ReviewGenes, chromosomes & cancer2019
The role of fork stalling and DNA structures in causing chromosome fragility.
Review in Genes, chromosomes & cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed.
- Beyond the genetic code: orchestrating epigenetic and immune landscapes with multivalent mRNA-exosome vaccines.Precision clinical medicine · 2026Review
- Determinants of dicentric chromosome breakage inbioRxiv : the preprint server for biology · 2026Article
- Genetic and Epigenetic Mechanisms Underlying Reversible Adaptive Responses in Fungi.Journal of fungi (Basel, Switzerland) · 2026Review
- Cruciform-forming AT/TA repeats are acted upon by structure-selective endonucleases and Rad51 prior to repositioning to the nuclear periphery for repair.Nucleic acids research · 2026Article
- Non-B DNA structures and their contributions to genetic diversity, aging, and disease.Nucleic acids research · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- AAV Kills Dividing Cells by Depleting PARP1 and Other DNA Damage Response Proteins.bioRxiv : the preprint server for biology · 2025Article
- Mechanistic insights into 16p13.3 microdeletions encompassing TBC1D24 and ATP6V0C through advanced sequencing approaches.European journal of human genetics : EJHG · 2025Article
- RNA G‑Quadruplex Reprogramming with Guanine-Rich Antisense Oligonucleotides Inhibits Monoamine Oxidase B's Translation.ACS bio & med chem Au · 2025Article
- DNA replication timing reveals genome-wide features of transcription and fragility.Nature communications · 2025Article
- Non-canonical DNA in human and other ape telomere-to-telomere genomes.Nucleic acids research · 2025Article
- Non-canonical DNA in human and other ape telomere-to-telomere genomes.bioRxiv : the preprint server for biology · 2025Article
- DNA polymerase zeta can efficiently replicate structures formed by AT/TA repeat sequences and prevent their deletion.Nucleic acids research · 2025Article
- HSATII RNA-dependent triplex formation in early human embryogenesis as a potential mechanism for Y chromosome loss in Turner syndrome.Frontiers in molecular biosciences · 2025Article
- Utilizing insights of DNA repair machinery to discover MMEJ deletions and novel mechanisms.Nucleic acids research · 2024Article
- Advances on the Mechanisms and Therapeutic Strategies in Non-coding CGG Repeat Expansion Diseases.Molecular neurobiology · 2024Review
- Replication fork stalling in late S-phase elicits nascent strand degradation by DNA mismatch repair.Nucleic acids research · 2024Article
- FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation.Functional & integrative genomics · 2024Article
- Somatic and intergenerational G4C2 hexanucleotide repeat instability in a human C9orf72 knock-in mouse model.Nucleic acids research · 2024Article
7 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.
Funding
Abstract
Alternative non-B form DNA structures, also called secondary structures, can form in certain DNA sequences under conditions that produce single-stranded DNA, such as during replication, transcription, and repair. Direct links between secondary structure formation, replication fork stalling, and genomic instability have been found for many repeated DNA sequences that cause disease when they expand. Common fragile sites (CFSs) are known to be AT-rich and break under replication stress, yet the molecular basis for their fragility is still being investigated. Over the past several years, new evidence has linked both the formation of secondary structures and transcription to fork stalling and fragility of CFSs. How these two events may synergize to cause fragility and the role of nuclease cleavage at secondary structures in rare and CFSs are discussed here. We also highlight evidence for a new hypothesis that secondary structures at CFSs not only initiate fragility but also inhibit healing, resulting in their characteristic appearance.
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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 Socratic graph.