ArticleBlood cancer journal2021
Dysregulated APOBEC3G causes DNA damage and promotes genomic instability in multiple myeloma.
Article in Blood cancer journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 47 citations in OpenAlex.
- A single-cell atlas of multiple myeloma defines malignant archetypes and proliferative states.Nature genetics · 2026Article
- Lamin B1 safeguards the B cell genome and shapes lymphoma outcome.HemaSphere · 2026Article
- Comprehensive repertoire of the chromosomal alteration and mutational signatures across 16 cancer types.Nature genetics · 2026Article
- Reprogramming tumor immunity through APOBEC3s-mediated mutagenesis: from genome instability to immune checkpoint interactions.Frontiers in immunology · 2026Review
- B-cell-specificBlood neoplasia · 2025Article
- APOBEC3C-Mediated NF-κB Activation Promotes Malignant Progression of Gliomas.Immunity, inflammation and disease · 2025Article
- Nonhypermutator Cancers Access Driver Mutations Through Reversals in Germline Mutational Bias.Molecular biology and evolution · 2025Article
- Next generation APOBEC3 inhibitors: optimally designed for potency and nuclease stability.Nucleic acids research · 2025Article
- Differential effects on tumor progression by APOBEC3A, APOBEC3B, and APOBEC3H Haplotype I in a breast cancer mouse xenograft model.Frontiers in genetics · 2025Article
- Next generation APOBEC3 inhibitors: Optimally designed for potency and nuclease stability.bioRxiv : the preprint server for biology · 2024Article
- Pan-cancer analysis of the interplay between mutational signatures and cellular signaling.iScience · 2024Article
- Cytidine deaminases APOBEC3C and APOBEC3D promote DNA replication stress resistance in pancreatic cancer cells.Nature cancer · 2024Article
- Article
- Anoikis-related genes signature development for clear cell renal cell carcinoma prognosis and tumor microenvironment.Scientific reports · 2023Article
- Review
- Molecular genetic aberrations in the pathogenesis of multiple myeloma.Asian biomedicine : research, reviews and news · 2023Review
- Alternative Splicing, RNA Editing, and the Current Limits of Next Generation Sequencing.Genes · 2023Article
- DNA Deamination Is Required for Human APOBEC3A-Driven Hepatocellular Carcinoma In Vivo.International journal of molecular sciences · 2023Article
- A Brief Review on Chemoresistance; Targeting Cancer Stem Cells as an Alternative Approach.International journal of molecular sciences · 2023Review
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Multiple myeloma (MM) is a heterogeneous disease characterized by significant genomic instability. Recently, a causal role for the AID/APOBEC deaminases in inducing somatic mutations in myeloma has been reported. We have identified APOBEC/AID as a prominent mutational signature at diagnosis with further increase at relapse in MM. In this study, we identified upregulation of several members of APOBEC3 family (A3A, A3B, A3C, and A3G) with A3G, as one of the most expressed APOBECs. We investigated the role of APOBEC3G in MM and observed that A3G expression and APOBEC deaminase activity is elevated in myeloma cell lines and patient samples. Loss-of and gain-of function studies demonstrated that APOBEC3G significantly contributes to increase in DNA damage (abasic sites and DNA breaks) in MM cells. Evaluation of the impact on genome stability, using SNP arrays and whole genome sequencing, indicated that elevated APOBEC3G contributes to ongoing acquisition of both the copy number and mutational changes in MM cells over time. Elevated APOBEC3G also contributed to increased homologous recombination activity, a mechanism that can utilize increased DNA breaks to mediate genomic rearrangements in cancer cells. These data identify APOBEC3G as a novel gene impacting genomic evolution and underlying mechanisms in MM.
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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.