ArticleGenes, chromosomes & cancer2013
Common chromosome fragile sites in human and murine epithelial cells and FHIT/FRA3B loss-induced global genome instability.
Article in Genes, chromosomes & cancer, 2013. 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 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
37 citing papers in PubMed, 60 citations in OpenAlex.
- Identification of Deregulated miRNAs and mRNAs Involved in Tumorigenesis and Detection of Glioblastoma Patients Applying Next-Generation RNA Sequencing.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The Clinical Role of miRNAs in the Development and Treatment of Glioblastoma.International journal of molecular sciences · 2025Review
- Review
- Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.Emerging topics in life sciences · 2023Article
- Review
- microRNAs (miRNAs) in Glioblastoma Multiforme (GBM)-Recent Literature Review.International journal of molecular sciences · 2023Review
- Global landscape of replicative DNA polymerase usage in the human genome.Nature communications · 2022Article
- Renal hypoxia-HIF-PHD-EPO signaling in transition metal nephrotoxicity: friend or foe?Archives of toxicology · 2022Review
- Locus-specific transcription silencing at the FHIT gene suppresses replication stress-induced copy number variant formation and associated replication delay.Nucleic acids research · 2021Article
- Genomic Adaption and Mutational Patterns in a HaCaT Subline Resistant to Alkylating Agents and Ionizing Radiation.International journal of molecular sciences · 2021Article
- Genome-wide high-resolution mapping of mitotic DNA synthesis sites and common fragile sites by direct sequencing.Cell research · 2020Article
- Common Fragile Sites Are Characterized by Faulty Condensin Loading after Replication Stress.Cell reports · 2020Article
- 3D genome organization contributes to genome instability at fragile sites.Nature communications · 2020Article
- Impaired Replication Timing Promotes Tissue-Specific Expression of Common Fragile Sites.Genes · 2020Article
- AT-dinucleotide rich sequences drive fragile site formation.Nucleic acids research · 2019Article
- The role of fork stalling and DNA structures in causing chromosome fragility.Genes, chromosomes & cancer · 2019Review
- DNA replication stress: oncogenes in the spotlight.Genetics and molecular biology · 2019Article
- Genome-wide Identification of Structure-Forming Repeats as Principal Sites of Fork Collapse upon ATR Inhibition.Molecular cell · 2018Article
- Pathways for maintenance of telomeres and common fragile sites during DNA replication stress.Open biology · 2018Review
- Karyotype reshufflings of Festuca pratensis × Lolium perenne hybrids.Protoplasma · 2018Article
Corrections and comments
- Erratum issuedErratum.2019
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Chromosomal positions of common fragile sites differ in lymphoblasts and fibroblasts, with positions dependent on the epigenetically determined density of replication origins at these loci. Because rearrangement of fragile loci and associated loss of fragile gene products are hallmarks of cancers, we aimed to map common fragile sites in epithelial cells, from which most cancers derive. Among the five most frequently activated sites in human epithelial cells were chromosome bands 2q33 and Xq22.1, which are not among top fragile sites identified in lymphoblasts or fibroblasts. FRA16D at 16q23 was among the top three fragile sites in the human epithelial cells examined, as it is in lymphoblasts and fibroblasts, while FRA3B at 3p14.2, the top fragile locus in lymphoblasts, was not fragile in most epithelial cell lines tested. Epithelial cells exhibited varying hierarchies of fragile sites; some frequent epithelial cell fragile sites are apparently not frequently altered in epithelial cancers and sites that are frequently deleted in epithelial cancers are not necessarily among the most fragile. Since we have reported that loss of expression of the FRA3B-encoded FHIT protein causes increased replication stress-induced DNA damage, we also examined the effect of FHIT-deficiency on markers of genome instability in epithelial cells. FHIT-deficient cells exhibited increases in fragile breaks and in γH2AX and 53BP1 foci in G1 phase cells, confirming in epithelial cells that the FHIT gene and encompassing FRA3B, is a "caretaker gene" necessary for maintenance of genome stability.
Indexed as
Identifiers
What OpenQuestion holds
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.