Transactivation of cyclin E gene by EWS-Fli1 and antitumor effects of cyclin dependent kinase inhibitor on Ewing's family tumor cells
Author:
Publisher
Wiley
Subject
Cancer Research,Oncology
Reference47 articles.
1. Biology of EWS/ETS fusions in Ewing's family tumors
2. Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumours
3. The Ewing's sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1.
4. Ewing sarcoma 11;22 translocation produces a chimeric transcription factor that requires the DNA-binding domain encoded by FLI1 for transformation.
5. Molecular Biology of the Ewing’s Sarcoma/Primitive Neuroectodermal Tumor Family
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1. Tumor-suppressive microRNA-152 inhibits the proliferation of Ewing’s sarcoma cells by targeting CDK5R1;Scientific Reports;2023-10-29
2. A logical model of Ewing sarcoma cell epithelial‐to‐mesenchymal transition supports the existence of hybrid cellular phenotypes;FEBS Letters;2023-08-28
3. Cell cycle arrest and apoptosis are early events in radiosensitization of EWS::FLI1 + Ewing sarcoma cells by Mithramycin A;International Journal of Radiation Biology;2023-04-20
4. Tumor-suppressive microRNA-152 inhibits the proliferation of Ewing’s sarcoma cells by targeting CDK5R1;2023-04-11
5. One oncogene, several vulnerabilities: EWS/FLI targeted therapies for Ewing sarcoma;Journal of Bone Oncology;2021-12
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