ArticleOncogene2002
Cloning and characterization of the common fragile site FRA6F harboring a replicative senescence gene and frequently deleted in human tumors.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 84 citations in OpenAlex.
- Cyclin C promotes pancreatic developmentand suppresses cancer initiation by maintenance of the autophagy-lysosome pathway.iScience · 2026Article
- Review
- Chromosomal Location of Genes Differentially Expressed in Tumor Cells Surviving High-Dose X-ray Irradiation: A Preliminary Study on Radio-Fragile Sites.Current issues in molecular biology · 2021Article
- Small RNAs, Big Diseases.International journal of molecular sciences · 2020Review
- Impaired Replication Timing Promotes Tissue-Specific Expression of Common Fragile Sites.Genes · 2020Article
- Double-Edged Sword of Tumour Suppressor Genes in Schizophrenia.Frontiers in molecular neuroscience · 2019Review
- Fragility Extraordinaire: Unsolved Mysteries of Chromosome Fragile Sites.Advances in experimental medicine and biology · 2017Review
- Characterization of chromosomal translocation breakpoint sequences in solid tumours: "an in silico analysis".The open medical informatics journal · 2015Article
- Article
- Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?Cellular and molecular life sciences : CMLS · 2014Review
- Molecular characterization of common fragile sites as a strategy to discover cancer susceptibility genes.Cellular and molecular life sciences : CMLS · 2014Review
- Common fragile sites: genomic hotspots of DNA damage and carcinogenesis.International journal of molecular sciences · 2012Review
- Genomic vulnerability to LINE-1 hypomethylation is a potential determinant of the clinicogenetic features of multiple myeloma.Genome medicine · 2012Article
- Translesion DNA synthesis in the context of cancer research.Cancer cell international · 2011Article
- A BEN-domain-containing protein associates with heterochromatin and represses transcription.Journal of cell science · 2011Article
- Schizophrenia, cancer and obstetric complications in an evolutionary perspective-an empirically based hypothesis.Psychiatry investigation · 2011Article
- DNA polymerases and cancer.Nature reviews. Cancer · 2011Review
- Mechanisms of genomic instabilities underlying two common fragile-site-associated loci, PARK2 and DMD, in germ cell and cancer cell lines.American journal of human genetics · 2010Article
- Article
- Inhibition of topoisomerase I prevents chromosome breakage at common fragile sites.DNA repair · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The common fragile site FRA6F, located at 6q21, is an extended region of about 1200 kb, with two hot spots of breakage each spanning about 200 kb. Transcription mapping of the FRA6F region identified 19 known genes, 10 within the FRA6F interval and nine in a proximal or distal position. The nucleotide sequence of FRA6F is rich in repetitive elements (LINE1 and LINE2, Alu, MIR, MER and endogenous retroviral sequences) as well as in matrix attachment regions (MARs), and shows several DNA segments with increased helix flexibility. We found that tight clusters of stem-loop structures were localized exclusively in the two regions with greater frequency of breakage. Chromosomal instability at FRA6F probably depends on a complex interaction of different factors, involving regions of greater DNA flexibility and MARs. We propose an additional mechanism of fragility at FRA6F, based on stem-loop structures which may cause delay or arrest in DNA replication. A senescence gene likely maps within FRA6F, as suggested by detection of deletion and translocation breakpoints involving this fragile site in immortal human-mouse cell hybrids and in SV40-immortalized human fibroblasts containing a human chromosome 6 deleted at q21. Deletion breakpoints within FRA6F are common in several types of human leukemias and solid tumors, suggesting the presence of a tumor suppressor gene in the region. Moreover, a gene associated to hereditary schizophrenia maps within FRA6F. Therefore, FRA6F may represent a landmark for the identification and cloning of genes involved in senescence, leukemia, cancer and schizophrenia.
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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.