ArticleCurrent genomics2010
DNA instability at chromosomal fragile sites in cancer.
Article in Current genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 97 citations in OpenAlex.
- Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025Review
- A post-irradiation-induced replication stress promotes RET proto-oncogene breakage.European thyroid journal · 2024Article
- DNA fragility at topologically associated domain boundaries is promoted by alternative DNA secondary structure and topoisomerase II activity.Nucleic acids research · 2024Article
- Time is ticking faster for long genes in aging.Trends in genetics : TIG · 2024Review
- Article
- Different classes of genomic inserts contribute to human antibody diversity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Functional mapping of PHF6 complexes in chromatin remodeling, replication dynamics, and DNA repair.Blood · 2022Article
- Unscrambling cancer genomes via integrated analysis of structural variation and copy number.Cell genomics · 2022Article
- Fragile sites, chromosomal lesions, tandem repeats, and disease.Frontiers in genetics · 2022Review
- Chromosomal Instability at Fragile Sites in Blue Foxes, Silver Foxes, and Their Interspecific Hybrids.Animals : an open access journal from MDPI · 2021Article
- Seminal plasma miRNAs in Klinefelter syndrome and in obstructive and non-obstructive azoospermia.Molecular biology reports · 2020Article
- Article
- Assessment of chromosome stability in boars.PloS one · 2020Article
- Genome-wide mapping and profiling of γH2AX binding hotspots in response to different replication stress inducers.BMC genomics · 2019Article
- BLM prevents instability of structure-forming DNA sequences at common fragile sites.PLoS genetics · 2018Article
- Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress.International journal of molecular sciences · 2018Review
- Pan-Cancer Analysis Reveals Differential Susceptibility of Bidirectional Gene Promoters to DNA Methylation, Somatic Mutations, and Copy Number Alterations.International journal of molecular sciences · 2018Article
- G2-seq: A High Throughput Sequencing-based Technique for Identifying Late Replicating Regions of the Genome.Journal of visualized experiments : JoVE · 2018Article
- Identifying RNA splicing factors usingOpen biology · 2018Article
- Karyotype reshufflings of Festuca pratensis × Lolium perenne hybrids.Protoplasma · 2018Article
4 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Human chromosomal fragile sites are specific genomic regions which exhibit gaps or breaks on metaphase chromosomes following conditions of partial replication stress. Fragile sites often coincide with genes that are frequently rearranged or deleted in human cancers, with over half of cancer-specific translocations containing breakpoints within fragile sites. But until recently, little direct evidence existed linking fragile site breakage to the formation of cancer-causing chromosomal aberrations. Studies have revealed that DNA breakage at fragile sites can induce formation of RET/PTC rearrangements, and deletions within the FHIT gene, resembling those observed in human tumors. These findings demonstrate the important role of fragile sites in cancer development, suggesting that a better understanding of the molecular basis of fragile site instability is crucial to insights in carcinogenesis. It is hypothesized that under conditions of replication stress, stable secondary structures form at fragile sites and stall replication fork progress, ultimately resulting in DNA breaks. A recent study examining an FRA16B fragment confirmed the formation of secondary structure and DNA polymerase stalling within this sequence in vitro, as well as reduced replication efficiency and increased instability in human cells. Polymerase stalling during synthesis of FRA16D has also been demonstrated. The ATR DNA damage checkpoint pathway plays a critical role in maintaining stability at fragile sites. Recent findings have confirmed binding of the ATR protein to three regions of FRA3B under conditions of mild replication stress. This review will discuss recent advances made in understanding the role and mechanism of fragile sites in cancer development.
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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.