ArticleCancer research2013
APOBEC3 cytidine deaminases in double-strand DNA break repair and cancer promotion.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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.
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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
34 citing papers in PubMed, 55 citations in OpenAlex.
- APOBEC3B regulates HPV replication by inducing R-loop formation and DNA damage.PLoS pathogens · 2026Article
- APOBEC3G protects the genome of human cultured cells and mice from radiation-induced damage.The FEBS journal · 2023Article
- APOBEC3-mediated mutagenesis in cancer: causes, clinical significance and therapeutic potential.Journal of hematology & oncology · 2023Review
- Influence network model uncovers relations between biological processes and mutational signatures.Genome medicine · 2023Article
- Research on the influence of APOBEC family on the occurrence, diagnosis, and treatment of various tumors.Journal of cancer research and clinical oncology · 2023Review
- Aberrant APOBEC3C expression induces characteristic genomic instability in pancreatic ductal adenocarcinoma.Oncogenesis · 2022Article
- Correlation-based and feature-driven mutation signature analyses to identify genetic features associated with DNA mutagenic processes in cancer genomes.Genomics & informatics · 2021Article
- Radiotherapy is associated with a deletion signature that contributes to poor outcomes in patients with cancer.Nature genetics · 2021Article
- Targeted Deep Sequencing of Bladder Tumors Reveals Novel Associations between Cancer Gene Mutations and Mutational Signatures with Major Risk Factors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead.Open biology · 2020Article
- Antitumor Effect of Sugar-Modified Cytosine Nucleosides on Growth of Adult T-Cell Leukemia Cells in Mice.Vaccines · 2020Article
- Alternative splicing of APOBEC3D generates functional diversity and its role as a DNA mutator.International journal of hematology · 2020Article
- Article
- Genomic heterogeneity in bladder cancer: challenges and possible solutions to improve outcomes.Nature reviews. Urology · 2020Review
- An Alu Element Insertion in Intron 1 Results in Aberrant Alternative Splicing of APOBEC3G Pre-mRNA in Northern Pig-Tailed Macaques (Journal of virology · 2020Article
- DNA Methylation-a Potential Source of Mitochondria DNA Base Mismatch in the Development of Diabetic Retinopathy.Molecular neurobiology · 2019Article
- Review
- Treatment resistance in urothelial carcinoma: an evolutionary perspective.Nature reviews. Clinical oncology · 2018Review
- Expressed HNSCC variants by HPV-status in a well-characterized Michigan cohort.Scientific reports · 2018Article
- APOBEC3B Activity Is Prevalent in Urothelial Carcinoma Cells and Only Slightly Affected by LINE-1 Expression.Frontiers in microbiology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
High frequency of cytidine to thymidine conversions was identified in the genome of several types of cancer cells. In breast cancer cells, these mutations are clustered in long DNA regions associated with single-strand DNA (ssDNA), double-strand DNA breaks (DSB), and genomic rearrangements. The observed mutational pattern resembles the deamination signature of cytidine to uridine carried out by members of the APOBEC3 family of cellular deaminases. Consistently, APOBEC3B (A3B) was recently identified as the mutational source in breast cancer cells. A3G is another member of the cytidine deaminases family predominantly expressed in lymphoma cells, where it is involved in mutational DSB repair following ionizing radiation treatments. This activity provides us with a new paradigm for cancer cell survival and tumor promotion and a mechanistic link between ssDNA, DSBs, and clustered mutations. Cancer Res; 73(12); 3494-8. ©2013 AACR.
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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.