ArticleBritish journal of cancer2017
Elevated APOBEC3B expression drives a kataegic-like mutation signature and replication stress-related therapeutic vulnerabilities in p53-defective cells.
Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 99 citations in OpenAlex.
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Effects of thymidylate synthase inhibitors differ in genomic uracilation and mutagenic potential.Life science alliance · 2026Article
- R-loop editing by DNA cytosine deaminase APOBEC3B modulates the activity of oestrogen receptor enhancers.Nature communications · 2026Article
- APOBEC3C coordinates DDX5 in R-loop resolution and dynamic control of Chk1-mediated stress-responsive circuitry as a prerequisite for gemcitabine resistance in p53-deficient cells.Cell death & disease · 2026Article
- Deaminase Modulation Driving a New Era in Drug Development.International journal of molecular sciences · 2025Review
- RNase H-sensitive accumulation of APOBEC3B in a nucleolus after DNA damage.Bioscience reports · 2025Article
- Article
- Cancer cells subvert the primate-specific KRAB zinc finger protein ZNF93 to control APOBEC3B.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Differential effects on tumor progression by APOBEC3A, APOBEC3B, and APOBEC3H Haplotype I in a breast cancer mouse xenograft model.Frontiers in genetics · 2025Article
- Article
- Targeting ATR in patients with cancer.Nature reviews. Clinical oncology · 2024Review
- Durable responses to ATR inhibition with ceralasertib in tumors with genomic defects and high inflammation.The Journal of clinical investigation · 2024Article
- The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance.Nature genetics · 2024Article
- Mutational impact of APOBEC3A and APOBEC3B in a human cell line and comparisons to breast cancer.PLoS genetics · 2023Article
- Human APOBEC3B promotes tumor development in vivo including signature mutations and metastases.Cell reports. Medicine · 2023Article
- Human cytomegalovirus mediates APOBEC3B relocalization early during infection through a ribonucleotide reductase-independent mechanism.Journal of virology · 2023Article
- APOBEC3B coordinates R-loop to promote replication stress and sensitize cancer cells to ATR/Chk1 inhibitors.Cell death & disease · 2023Article
- APOBEC3-mediated mutagenesis in cancer: causes, clinical significance and therapeutic potential.Journal of hematology & oncology · 2023Review
- Human cytomegalovirus mediates APOBEC3B relocalization early during infection through a ribonucleotide reductase-independent mechanism.bioRxiv : the preprint server for biology · 2023Article
- APOBEC3 as a driver of genetic intratumor heterogeneity.Molecular & cellular oncology · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundElevated APOBEC3B expression in tumours correlates with a kataegic pattern of localised hypermutation. We assessed the cellular phenotypes associated with high-level APOBEC3B expression and the influence of p53 status on these phenotypes using an isogenic system.
methodsWe used RNA interference of p53 in cells with inducible APOBEC3B and assessed DNA damage response (DDR) biomarkers. The mutational effects of APOBEC3B were assessed using whole-genome sequencing. In vitro small-molecule inhibitor sensitivity profiling was used to identify candidate therapeutic vulnerabilities.
resultsAlthough APOBEC3B expression increased the incorporation of genomic uracil, invoked DDR biomarkers and caused cell cycle arrest, inactivation of p53 circumvented APOBEC3B-induced cell cycle arrest without reversing the increase in genomic uracil or DDR biomarkers. The continued expression of APOBEC3B in p53-defective cells not only caused a kataegic mutational signature but also caused hypersensitivity to small-molecule DDR inhibitors (ATR, CHEK1, CHEK2, PARP, WEE1 inhibitors) as well as cisplatin/ATR inhibitor and ATR/PARP inhibitor combinations.
conclusionsAlthough loss of p53 might allow tumour cells to tolerate elevated APOBEC3B expression, continued expression of this enzyme might impart a number of therapeutic vulnerabilities upon tumour cells.
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