ArticleCancer research2008
EWS-FLI1 induces developmental abnormalities and accelerates sarcoma formation in a transgenic mouse model.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 93 citations in OpenAlex.
- Genetically Modified Mouse Models for Sarcoma Research: A Comprehensive Review.Current oncology reports · 2025Review
- YAP1 is a key regulator of EWS::FLI1-dependent malignant transformation upon IGF-1-mediated reprogramming of bone mesenchymal stem cells.Cell reports · 2025Article
- Primary Bone Tumors and Breast Cancer-Induced Bone Metastases: In Vivo Animal Models and New Alternative Approaches.Biomedicines · 2024Review
- Preclinical models for the study of pediatric solid tumors: focus on bone sarcomas.Frontiers in oncology · 2024Review
- Mesenchymal loss of p53 alters stem cell capacity and models human soft tissue sarcoma traits.Stem cell reports · 2023Article
- Human EWS-FLI protein recapitulates in Drosophila the neomorphic functions that induce Ewing sarcoma tumorigenesis.PNAS nexus · 2022Article
- Latest developments in the pathobiology of Ewing sarcoma.Journal of bone oncology · 2022Review
- Fli1 Promotes Vascular Morphogenesis by Regulating Endothelial Potential of Multipotent Myogenic Progenitors.Circulation research · 2021Article
- Challenges in modeling EWS-FLI1-driven transgenic mouse model for Ewing sarcoma.American journal of translational research · 2021Review
- Extracellular Vesicles in Reprogramming of the Ewing Sarcoma Tumor Microenvironment.Frontiers in cell and developmental biology · 2021Review
- CDKs in Sarcoma: Mediators of Disease and Emerging Therapeutic Targets.International journal of molecular sciences · 2020Review
- Article
- Newly identified LMO3-BORCS5 fusion oncogene in Ewing sarcoma at relapse is a driver of tumor progression.Oncogene · 2019Article
- Discovery of New Fusion Transcripts in a Cohort of Pediatric Solid Cancers at Relapse and Relevance for Personalized Medicine.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Small animal models for the study of bone sarcoma pathogenesis:characteristics, therapeutic interests and limitations.Journal of bone oncology · 2018Review
- Translocations involving ETS family proteins in human cancer.Integrative cancer science and therapeutics · 2018Article
- Combined experience of six independent laboratories attempting to create an Ewing sarcoma mouse model.Oncotarget · 2017Article
- Relevance of Fusion Genes in Pediatric Cancers: Toward Precision Medicine.Molecular therapy. Nucleic acids · 2017Review
- Widespread Chromatin Accessibility at Repetitive Elements Links Stem Cells with Human Cancer.Cell reports · 2016Article
- Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation.Cell death & disease · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Ewing's sarcoma is characterized by the t(11;22)(q24:q12) reciprocal translocation. To study the effects of the fusion gene EWS-FLI1 on development and tumor formation, a transgenic mouse model was created. A strategy of conditional expression was used to limit the potentially deleterious effects of EWS-FLI1 to certain tissues. In the absence of Cre recombinase, EWS-FLI1 was not expressed in the EWS-FLI1 transgenic mice, and they had a normal phenotype. When crossed to the Prx1-Cre transgenic mouse, which expresses Cre recombinase in the primitive mesenchymal cells of the embryonic limb bud, the EF mice were noted to have a number of developmental defects of the limbs. These included shortening of the limbs, muscle atrophy, cartilage dysplasia, and immature bone. By itself, EWS-FLI1 did not induce the formation of tumors in the EF transgenic mice. However, in the setting of p53 deletion, EWS-FLI1 accelerated the formation of sarcomas from a median time of 50 to 21 weeks. Furthermore, EWS-FLI1 altered the type of tumor that formed. Conditional deletion of p53 in mesenchymal cells (Prx1-Cre p53(lox/lox)) produced osteosarcomas as the predominant tumor. The presence of EWS-FLI1 shifted the tumor phenotype to a poorly differentiated sarcoma. The results taken together suggest that EWS-FLI1 inhibits normal limb development and accelerates the formation of poorly differentiated sarcomas.
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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 Socratic graph.