ArticlePloS one2013
DNA topoisomerases participate in fragility of the oncogene RET.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- Article
- DNA fragility at topologically associated domain boundaries is promoted by alternative DNA secondary structure and topoisomerase II activity.Nucleic acids research · 2024Article
- Review
- Assessing acute myeloid leukemia susceptibility in rearrangement-driven patients by DNA breakage at topoisomerase II and CCCTC-binding factor/cohesin binding sites.Genes, chromosomes & cancer · 2021Article
- Effects of Topically Applied Betulinic Acid and NVX-207 on Melanocytic Tumors in 18 Horses.Animals : an open access journal from MDPI · 2021Article
- The relationship between chimeric RNAs and gene fusions: Potential implications of reciprocity in cancer.Journal of genetics and genomics = Yi chuan xue bao · 2020Article
- Topoisomerase II contributes to DNA secondary structure-mediated double-stranded breaks.Nucleic acids research · 2020Article
- Review
- Review
- DNA fragile site breakage as a measure of chemical exposure and predictor of individual susceptibility to form oncogenic rearrangements.Carcinogenesis · 2017Article
- Linking Pesticide Exposure with Pediatric Leukemia: Potential Underlying Mechanisms.International journal of molecular sciences · 2016Review
- Molecular Process Producing Oncogene Fusion in Lung Cancer Cells by Illegitimate Repair of DNA Double-Strand Breaks.Biomolecules · 2015Review
- Environmental and chemotherapeutic agents induce breakage at genes involved in leukemia-causing gene rearrangements in human hematopoietic stem/progenitor cells.Mutation research · 2015Article
- DNA secondary structure at chromosomal fragile sites in human disease.Current genomics · 2015Article
- Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?Cellular and molecular life sciences : CMLS · 2014Review
- RET revisited: expanding the oncogenic portfolio.Nature reviews. Cancer · 2014Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Fragile site breakage was previously shown to result in rearrangement of the RET oncogene, resembling the rearrangements found in thyroid cancer. Common fragile sites are specific regions of the genome with a high susceptibility to DNA breakage under conditions that partially inhibit DNA replication, and often coincide with genes deleted, amplified, or rearranged in cancer. While a substantial amount of work has been performed investigating DNA repair and cell cycle checkpoint proteins vital for maintaining stability at fragile sites, little is known about the initial events leading to DNA breakage at these sites. The purpose of this study was to investigate these initial events through the detection of aphidicolin (APH)-induced DNA breakage within the RET oncogene, in which 144 APH-induced DNA breakpoints were mapped on the nucleotide level in human thyroid cells within intron 11 of RET, the breakpoint cluster region found in patients. These breakpoints were located at or near DNA topoisomerase I and/or II predicted cleavage sites, as well as at DNA secondary structural features recognized and preferentially cleaved by DNA topoisomerases I and II. Co-treatment of thyroid cells with APH and the topoisomerase catalytic inhibitors, betulinic acid and merbarone, significantly decreased APH-induced fragile site breakage within RET intron 11 and within the common fragile site FRA3B. These data demonstrate that DNA topoisomerases I and II are involved in initiating APH-induced common fragile site breakage at RET, and may engage the recognition of DNA secondary structures formed during perturbed DNA replication.
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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.