ArticleBlood2016
AID-associated DNA repair pathways regulate malignant transformation in a murine model of BCL6-driven diffuse large B-cell lymphoma.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Adverse Prognostic Significance of Activation-Induced Cytidine Deaminase in Diffuse Large B-Cell Lymphoma Patients Treated With R-CHOP.Cancer reports (Hoboken, N.J.) · 2026Article
- Identification of primary mediastinal B-cell lymphomas with higher clonal dominance and poorer outcome using 5'RACE.Blood advances · 2025Article
- DNA mismatch repair defect and intratumor heterogeneous deficiency differently impact immune responses in diffuse large B-cell lymphoma.Oncoimmunology · 2024Article
- HBV-associated DLBCL of poor prognosis: advance in pathogenesis, immunity and therapy.Frontiers in immunology · 2023Review
- Synthesis and Biological Evaluation of PEGylated MWOMolecules (Basel, Switzerland) · 2022Article
- Mutational landscape of high-grade B-cell lymphoma withHaematologica · 2022Article
- SETD2 Haploinsufficiency Enhances Germinal Center-Associated AICDA Somatic Hypermutation to Drive B-cell Lymphomagenesis.Cancer discovery · 2022Article
- Genomic Uracil and Aberrant Profile of Demethylation Intermediates in Epigenetics and Hematologic Malignancies.International journal of molecular sciences · 2021Review
- Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphoma.PLoS genetics · 2020Article
- Bovine Leukemia Virus Infection Affects Host Gene Expression Associated with DNA Mismatch Repair.Pathogens (Basel, Switzerland) · 2020Article
- Optimized high-fidelity 3DPCR to assess potential mitochondrial targeting by activation-induced cytidine deaminase.FEBS open bio · 2020Article
- The uracil-DNA glycosylase UNG protects the fitness of normal and cancer B cells expressing AID.NAR cancer · 2020Article
- TRAF3 Acts as a Checkpoint of B Cell Receptor Signaling to Control Antibody Class Switch Recombination and Anergy.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- WEE1 inhibition synergizes with CHOP chemotherapy and radiation therapy through induction of premature mitotic entry and DNA damage in diffuse large B-cell lymphoma.Therapeutic advances in hematology · 2020Article
- TEOA Inhibits Proliferation and Induces DNA Damage of Diffuse Large B-Cell Lymphoma Cells Through Activation of the ROS-Dependent p38 MAPK Signaling Pathway.Frontiers in pharmacology · 2020Article
- [Proteomic analysis and verification of protein expression after upregulation of human CD99 in Hodgkin lymphoma cell line L428].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
- AID modulates carcinogenesis network via DNA demethylation in bladder urothelial cell carcinoma.Cell death & disease · 2019Article
- Pan-SRC kinase inhibition blocks B-cell receptor oncogenic signaling in non-Hodgkin lymphoma.Blood · 2018Article
- Establishment of induced pluripotent stem cells from normal B cells and inducing AID expression in their differentiation into hematopoietic progenitor cells.Scientific reports · 2017Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Somatic hypermutation and class-switch recombination of the immunoglobulin (Ig) genes occur in germinal center (GC) B cells and are initiated through deamination of cytidine to uracil by activation-induced cytidine deaminase (AID). Resulting uracil-guanine mismatches are processed by uracil DNA glycosylase (UNG)-mediated base-excision repair and MSH2-mediated mismatch repair (MMR) to yield mutations and DNA strand lesions. Although off-target AID activity also contributes to oncogenic point mutations and chromosome translocations associated with GC and post-GC B-cell lymphomas, the role of downstream AID-associated DNA repair pathways in the pathogenesis of lymphoma is unknown. Here, we show that simultaneous deficiency of UNG and MSH2 or MSH2 alone causes genomic instability and a shorter latency to the development of BCL6-driven diffuse large B-cell lymphoma (DLBCL) in a murine model. The additional development of several BCL6-independent malignancies in these mice underscores the critical role of MMR in maintaining general genomic stability. In contrast, absence of UNG alone is highly protective and prevents the development of BCL6-driven DLBCL. We further demonstrate that clonal and nonclonal mutations arise within non-Ig AID target genes in the combined absence of UNG and MSH2 and that DNA strand lesions arise in an UNG-dependent manner but are offset by MSH2. These findings lend insight into a complex interplay whereby potentially deleterious UNG activity and general genomic instability are opposed by the protective influence of MSH2, producing a net protective effect that promotes immune diversification while simultaneously attenuating malignant transformation of GC B cells.
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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.