ArticleBlood2012
IGHV-unmutated and IGHV-mutated chronic lymphocytic leukemia cells produce activation-induced deaminase protein with a full range of biologic functions.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- Ibrutinib therapy downregulates AID enzyme and proliferative fractions in chronic lymphocytic leukemia.Blood · 2019Trial
- AID induces intraclonal diversity and genomic damage in CD86(+) chronic lymphocytic leukemia cells.European journal of immunology · 2014Trial
- Early-onset CLL is characterized by enhanced microenvironment-driven metabolic fitness, increased proliferative bias, and accelerated disease progression.Frontiers in immunology · 2026Article
- Proliferating CLL cells express high levels of CXCR4 and CD5.HemaSphere · 2024Article
- BCL2 Protein Progressively Declines during Robust CLL Clonal Expansion: Potential Impact on Venetoclax Clinical Efficacy and Insights on Mechanism.Lymphatics · 2024Article
- IGH 3'RR recombination uncovers a non-germinal center imprint and c-MYC-dependent IGH rearrangement in unmutated chronic lymphocytic leukemia.Haematologica · 2024Article
- Article
- B Cell Chronic Lymphocytic Leukemia Development in Mice with Chronic Lung Exposure to Coccidioides Fungal Arthroconidia.ImmunoHorizons · 2023Article
- Implementation of International Prognostic Index with flow cytometry immunophenotyping for better risk stratification of chronic lymphocytic leukemia.European journal of haematology · 2022Article
- Loss of AID exacerbates the malignant progression of CLL.Leukemia · 2022Article
- Multi-platform profiling characterizes molecular subgroups and resistance networks in chronic lymphocytic leukemia.Nature communications · 2021Article
- 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
- Musashi 2 influences chronic lymphocytic leukemia cell survival and growth making it a potential therapeutic target.Leukemia · 2021Article
- Chronic Lymphocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2021Review
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- The Determinants of B Cell Receptor Signaling as Prototype Molecular Biomarkers of Leukemia.Frontiers in oncology · 2021Article
- Article
- B Cell Receptor Immunogenetics in B Cell Lymphomas: Immunoglobulin Genes as Key to Ontogeny and Clinical Decision Making.Frontiers in oncology · 2020Review
- Novel CHK1 inhibitor MU380 exhibits significant single-agent activity in TP53-mutated chronic lymphocytic leukemia cells.Haematologica · 2019Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
Abstract
Clonal evolution occurs during the course of chronic lymphocytic leukemia (CLL) and activation-induced deaminase (AID) could influence this process. However, this possibility has been questioned in CLL because the number of circulating AID mRNA(+) cells is exceedingly low; synthesis of AID protein by blood CLL cells has not been demonstrated; the full range of AID functions is lacking in unmutated CLL (U-CLL), and no prospective analysis linking AID expression and disease severity has been reported. The results of the present study show that circulating CLL cells and those within secondary lymphoid tissues can make AID mRNA and protein. This production is related to cell division because more AID mRNA was detected in recently divided cells and AID protein was limited to the dividing fraction and was up-regulated on induction of cell division. AID protein was functional because AID(+) dividing cells exhibited more double-stranded DNA breaks, IGH class switching, and new IGHV-D-J mutations. Each of these actions was documented in U-CLL and mutated CLL (M-CLL). Furthermore, AID protein was associated with worse patient outcome and adverse cytogenetics. We conclude that the production of fully functional AID protein by U-CLL and M-CLL cells could be involved in clonal evolution of the disease.
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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.