ReviewCurrent opinion in genetics & development2012
Replication stress and mechanisms of CNV formation.
Review in Current opinion in genetics & development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed, 130 citations in OpenAlex.
- Recurrent DNA break clusters drive replication-stress-induced copy number variants and genome diversification.Nature communications · 2026Article
- Replication stress increases de novo CNVs across the malaria parasite genome.Nucleic acids research · 2026Article
- Digital droplet PCR is an accurate and precise method to measure DNA copy number.Scientific reports · 2025Article
- Replication stress increases de novo CNVs across the malaria parasite genome.bioRxiv : the preprint server for biology · 2025Article
- Detection and functional assessment of structural variants using whole-genome re-sequencing data in Nellore cattle.Scientific reports · 2025Article
- Genome-Wide Analyses of Copy Number Variants in 751 Populus trichocarpa Individuals From Natural Populations.Genome biology and evolution · 2025Article
- Formation of chromosomal rearrangements inbioRxiv : the preprint server for biology · 2025Article
- The Slx4-Rad1-Rad10 nuclease differentially regulates deletions and duplications induced by a replication fork barrier.PLoS genetics · 2025Article
- Template switching during DNA replication is a prevalent source of adaptive gene amplification.eLife · 2025Article
- The known structural variations in hearing loss and their diagnostic approaches: a comprehensive review.Molecular biology reports · 2025Review
- Chromoanasynthesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Template switching during DNA replication is a prevalent source of adaptive gene amplification.bioRxiv : the preprint server for biology · 2024Article
- FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation.Functional & integrative genomics · 2024Article
- Article
- Analysis of parental origin of de novo pathogenic CNVs in patients with intellectual disability.Genetics and molecular biology · 2024Article
- Copy Number Variations in Pancreatic Cancer: From Biological Significance to Clinical Utility.International journal of molecular sciences · 2023Review
- Mycoplasma DnaK increases DNA copy number variants in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- G-Quadruplex Structures Are Key Modulators of Somatic Structural Variants in Cancers.Cancer research · 2023Article
- Article
- Incorporation of a histone mutant with H3K56 site substitution perturbs the replication machinery in mouse embryonic stem cells.Journal of molecular cell biology · 2022Article
12 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Copy number variants (CNVs) are widely distributed throughout the human genome, where they contribute to genetic variation and phenotypic diversity. De novo CNVs are also a major cause of numerous genetic and developmental disorders. However, unlike many other types of mutations, little is known about the genetic and environmental risk factors for new and deleterious CNVs. DNA replication errors have been implicated in the generation of a major class of CNVs, the nonrecurrent CNVs. We have found that agents that perturb normal replication and create conditions of replication stress, including hydroxyurea and aphidicolin, are potent inducers of nonrecurrent CNVs in cultured human cells. These findings have broad implications for identifying CNV risk factors and for hydroxyurea-related therapies in humans.
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.