ReviewCurrent opinion in genetics & development2014
Complex correlations: replication timing and mutational landscapes during cancer and genome evolution.
Review in Current opinion in genetics & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 76 citations in OpenAlex.
- Review
- Most human DNA replication initiation is dispersed throughout the genome with only a minority within previously identified initiation zones.Genome biology · 2025Article
- Global chromatin reorganization and regulation of genes with specific evolutionary ages during differentiation and cancer.Nucleic acids research · 2025Article
- R-loops acted on by RNase H1 influence DNA replication timing and genome stability in Leishmania.Nature communications · 2025Article
- Global chromatin reorganization and regulation of genes with specific evolutionary ages during differentiation and cancer.bioRxiv : the preprint server for biology · 2024Article
- RIF1 regulates early replication timing in murine B cells.Nature communications · 2023Article
- Kronos scRT: a uniform framework for single-cell replication timing analysis.Nature communications · 2022Article
- Rif1-Dependent Control of Replication Timing.Genes · 2022Review
- Mutational Signatures of Replication Timing and Epigenetic Modification Persist through the Global Divergence of Mutation Spectra across the Great Ape Phylogeny.Genome biology and evolution · 2022Article
- Mapping Replication Timing in Single Mammalian Cells.Current protocols · 2022Article
- Convergent evolution of a genomic rearrangement may explain cancer resistance in hystrico- and sciuromorpha rodents.NPJ aging and mechanisms of disease · 2021Article
- Analysis of gene expression and mutation data points on contribution of transcription to the mutagenesis by APOBEC enzymes.NAR cancer · 2021Article
- Article
- Targeting Loss of Heterozygosity: A Novel Paradigm for Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Diverse noncoding mutations contribute to deregulation of cis-regulatory landscape in pediatric cancers.Science advances · 2020Article
- Control of DNA replication timing in the 3D genome.Nature reviews. Molecular cell biology · 2019Review
- Repair of multiple simultaneous double-strand breaks causes bursts of genome-wide clustered hypermutation.PLoS biology · 2019Article
- Linking the organization of DNA replication with genome maintenance.Current genetics · 2019Review
- Genome-wide analysis of DNA replication timing in single cells: Yes! We're all individuals.Genome biology · 2019Article
- Modeling double strand break susceptibility to interrogate structural variation in cancer.Genome biology · 2019Article
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 1 institution in 1 country.
Funding
Abstract
A recent flurry of reports correlates replication timing (RT) with mutation rates during both evolution and cancer. Specifically, point mutations and copy number losses correlate with late replication, while copy number gains and other rearrangements correlate with early replication. In some cases, plausible mechanisms have been proposed. Point mutation rates may reflect temporal variation in repair mechanisms. Transcription-induced double-strand breaks are expected to occur in transcriptionally active early replicating chromatin. Fusion partners are generally in close proximity, and chromatin in close proximity replicates at similar times. However, temporal enrichment of copy number gains and losses remains an enigma. Moreover, many conclusions are compromised by a lack of matched RT and sequence datasets, the filtering out of developmental variation in RT, and the use of somatic cell lines to make inferences about germline evolution.
Indexed as
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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.