ReviewSeminars in cancer biology2013
DNA replication timing, genome stability and cancer: late and/or delayed DNA replication timing is associated with increased genomic instability.
Review in Seminars in cancer biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
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.
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Who cites it
63 citing papers in PubMed, 129 citations in OpenAlex.
- Structural insights into Sld3-Sld7-dependent Cdc45 loading during replication initiation.Nature communications · 2026Article
- MTHFD1L in muscle invasive bladder cancer: a multi-cohort study on prognosis and therapeutic response.World journal of surgical oncology · 2026Article
- ResNet-Powered Multi-Class Identification of Sequence Patterns for Genome Replication Timing Analysis.Interdisciplinary sciences, computational life sciences · 2025Article
- Article
- Single cell multiomics approach to analyze replication timing and gene expression in mouse preimplantation embryos.Communications biology · 2025Article
- Z-form DNA-RNA hybrid blocks DNA replication.Nucleic acids research · 2025Article
- Infection-related pathway activation and vulnerability to arsenic trioxide in acute promyelocytic leukemia with TTMV::RARA.Leukemia · 2025Article
- Article
- Characterizing the evolutionary dynamics of cancer proliferation in single-cell clones with SPRINTER.Nature genetics · 2025Article
- Sir2 and Fun30 regulate ribosomal DNA replication timing via MCM helicase positioning and nucleosome occupancy.bioRxiv : the preprint server for biology · 2024Article
- Inferring replication timing and proliferation dynamics from single-cell DNA sequencing data.Nature communications · 2024Article
- Ultrasensitive plasma-based monitoring of tumor burden using machine-learning-guided signal enrichment.Nature medicine · 2024Article
- Unveiling human origins of replication using deep learning: accurate prediction and comprehensive analysis.Briefings in bioinformatics · 2023Article
- Giemsa-negative chromosome bands preferentially recombine in cancer-associated translocations and gene fusions.Genes, chromosomes & cancer · 2023Article
- Chromosomal Rearrangements and Altered Nuclear Organization: Recent Mechanistic Models in Cancer.Cancers · 2021Review
- DNA polymerase zeta contributes to heterochromatin replication to prevent genome instability.The EMBO journal · 2021Article
- RIF1 Links Replication Timing with Fork Reactivation and DNA Double-Strand Break Repair.International journal of molecular sciences · 2021Review
- The CRL4DTL E3 ligase induces degradation of the DNA replication initiation factor TICRR/TRESLIN specifically during S phase.Nucleic acids research · 2021Article
- Analysis of gene expression and mutation data points on contribution of transcription to the mutagenesis by APOBEC enzymes.NAR cancer · 2021Article
- Mammalian DNA Replication Timing.Cold Spring Harbor perspectives in biology · 2021Review
3 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Normal cellular division requires that the genome be faithfully replicated to ensure that unaltered genomic information is passed from one generation to the next. DNA replication initiates from thousands of origins scattered throughout the genome every cell cycle; however, not all origins initiate replication at the same time. A vast amount of work over the years indicates that different origins along each eukaryotic chromosome are activated in early, middle or late S phase. This temporal control of DNA replication is referred to as the replication-timing program. The replication-timing program represents a very stable epigenetic feature of chromosomes. Recent evidence has indicated that the replication-timing program can influence the spatial distribution of mutagenic events such that certain regions of the genome experience increased spontaneous mutagenesis compared to surrounding regions. This influence has helped shape the genomes of humans and other multicellular organisms and can affect the distribution of mutations in somatic cells. It is also becoming clear that the replication-timing program is deregulated in many disease states, including cancer. Aberrant DNA replication timing is associated with changes in gene expression, changes in epigenetic modifications and an increased frequency of structural rearrangements. Furthermore, certain replication timing changes can directly lead to overt genomic instability and may explain unique mutational signatures that are present in cells that have undergone the recently described processes of "chromothripsis" and "kataegis". In this review, we will discuss how the normal replication timing program, as well as how alterations to this program, can contribute to the evolution of the genomic landscape in normal and cancerous cells.
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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.