ArticleDNA repair2010
Inhibition of topoisomerase I prevents chromosome breakage at common fragile sites.
Article in DNA repair, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 31 citations in OpenAlex.
- Impact of treatment history on drug resistance of metastatic colorectal cancer organoids.iScience · 2025Article
- TDP1 phosphorylation by CDK1 in mitosis promotes MUS81-dependent repair of trapped Top1-DNA covalent complexes.The EMBO journal · 2024Article
- Fragile sites, chromosomal lesions, tandem repeats, and disease.Frontiers in genetics · 2022Review
- Impaired Replication Timing Promotes Tissue-Specific Expression of Common Fragile Sites.Genes · 2020Article
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
- Review
- Pyrimidine Pool Disequilibrium Induced by a Cytidine Deaminase Deficiency Inhibits PARP-1 Activity, Leading to the Under Replication of DNA.PLoS genetics · 2015Article
- DNA secondary structure at chromosomal fragile sites in human disease.Current genomics · 2015Article
- Topoisomerase-I PS506 as a Dual Function Cancer Biomarker.PloS one · 2015Article
- Interplay between genetic and epigenetic factors governs common fragile site instability in cancer.Cellular and molecular life sciences : CMLS · 2014Review
- Chromosome fragility and the abnormal replication of the FMR1 locus in fragile X syndrome.Human molecular genetics · 2014Article
- Genome-wide high-resolution mapping of chromosome fragile sites in Saccharomyces cerevisiae.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- DNA double-strand breaks coupled with PARP1 and HNRNPA2B1 binding sites flank coordinately expressed domains in human chromosomes.PLoS genetics · 2013Article
- Separation of intra-S checkpoint protein contributions to DNA replication fork protection and genomic stability in normal human fibroblasts.Cell cycle (Georgetown, Tex.) · 2013Article
- Article
- Article
- Genomic rearrangements at the FRA2H common fragile site frequently involve non-homologous recombination events across LTR and L1(LINE) repeats.Human genetics · 2012Article
- Chromatin changes in the development and pathology of the Fragile X-associated disorders and Friedreich ataxia.Biochimica et biophysica acta · 2012Review
- Article
- Common fragile sites: genomic hotspots of DNA damage and carcinogenesis.International journal of molecular sciences · 2012Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Common fragile sites are loci that preferentially form gaps and breaks on metaphase chromosomes when DNA synthesis is perturbed, particularly after treatment with the DNA polymerase inhibitor, aphidicolin. We and others have identified several cell cycle checkpoint and DNA repair proteins that influence common fragile site stability. However, the initial events underlying fragile site breakage remain poorly understood. We demonstrate here that aphidicolin-induced gaps and breaks at fragile sites are prevented when cells are co-treated with low concentrations of the topoisomerase I inhibitor, camptothecin. This reduction in breakage is accompanied by a reduction in aphidicolin-induced RPA foci, CHK1 and RPA2 phosphorylation, and PCNA monoubiquitination, indicative of reduced levels of single stranded DNA. Furthermore, camptothecin reduces spontaneous fragile site breakage seen in cells lacking ATR, even in the absence of aphidicolin. These data from cultured human cells demonstrate that topoisomerase I activity is required for DNA common fragile site breaks and suggest that polymerase-helicase uncoupling is a key initial event in this process.
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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.