ArticleNucleic acids research2018
Developmental and cancer-associated plasticity of DNA replication preferentially targets GC-poor, lowly expressed and late-replicating regions.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 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.
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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
20 citing papers in PubMed, 55 citations in OpenAlex.
- Decoding DNA metabolism and its clinical relevance through the lens of high-throughput sequencing assays.Medical review (2021) · 2026Review
- The CGG triplet repeat binding protein 1 counteracts R-loop induced transcription-replication stress.EMBO reports · 2025Article
- The double life of mammalian DNA replication origins.Genes & development · 2025Review
- Genome-wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression.Genome biology · 2024Article
- Transcription elongation defects link oncogenic SF3B1 mutations to targetable alterations in chromatin landscape.Molecular cell · 2024Article
- Article
- The chromatin network helps prevent cancer-associated mutagenesis at transcription-replication conflicts.Nature communications · 2023Article
- Cohesin maintains replication timing to suppress DNA damage on cancer genes.Nature genetics · 2023Article
- Neural network and kinetic modelling of human genome replication reveal replication origin locations and strengths.PLoS computational biology · 2023Article
- Genome-wide measurement of DNA replication fork directionality and quantification of DNA replication initiation and termination with Okazaki fragment sequencing.Nature protocols · 2023Review
- OKseqHMM: a genome-wide replication fork directionality analysis toolkit.Nucleic acids research · 2023Article
- 3D chromatin connectivity underlies replication origin efficiency in mouse embryonic stem cells.Nucleic acids research · 2022Article
- Effects of replication domains on genome-wide UV-induced DNA damage and repair.PLoS genetics · 2022Article
- Determination of human DNA replication origin position and efficiency reveals principles of initiation zone organisation.Nucleic acids research · 2022Article
- The SWI/SNF chromatin remodeling complex helps resolve R-loop-mediated transcription-replication conflicts.Nature genetics · 2021Article
- Transcription shapes DNA replication initiation to preserve genome integrity.Genome biology · 2021Article
- Article
- Discovery and Protein Modeling Studies of Novel Compound Mutations Causing Resistance to Multiple Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Identification of new driver and passenger mutations within APOBEC-induced hotspot mutations in bladder cancer.Genome medicine · 2020Article
- Genomic methods for measuring DNA replication dynamics.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spatiotemporal program of metazoan DNA replication is regulated during development and altered in cancers. We have generated novel OK-seq, Repli-seq and RNA-seq data to compare the DNA replication and gene expression programs of twelve cancer and non-cancer human cell types. Changes in replication fork directionality (RFD) determined by OK-seq are widespread but more frequent within GC-poor isochores and largely disconnected from transcription changes. Cancer cell RFD profiles cluster with non-cancer cells of similar developmental origin but not with different cancer types. Importantly, recurrent RFD changes are detected in specific tumour progression pathways. Using a model for establishment and early progression of chronic myeloid leukemia (CML), we identify 1027 replication initiation zones (IZs) that progressively change efficiency during long-term expression of the BCR-ABL1 oncogene, being twice more often downregulated than upregulated. Prolonged expression of BCR-ABL1 results in targeting of new IZs and accentuation of previous efficiency changes. Targeted IZs are predominantly located in GC-poor, late replicating gene deserts and frequently silenced in late CML. Prolonged expression of BCR-ABL1 results in massive deletion of GC-poor, late replicating DNA sequences enriched in origin silencing events. We conclude that BCR-ABL1 expression progressively affects replication and stability of GC-poor, late-replicating regions during CML progression.
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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.