| Both isoforms of the EWS/WT1 fusion protein can function as an oncogene in desmoplastic small round cell tumors. | None |
| The oncogenic properties of EWS/WT1 of desmoplastic small round cell tumors are unmasked by loss of p53 in murine embryonic fibroblasts. | None |
| EWS-FLI1 establishes an oncogenic regulatory program governing both tumor survival and differentiation. | None |
| RNA helicase A activity is inhibited by oncogenic transcription factor EWS-FLI1. | None |
| Epigenome mapping reveals distinct modes of gene regulation and widespread enhancer reprogramming by the oncogenic fusion protein EWS-FLI1. | None |
| Oncogenic fusion protein EWS-FLI1 is a network hub that regulates alternative splicing. | None |
| These experiments establish systemic alternative splicing as an oncogenic process modulated by EWS-FLI1. | None |
| Fusion of short fragments of EWSR1 to FLI1 is sufficient to recapitulate BAF complex retargeting and EWS-FLI1 activities; studies thus demonstrate that the physical properties of prion-like domains can retarget critical chromatin regulatory complexes to establish and maintain oncogenic gene expression programs. | None |
| Promoters containing ATF-binding sites are de-regulated in cells that express the EWS/ATF1 oncogene. | None |
| A novel effector domain from the RNA-binding protein TLS or EWS is required for oncogenic transformation by CHOP. | None |
| Chromosome translocation-mediated conversion of a tumor suppressor gene into a dominant oncogene: fusion of EWS1 to WT1 in desmoplastic small round cell tumors. | None |
| The DNA binding domains of the WT1 tumor suppressor gene product and chimeric EWS/WT1 oncoprotein are functionally distinct. | None |
| MMSP tumor cells expressing the EWS/ATF1 oncogene do not support cAMP-inducible transcription. | None |
| The desmoplastic small round cell tumor t(11;22) translocation produces EWS/WT1 isoforms with differing oncogenic properties. | None |