic leukemia (CLL), a clear analysis of in vivo AID activity in this B-cell malignancy remained elusive. In this study performed on primary human CLL samples, we report that, despite the presence of a dominant VDJ heavy chain region, a substantial intraclonal diversity was observed at VDJ as well as at IgM switch regions (Sμ), showing ongoing AID activity in vivo during disease progression. This AID-mediated heterogeneity was higher in CLL subclones expressing CD86, which we identified as the proliferative CLL fraction. Finally, CD86 expression correlated with shortened time to first treatment and increased γ-H2AX focus formation. Our data demonstrate that AID is active in CLL in vivo and thus, AID likely contributes to clonal evolution of CLL.
Indexed as
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.