ArticlePloS one2016
Mutation Processes in 293-Based Clones Overexpressing the DNA Cytosine Deaminase APOBEC3B.
Article in PloS one, 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, 36 citations in OpenAlex.
- R-loop editing by DNA cytosine deaminase APOBEC3B modulates the activity of oestrogen receptor enhancers.Nature communications · 2026Article
- APOBEC3 Activity Promotes the Survival and Evolution of Drug-Tolerant Persister Cells during EGFR Inhibitor Resistance in Lung Cancer.Cancer research communications · 2025Article
- APOBEC3B expression in 293T viral producer cells drives mutations in chimeric antigen receptors and reduces CAR T cell efficacy.Molecular therapy. Oncology · 2024Article
- Mutational impact of APOBEC3A and APOBEC3B in a human cell line and comparisons to breast cancer.PLoS genetics · 2023Article
- Quantification of APOBEC3 Mutation Rates Affecting theViruses · 2022Article
- Prospectively defined patterns of APOBEC3A mutagenesis are prevalent in human cancers.Cell reports · 2022Article
- Loss of the abasic site sensor HMCES is synthetic lethal with the activity of the APOBEC3A cytosine deaminase in cancer cells.PLoS biology · 2021Article
- MEK1/2 regulates APOBEC3B and polymerase iota-induced mutagenesis in head and neck cancer cells.American journal of cancer research · 2021Article
- Involvement of APOBEC3B in mutation induction by irradiation.Journal of radiation research · 2020Article
- Evaluation and minimization of Cas9-independent off-target DNA editing by cytosine base editors.Nature biotechnology · 2020Article
- APOBEC3B reporter myeloma cell lines identify DNA damage response pathways leading to APOBEC3B expression.PloS one · 2020Article
- Targeting specificity of APOBEC-based cytosine base editor in human iPSCs determined by whole genome sequencing.Nature communications · 2019Article
- A Rabbit Monoclonal Antibody against the Antiviral and Cancer Genomic DNA Mutating Enzyme APOBEC3B.Antibodies (Basel, Switzerland) · 2019Article
- Endogenous APOBEC3B Overexpression Constitutively Generates DNA Substitutions and Deletions in Myeloma Cells.Scientific reports · 2019Article
- APOBEC Mutagenesis and Copy-Number Alterations Are Drivers of Proteogenomic Tumor Evolution and Heterogeneity in Metastatic Thoracic Tumors.Cell reports · 2019Article
- A lentivirus-based system for Cas9/gRNA expression and subsequent removal by Cre-mediated recombination.Methods (San Diego, Calif.) · 2019Article
- Pan-cancer transcriptomic analysis dissects immune and proliferative functions of APOBEC3 cytidine deaminases.Nucleic acids research · 2019Article
- Computational approaches for discovery of mutational signatures in cancer.Briefings in bioinformatics · 2019Review
- Perspective: APOBEC mutagenesis in drug resistance and immune escape in HIV and cancer evolution.Annals of oncology : official journal of the European Society for Medical Oncology · 2018Review
- p53 controls expression of the DNA deaminase APOBEC3B to limit its potential mutagenic activity in cancer cells.Nucleic acids research · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Molecular, cellular, and clinical studies have combined to demonstrate a contribution from the DNA cytosine deaminase APOBEC3B (A3B) to the overall mutation load in breast, head/neck, lung, bladder, cervical, ovarian, and other cancer types. However, the complete landscape of mutations attributable to this enzyme has yet to be determined in a controlled human cell system. We report a conditional and isogenic system for A3B induction, genomic DNA deamination, and mutagenesis. Human 293-derived cells were engineered to express doxycycline-inducible A3B-eGFP or eGFP constructs. Cells were subjected to 10 rounds of A3B-eGFP exposure that each caused 80-90% cell death. Control pools were subjected to parallel rounds of non-toxic eGFP exposure, and dilutions were done each round to mimic A3B-eGFP induced population fluctuations. Targeted sequencing of portions of TP53 and MYC demonstrated greater mutation accumulation in the A3B-eGFP exposed pools. Clones were generated and microarray analyses were used to identify those with the greatest number of SNP alterations for whole genome sequencing. A3B-eGFP exposed clones showed global increases in C-to-T transition mutations, enrichments for cytosine mutations within A3B-preferred trinucleotide motifs, and more copy number aberrations. Surprisingly, both control and A3B-eGFP clones also elicited strong mutator phenotypes characteristic of defective mismatch repair. Despite this additional mutational process, the 293-based system characterized here still yielded a genome-wide view of A3B-catalyzed mutagenesis in human cells and a system for additional studies on the compounded effects of simultaneous mutation mechanisms in cancer cells.
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