ArticleNature communications2019
Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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Who cites it
69 citing papers in PubMed, 108 citations in OpenAlex.
- Article
- Article
- Towards implementation of precision medicine biomarkers in early detection and prognostication of prostate cancer.Cancer metastasis reviews · 2026Review
- ATF4 coordinates amino acid and nucleotide synthesis with selective protein translation to ensure proper DNA replication timing in leukemia cells.Nature communications · 2026Article
- DNMT1 loss leads to hypermethylation of a subset of late replicating domains by DNMT3A.PLoS genetics · 2026Article
- Transcription at an inducible common fragile site reveals replication origin strength hierarchy.Nucleic acids research · 2026Article
- The urinary eccDNA landscape in prostate cancer reveals associations with genome instability and vital roles in cancer progression.Journal of advanced research · 2025Article
- Evolutionarily recent transcription factors partake in human cell cycle regulation.Cell genomics · 2025Article
- Mitigating Cell Cycle Effects in Multi-Omics Data: Solutions and Analytical Frameworks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- T-DNAreader: fast and precise identification of T-DNA insertion sites in plant genomes using RNA sequencing data.Genome biology · 2025Article
- Centromeric transposable elements and epigenetic status drive karyotypic variation in the eastern hoolock gibbon.Cell genomics · 2025Article
- A sequence context-based approach for classifying tumor structural variants without paired normal samples.Cell reports methods · 2025Article
- Heterochromatin fidelity is a therapeutic vulnerability in lymphoma and other human cancers.bioRxiv : the preprint server for biology · 2025Article
- Methylomes of human CD4 and CD8 memory T lymphocytes reveal tissue-specific epigenetic signatures for maintenance and recall function.Immunity & inflammation · 2025Article
- Characterizing the evolutionary dynamics of cancer proliferation in single-cell clones with SPRINTER.Nature genetics · 2025Article
- Single-cell genomics breaks new ground in cell cycle detection.Nature genetics · 2025Article
- Multi-omics approaches reveal that diffuse midline gliomas present altered DNA replication and are susceptible to replication stress therapy.Genome biology · 2024Article
- UHRF1 ubiquitin ligase activity supports the maintenance of low-density CpG methylation.Nucleic acids research · 2024Article
- Genome-wide profiling of DNA repair proteins in single cells.Nature communications · 2024Article
- Inferring replication timing and proliferation dynamics from single-cell DNA sequencing data.Nature communications · 2024Article
9 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
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA replication timing is known to facilitate the establishment of the epigenome, however, the intimate connection between replication timing and changes to the genome and epigenome in cancer remain largely uncharacterised. Here, we perform Repli-Seq and integrated epigenome analyses and demonstrate that genomic regions that undergo long-range epigenetic deregulation in prostate cancer also show concordant differences in replication timing. A subset of altered replication timing domains are conserved across cancers from different tissue origins. Notably, late-replicating regions in cancer cells display a loss of DNA methylation, and a switch in heterochromatin features from H3K9me3-marked constitutive to H3K27me3-marked facultative heterochromatin. Finally, analysis of 214 prostate and 35 breast cancer genomes reveal that late-replicating regions are prone to cis and early-replication to trans chromosomal rearrangements. Together, our data suggests that the nature of chromosomal rearrangement in cancer is related to the spatial and temporal positioning and altered epigenetic states of early-replicating compared to late-replicating loci.
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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.