ArticleBioEssays : news and reviews in molecular, cellular and developmental biology2014
Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness.
Article in BioEssays : news and reviews in molecular, cellular and developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- A practical framework RNMF for exploring the association between mutational signatures and genes using gene cumulative contribution abundance.Cancer medicine · 2022Pooled it
- The Role of Nuclear APOBEC Enzymes in Neoplastic Progression of Ulcerative Colitis.Clinical and experimental gastroenterology · 2026Article
- Reprogramming tumor immunity through APOBEC3s-mediated mutagenesis: from genome instability to immune checkpoint interactions.Frontiers in immunology · 2026Review
- Tobacco smoke carcinogens exacerbate APOBEC mutagenesis and carcinogenesis.Research square · 2025Article
- Tobacco smoke carcinogens exacerbate APOBEC mutagenesis and carcinogenesis.bioRxiv : the preprint server for biology · 2025Article
- Exploring the Role of Clustered Mutations in Carcinogenesis and Their Potential Clinical Implications in Cancer.International journal of molecular sciences · 2024Review
- Meiosis and beyond - understanding the mechanistic and evolutionary processes shaping the germline genome.Biological reviews of the Cambridge Philosophical Society · 2021Review
- Investigation of Break-Induced Replication in Yeast.Methods in molecular biology (Clifton, N.J.) · 2021Article
- The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead.Open biology · 2020Article
- Single-nucleotide polymorphism of the DNA cytosine deaminase APOBEC3H haplotype I leads to enzyme destabilization and correlates with lung cancer.NAR cancer · 2020Article
- The spectrum of APOBEC3 activity: From anti-viral agents to anti-cancer opportunities.DNA repair · 2019Review
- Repair of base damage within break-induced replication intermediates promotes kataegis associated with chromosome rearrangements.Nucleic acids research · 2019Article
- A practical guide for mutational signature analysis in hematological malignancies.Nature communications · 2019Article
- In Silico Genetics Revealing 5 Mutations inCancer informatics · 2019Article
- Mutational signatures and mutable motifs in cancer genomes.Briefings in bioinformatics · 2018Review
- Transient AID expression for in situ mutagenesis with improved cellular fitness.Scientific reports · 2018Article
- *K-means and cluster models for cancer signatures.Biomolecular detection and quantification · 2017Article
- Review
- Base changes in tumour DNA have the power to reveal the causes and evolution of cancer.Oncogene · 2017Review
- Recombination Is Responsible for the Increased Recovery of Drug-Resistant Mutants with Hypermutated Genomes in Resting Yeast Diploids Expressing APOBEC Deaminases.Frontiers in genetics · 2017Article
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 2 institutions in 1 country.
Funding
Abstract
The gain of a selective advantage in cancer as well as the establishment of complex traits during evolution require multiple genetic alterations, but how these mutations accumulate over time is currently unclear. There is increasing evidence that a mutator phenotype perpetuates the development of many human cancers. While in some cases the increased mutation rate is the result of a genetic disruption of DNA repair and replication or environmental exposures, other evidence suggests that endogenous DNA damage induced by AID/APOBEC cytidine deaminases can result in transient localized hypermutation generating simultaneous, closely spaced (i.e. "clustered") multiple mutations. Here, we discuss mechanisms that lead to mutation cluster formation, the biological consequences of their formation in cancer and evidence suggesting that APOBEC mutagenesis can also occur genome-wide. This raises the possibility that dysregulation of these enzymes may enable rapid malignant transformation by increasing mutation rates without the loss of fitness associated with permanent mutators.
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.