ArticleBMC cancer2020
Loss of Stag2 cooperates with EWS-FLI1 to transform murine Mesenchymal stem cells.
Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Analysis of Migration and Invasion in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Emerging roles of cohesin-STAG2 in cancer.Oncogene · 2025Review
- Identification and validation of HOXC6 as a diagnostic biomarker for Ewing sarcoma: insights from machine learning algorithms andFrontiers in immunology · 2025Article
- Recent advances in sarcoma therapy: new agents, strategies and predictive biomarkers.Journal of hematology & oncology · 2024Review
- The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024Review
- Bioinformatic Analysis of Recurrent Genomic Alterations and Corresponding Pathway Alterations in Ewing Sarcoma.Journal of personalized medicine · 2023Article
- Children's Oncology Group's 2023 blueprint for research: Bone tumors.Pediatric blood & cancer · 2023Article
- Novel patient-derived models of desmoplastic small round cell tumor confirm a targetable dependency on ERBB signaling.Disease models & mechanisms · 2022Article
- Unraveling Ewing Sarcoma Tumorigenesis Originating from Patient-Derived Mesenchymal Stem Cells.Cancer research · 2021Article
- Article
- A cohesive look at leukemogenesis: The cohesin complex and other driving mutations in AML.Neoplasia (New York, N.Y.) · 2021Review
- Challenges in modeling EWS-FLI1-driven transgenic mouse model for Ewing sarcoma.American journal of translational research · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundEwing sarcoma is a malignancy of primitive cells, possibly of mesenchymal origin. It is probable that genetic perturbations other than EWS-FLI1 cooperate with it to produce the tumor. Sequencing studies identified STAG2 mutations in approximately 15% of cases in humans. In the present study, we hypothesize that loss of Stag2 cooperates with EWS-FLI1 in generating sarcomas derived from murine mesenchymal stem cells (MSCs).
methodsMice bearing an inducible EWS-FLI1 transgene were crossed to p53
resultsPrimary murine MSCs with the genotype EWS-FLI1 p53
conclusionLoss of Stag2 has a synergistic effect with EWS-FLI1 in the production of sarcomas from murine MSCs, but the mechanism may not relate to increased proliferation or chromosomal instability. Primary murine MSCs are resistant to transformation, and the combination of p53 null mutation, EWS-FLI1, and Stag2 inhibition does not confer immediate conversion of MSCs to sarcomas. Irradiation is necessary in this model, suggesting that perturbations of other genes beside Stag2 and p53 are likely to be essential in the development of EWS-FLI1-driven sarcomas from MSCs.
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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.