ArticleGenome biology2014
The RNA editing enzyme APOBEC1 induces somatic mutations and a compatible mutational signature is present in esophageal adenocarcinomas.
Article in Genome biology, 2014. 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 66 papers.
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Who cites it
66 citing papers in PubMed, 76 citations in OpenAlex.
- Effects of thymidylate synthase inhibitors differ in genomic uracilation and mutagenic potential.Life science alliance · 2026Article
- Comparing self-reported race and genetic ancestry for identifying potential differentially methylated sites in endometrial cancer: insights from African ancestry proportions using machine learning models.Molecular oncology · 2025Article
- Machine learning-driven classification and prognostic prediction of kidney renal clear cell carcinoma using APOBEC family expression signatures.Scientific reports · 2025Article
- Article
- Structure-guided discovery of highly efficient cytidine deaminases with sequence-context independence.Nature biomedical engineering · 2025Article
- APOBEC in breast cancer: a dual player in tumor evolution and therapeutic response.Frontiers in molecular biosciences · 2025Review
- Efficient Rescue of Retinal Degeneration in Pde6a Mice by Engineered Base Editing and Prime Editing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Simultaneous multiplex genome loci editing ofSynthetic and systems biotechnology · 2024Article
- CRISPR Base Editing to Create Potential Charcot-Marie-Tooth Disease Models with High Editing Efficiency: Human Induced Pluripotent Stem Cell HarboringBiomedicines · 2024Article
- Identification of RBM46 as a novel APOBEC1 cofactor for C-to-U RNA-editing activity.Journal of molecular biology · 2023Article
- Engineered deaminases as a key component of DNA and RNA editing tools.Molecular therapy. Nucleic acids · 2023Review
- Acute expression of human APOBEC3B in mice results in RNA editing and lethality.Genome biology · 2023Article
- Article
- Proteogenomics of different urothelial bladder cancer stages reveals distinct molecular features for papillary cancer and carcinoma in situ.Nature communications · 2023Article
- Loss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer.Cancer cell · 2023Article
- RNA recording in single bacterial cells using reprogrammed tracrRNAs.Nature biotechnology · 2023Article
- Detect-seq, a chemical labeling and biotin pull-down approach for the unbiased and genome-wide off-target evaluation of programmable cytosine base editors.Nature protocols · 2023Review
- The Design and Application of DNA-Editing Enzymes as Base Editors.Annual review of biochemistry · 2023Review
- Evolutionary honing in and mutational replacement: how long-term directed mutational responses to specific environmental pressures are possible.Theory in biosciences = Theorie in den Biowissenschaften · 2023Review
- APOBEC mutagenesis is a common process in normal human small intestine.Nature genetics · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe AID/APOBECs are deaminases that act on cytosines in a diverse set of pathways and some of them have been linked to the onset of genetic alterations in cancer. Among them, APOBEC1 is the only family member to physiologically target RNA, as the catalytic subunit in the Apolipoprotein B mRNA editing complex. APOBEC1 has been linked to cancer development in mice but its oncogenic mechanisms are not yet well understood.
resultsWe analyze whether expression of APOBEC1 induces a mutator phenotype in vertebrate cells, likely through direct targeting of genomic DNA. We show its ability to increase the inactivation of a stably inserted reporter gene in a chicken cell line that lacks any other AID/APOBEC proteins, and to increase the number of imatinib-resistant clones in a human cellular model for chronic myeloid leukemia through induction of mutations in the BCR-ABL1 fusion gene. Moreover, we find the presence of an AID/APOBEC mutational signature in esophageal adenocarcinomas, a type of tumor where APOBEC1 is expressed, that mimics the one preferred by APOBEC1 in vitro.
conclusionsOur findings suggest that the ability of APOBEC1 to trigger genetic alterations represents a major layer in its oncogenic potential. Such APOBEC1-induced mutator phenotypes could play a role in the onset of esophageal adenocarcinomas. APOBEC1 could be involved in cancer promotion at the very early stages of carcinogenesis, as it is highly expressed in Barrett's esophagus, a condition often associated with esophageal adenocarcinoma.
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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.