ReviewDNA repair2019
The spectrum of APOBEC3 activity: From anti-viral agents to anti-cancer opportunities.
Review in DNA repair, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 85 citations in OpenAlex.
- Replication stress in cancer: origins, consequences and therapeutic opportunities.Nature reviews. Cancer · 2026Review
- APOBEC3A is the predominant global editor of cytosines in human mRNAs and in single-strand RNA viruses.G3 (Bethesda, Md.) · 2026Article
- Single base focal hypermutation cooccurs with structural variation as an early event in advanced prostate tumourigenesis with ancestry specific independence: a multi-ancestral observational study.Genome medicine · 2026Observational
- HAMMER: hairpin-based APOBEC3A-mediated mRNA editing reporter.Nucleic acids research · 2026Article
- R-loop editing by DNA cytosine deaminase APOBEC3B modulates the activity of oestrogen receptor enhancers.Nature communications · 2026Article
- HAMMER: Hairpin-based APOBEC3A-mediated mRNA editing reporter.bioRxiv : the preprint server for biology · 2026Article
- APOBEC3A is the predominant global editor of cytosines in human mRNAs and in single-strand RNA viruses.bioRxiv : the preprint server for biology · 2026Article
- Single base focal hypermutation cooccurs with structural variation as an early event in advanced prostate tumourigenesis with ancestry specific independence: a multi-ancestral observational study.Research square · 2025Article
- Kaposi's sarcoma-associated herpesvirus ORF61 protein sequesters APOBEC3B in filamentous aggregates.Journal of virology · 2025Article
- Inactivation of GSK3β by SerCell death and differentiation · 2025Article
- APOBEC3 Proteins: From Antiviral Immunity to Oncogenic Drivers in HPV-Positive Cancers.Viruses · 2025Review
- Characterisation of APOBEC3B-Mediated RNA editing in breast cancer cells reveals regulatory roles of NEAT1 and MALAT1 lncRNAs.Oncogene · 2024Article
- Molecular mechanism for regulating APOBEC3G DNA editing function by the non-catalytic domain.Nature communications · 2024Article
- Article
- Kataegis associated mutational processes linked to adverse prostate cancer presentation in African men.Research square · 2024Article
- Molecular mechanism for regulating APOBEC3G DNA editing function by the non-catalytic domain.bioRxiv : the preprint server for biology · 2024Article
- Prognostic value of APOBEC3A in patients with cervical squamous cell carcinoma in a major urban center in China: a retrospective study.Translational cancer research · 2023Article
- APOBEC3B regulates R-loops and promotes transcription-associated mutagenesis in cancer.Nature genetics · 2023Article
- Human cytomegalovirus mediates APOBEC3B relocalization early during infection through a ribonucleotide reductase-independent mechanism.Journal of virology · 2023Article
- Structural basis of sequence-specific cytosine deamination by double-stranded DNA deaminase toxin DddA.Nature structural & molecular biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The APOBEC3 family of cytosine deaminases are part of the innate immune response to viral infection, but also have the capacity to damage cellular DNA. Detection of mutational signatures consistent with APOBEC3 activity, together with elevated APOBEC3 expression in cancer cells, has raised the possibility that these enzymes contribute to oncogenesis. Genome deamination by APOBEC3 enzymes also elicits DNA damage response signaling and presents therapeutic vulnerabilities for cancer cells. Here, we discuss implications of APOBEC3 activity in cancer and the potential to exploit their mutagenic activity for targeted cancer therapies.
Indexed as
Identifiers
What OpenQuestion holds
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.