ArticleGenome medicine2010
Downstream EWS/FLI1 - upstream Ewing's sarcoma.
Article in Genome medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 64 citations in OpenAlex.
- A Practical Compass to Biological Digital Resources and Omics Integration in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Pediatric sarcomas: challenges and opportunities.Genes & development · 2026Review
- EWS-FLI1 and Activator Protein-1 (AP-1) Reciprocally Regulate Extracellular-Matrix Proteins in Ewing sarcoma Cells.International journal of molecular sciences · 2024Article
- Recurrent Intracranial Ewing Sarcoma.Ochsner journal · 2024Article
- Auranofin and reactive oxygen species inhibit protein synthesis and regulate the level of the PLK1 protein in Ewing sarcoma cells.Frontiers in oncology · 2024Article
- Dissociation protocols used for sarcoma tissues bias the transcriptome observed in single-cell and single-nucleus RNA sequencing.BMC cancer · 2023Article
- Review
- Ewing sarcoma from molecular biology to the clinic.Frontiers in cell and developmental biology · 2023Review
- Polymorphic variants ofFrontiers in oncology · 2022Article
- Chromatin Immunoprecipitation Followed by Next-Generation Sequencing (ChIP-Seq) Analysis in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Identifying the druggable interactome of EWS-FLI1 reveals MCL-1 dependent differential sensitivities of Ewing sarcoma cells to apoptosis inducers.Oncotarget · 2018Article
- Using biology to guide the treatment of sarcomas and aggressive connective-tissue tumours.Nature reviews. Clinical oncology · 2018Review
- EWS-FLI1 perturbs MRTFB/YAP-1/TEAD target gene regulation inhibiting cytoskeletal autoregulatory feedback in Ewing sarcoma.Oncogene · 2017Article
- Inhibition of CHK1 sensitizes Ewing sarcoma cells to the ribonucleotide reductase inhibitor gemcitabine.Oncotarget · 2017Article
- Gene expression signature based screening identifies ribonucleotide reductase as a candidate therapeutic target in Ewing sarcoma.Oncotarget · 2016Article
- Englerin A Inhibits EWS-FLI1 DNA Binding in Ewing Sarcoma Cells.The Journal of biological chemistry · 2016Article
- Targeting the epigenetic readers in Ewing sarcoma inhibits the oncogenic transcription factor EWS/Fli1.Oncotarget · 2016Article
- EWS-FLI1 employs an E2F switch to drive target gene expression.Nucleic acids research · 2015Article
- Epigenome mapping reveals distinct modes of gene regulation and widespread enhancer reprogramming by the oncogenic fusion protein EWS-FLI1.Cell reports · 2015Article
- Structure-function based molecular relationships in Ewing's sarcoma.BioMed research international · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ewing's sarcoma family tumors are a good example of how genome research has advanced our understanding of the molecular pathogenesis of an otherwise enigmatic disease. This group of embryonal bone tumors is characterized by the expression of a chimeric ETS-family oncogene, predominantly EWS/FLI1. There is now convincing evidence for a mesenchymal descent from an early pluripotent progenitor. EWS/FLI1 has been shown to drive proliferation of Ewing's sarcoma cells and block most of the differentiation potential except for a partial neural gene expression program. The EWS/FLI1 fusion protein acts mainly as a gene activator, directly interacting with chromatin at two kinds of binding site: distant enhancers enriched in GGAA microsatellites, and proximal promoters containing classical ETS-binding motifs and recognition motifs for other transcription factors. EWS/FLI1 also represses a large number of genes, mainly indirectly, presumably by altering microRNA expression and epigenetic mechanisms, and potentially affecting post-transcriptional gene regulation. Modulation of EWS/FLI1 expression is not only a desirable therapeutic goal, but may also occur under physiological conditions and influence the course of the disease.
Identifiers
What Socratic 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 Socratic graph.