ArticleScientific reports2019
Endogenous APOBEC3B Overexpression Constitutively Generates DNA Substitutions and Deletions in Myeloma Cells.
Article in Scientific reports, 2019. 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, 35 citations in OpenAlex.
- When Myeloma Escapes the Bone Marrow: Extramedullary Disease in the Immunotherapy Era.Cancers · 2026Review
- Research progress on resistance mechanisms to CAR-T cell therapy in diffuse large B-cell lymphoma.Frontiers in oncology · 2026Review
- APOBEC3B Does Not Promote Tumor Progression in Tp53 Hemizygous Mice.Cancer reports (Hoboken, N.J.) · 2025Article
- Untargeted Mutation Triggered by Ribonucleoside Embedded in DNA.International journal of molecular sciences · 2024Article
- Mutational impact of APOBEC3A and APOBEC3B in a human cell line and comparisons to breast cancer.PLoS genetics · 2023Article
- Molecular genetic aberrations in the pathogenesis of multiple myeloma.Asian biomedicine : research, reviews and news · 2023Review
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
- CORN-Condition Orientated Regulatory Networks: bridging conditions to gene networks.Briefings in bioinformatics · 2022Article
- Article
- A panel of nanobodies recognizing conserved hidden clefts of all SARS-CoV-2 spike variants including Omicron.Communications biology · 2022Article
- APOBEC mediated mutagenesis drives genomic heterogeneity in endometriosis.Journal of human genetics · 2022Article
- ILF2 enhances the DNA cytosine deaminase activity of tumor mutator APOBEC3B in multiple myeloma cells.Scientific reports · 2022Article
- Characterizing the mutational landscape of MM and its precursor MGUS.American journal of cancer research · 2022Article
- Prognostic Value of HPV E6 and APOBEC3B in Upper Urinary Tract Urothelial Carcinoma.Disease markers · 2022Article
- Aberrantly Activated APOBEC3B Is Associated With Mutant p53-Driven Refractory/Relapsed Diffuse Large B-Cell Lymphoma.Frontiers in immunology · 2022Article
- Dysregulated APOBEC3G causes DNA damage and promotes genomic instability in multiple myeloma.Blood cancer journal · 2021Article
- Review
- Correlation Between APOBEC3B Expression and Clinical Characterization in Lower-Grade Gliomas.Frontiers in oncology · 2021Article
- Pan-Cancer Survey of Tumor Mass Dormancy and Underlying Mutational Processes.Frontiers in cell and developmental biology · 2021Article
- APOBEC3A catalyzes mutation and drives carcinogenesis in vivo.The Journal of experimental medicine · 2020Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) DNA cytosine deaminases have emerged as potential genomic mutators in various cancers. Multiple myeloma accumulates APOBEC signature mutations as it progresses; however, the mechanisms underlying APOBEC signature acquisition and its consequences remain elusive. In this study, we examined the significance and clinical impact of APOBEC3B (A3B) activity in multiple myeloma. Among APOBECs, only highly expressed A3B was associated with poor prognosis in myeloma patients, independent of other known poor prognostic factors. Quantitative PCR revealed that CD138-positive primary myeloma cells and myeloma cell lines exhibited remarkably high A3B expression levels. Interestingly, lentiviral A3B knockdown prevented the generation of deletion and loss-of-function mutations in exogenous DNA, whereas in control cells, these mutations accumulated with time. A3B knockdown also decreased the basal levels of γ-H2AX foci, suggesting that A3B promotes constitutive DNA double-strand breaks in myeloma cells. Importantly, among control shRNA-transduced cells, we observed the generation of clones that harboured diverse mutations in exogenous genes and several endogenous genes frequently mutated in myeloma, including TP53. Taken together, the results suggest that A3B constitutively mutates the tumour genome beyond the protection of the DNA repair system, which may lead to clonal evolution and genomic instability in myeloma.
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