ArticlePloS one2014
Clinical and biochemical function of polymorphic NR0B1 GGAA-microsatellites in Ewing sarcoma: a report from the Children's Oncology Group.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 39 citations in OpenAlex.
- A Drosophila Study Model for EWS::FLI1-Induced Molecular Pathways.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Ancient and animal-specific regulatory modes of EWS::FLI1 revealed by a minimal yeast model.PNAS nexus · 2026Article
- Long-read analysis of tetrameric microsatellites with vmwhere supports GGAA repeat length-dependent chromatin state association in Ewing sarcoma.bioRxiv : the preprint server for biology · 2026Article
- EWS/FLI1 Characterization, Activation, Repression, Target Genes and Therapeutic Opportunities in Ewing Sarcoma.International journal of molecular sciences · 2023Review
- Targeted Therapy for EWS-FLI1 in Ewing Sarcoma.Cancers · 2023Review
- ETV6 dependency in Ewing sarcoma by antagonism of EWS-FLI1-mediated enhancer activation.Nature cell biology · 2023Article
- Systematic multi-omics cell line profiling uncovers principles of Ewing sarcoma fusion oncogene-mediated gene regulation.Cell reports · 2022Article
- Mitochondrial DNA haplogroup, genetic ancestry, and susceptibility to Ewing sarcoma.Mitochondrion · 2022Article
- EWS/FLI mediated reprogramming of 3D chromatin promotes an altered transcriptional state in Ewing sarcoma.Nucleic acids research · 2022Article
- Human EWS-FLI protein recapitulates in Drosophila the neomorphic functions that induce Ewing sarcoma tumorigenesis.PNAS nexus · 2022Article
- Epigenetic and Transcriptional Signaling in Ewing Sarcoma-Disease Etiology and Therapeutic Opportunities.Biomedicines · 2022Review
- Polymorphic variants ofFrontiers in oncology · 2022Article
- Loci-specific phase separation of FET fusion oncoproteins promotes gene transcription.Nature communications · 2021Article
- Review: Ewing Sarcoma Predisposition.Pathology oncology research : POR · 2020Review
- Oncogenic hijacking of a developmental transcription factor evokes vulnerability toward oxidative stress in Ewing sarcoma.Nature communications · 2020Article
- SOX6: a double-edged sword for Ewing sarcoma.Molecular & cellular oncology · 2020Article
- Gene expression and immunohistochemical analyses identify SOX2 as major risk factor for overall survival and relapse in Ewing sarcoma patients.EBioMedicine · 2019Article
- Transcriptomic analysis functionally maps the intrinsically disordered domain of EWS/FLI and reveals novel transcriptional dependencies for oncogenesis.Genes & cancer · 2019Article
- PAX7 expression in sarcomas bearing the EWSR1-NFATC2 translocation.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019Article
- Are EWSR1-NFATc2-positive sarcomas really Ewing sarcomas?Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
Corrections and comments
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Authors and funding
15 authors at 8 institutions in 1 country.
Funding
Abstract
backgroundThe genetics involved in Ewing sarcoma susceptibility and prognosis are poorly understood. EWS/FLI and related EWS/ETS chimeras upregulate numerous gene targets via promoter-based GGAA-microsatellite response elements. These microsatellites are highly polymorphic in humans, and preliminary evidence suggests EWS/FLI-mediated gene expression is highly dependent on the number of GGAA motifs within the microsatellite.
objectivesHere we sought to examine the polymorphic spectrum of a GGAA-microsatellite within the NR0B1 promoter (a critical EWS/FLI target) in primary Ewing sarcoma tumors, and characterize how this polymorphism influences gene expression and clinical outcomes.
resultsA complex, bimodal pattern of EWS/FLI-mediated gene expression was observed across a wide range of GGAA motifs, with maximal expression observed in constructs containing 20-26 GGAA motifs. Relative to white European and African controls, the NR0B1 GGAA-microsatellite in tumor cells demonstrated a strong bias for haplotypes containing 21-25 GGAA motifs suggesting a relationship between microsatellite function and disease susceptibility. This selection bias was not a product of microsatellite instability in tumor samples, nor was there a correlation between NR0B1 GGAA-microsatellite polymorphisms and survival outcomes.
conclusionsThese data suggest that GGAA-microsatellite polymorphisms observed in human populations modulate EWS/FLI-mediated gene expression and may influence disease susceptibility in Ewing sarcoma.
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