ArticleNature genetics2014
Association of a germline copy number polymorphism of APOBEC3A and APOBEC3B with burden of putative APOBEC-dependent mutations in breast cancer.
Article in Nature genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 1 of them a synthesis that pooled it.
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
193 citing papers in PubMed, 1 synthesis or guideline pooled it, 288 citations in OpenAlex.
- Pooled it
- Genomic Features Do Not Account for Differences in Multiple Myeloma Risk by Ancestry.Blood cancer discovery · 2026Article
- Motif-centered analyses reveal universal and tissue-specific mutagenic mechanisms operating in the human body.NAR cancer · 2026Article
- APOBEC3A is the predominant global editor of cytosines in human mRNAs and in single-strand RNA viruses.G3 (Bethesda, Md.) · 2026Article
- Motif-Centered Analyses Reveal Universal and Tissue-Specific Mutagenic Mechanisms Operating in the Human Body.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.Genome medicine · 2026Observational
- APOBEC3A is the predominant global editor of cytosines in human mRNAs and in single-strand RNA viruses.bioRxiv : the preprint server for biology · 2026Article
- Hypoxia-mimicked mitochondrial stress triggers APOBEC3A-mediated DNA damage via non-canonical innate immune activation.NAR molecular medicine · 2026Article
- Whole-genome landscapes of 1,364 breast cancers.Nature · 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
- Identification and characterization of lLF2 as a prognostic biomarker in HER2-positive breast cancer using Mendelian randomization and machine learning.Discover oncology · 2025Article
- Germline genetic variation impacts clonal hematopoiesis landscape and progression to malignancy.Nature genetics · 2025Article
- Pembrolizumab monotherapy for previously treated metastatic HER2-negative breast cancer with germlineThe Lancet regional health. Western Pacific · 2025Article
- Mechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastrophe.Science advances · 2025Article
- APOBEC3 Proteins: From Antiviral Immunity to Oncogenic Drivers in HPV-Positive Cancers.Viruses · 2025Review
- APOBEC3A drives ovarian cancer metastasis by altering epithelial-mesenchymal transition.JCI insight · 2025Article
- Complex rearrangements fuel ERNature · 2025Article
- An overview of the functions and mechanisms of APOBEC3A in tumorigenesis.Acta pharmaceutica Sinica. B · 2024Review
- Systematically Evaluating Cell-Free DNA Fragmentation Patterns for Cancer Diagnosis and Enhanced Cancer Detection via Integrating Multiple Fragmentation Patterns.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The role of distinct APOBEC/ADAR mRNA levels in mutational signatures linked to aging and ultraviolet radiation.Scientific reports · 2024Article
133 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
The somatic mutations in a cancer genome are the aggregate outcome of one or more mutational processes operative through the lifetime of the individual with cancer. Each mutational process leaves a characteristic mutational signature determined by the mechanisms of DNA damage and repair that constitute it. A role was recently proposed for the APOBEC family of cytidine deaminases in generating particular genome-wide mutational signatures and a signature of localized hypermutation called kataegis. A germline copy number polymorphism involving APOBEC3A and APOBEC3B, which effectively deletes APOBEC3B, has been associated with modestly increased risk of breast cancer. Here we show that breast cancers in carriers of the deletion show more mutations of the putative APOBEC-dependent genome-wide signatures than cancers in non-carriers. The results suggest that the APOBEC3A-APOBEC3B germline deletion allele confers cancer susceptibility through increased activity of APOBEC-dependent mutational processes, although the mechanism by which this increase in activity occurs remains unknown.
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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.