| BRD4-NUT fusion oncogene: a novel mechanism in aggressive carcinoma. | None |
| Midline carcinoma with t(15;19) and BRD4-NUT fusion oncogene in a 30-year-old female with response to docetaxel and radiotherapy. | None |
| Using a patient-derived cell line, the authors show that p300 sequestration into the chromatin-bound BRD4-NUT fusion protein foci is the principal oncogenic mechanism leading to p53 inactivation. | None |
| Perturbation of BRD4 protein function by BRD4-NUT protein abrogates cellular differentiation in NUT midline carcinoma. | None |
| study provides a novel mechanism by which the BRD4-NUT oncogene perturbs BRD4 functions to block cellular differentiation and to contribute to the oncogenic progression in the highly aggressive NUT midline carcinoma | None |
| The novel BRD4-NUT fusion in which Exon 15 of BRD4 was fused to Exon 2 of NUT encodes a functional protein that is central to the oncogenic mechanism in these cells. | None |
| Activation of SOX2 expression by BRD4-NUT oncogenic fusion drives neoplastic transformation in NUT midline carcinoma. | None |
| NSD3-NUT fusion oncoprotein in NUT midline carcinoma: implications for a novel oncogenic mechanism. | None |
| The involvement of the NSD3 methyltransferase as a component of the NUT fusion protein oncogenic complex identifies a new potential therapeutic target. | None |
| Data support a model in which BRD4-NUT-stimulated histone hyperacetylation recruits additional BRD4 and interacting partners to support transcriptional activation, which underlies the BRD4-NUT oncogenic mechanism in NMC. | None |