| BRD4 amplification in cancer has oncogenic potential; BRD4-amplified High-grade Serous Ovarian Cancer is a potential patient population that could benefit from BET inhibitors | ovarian, |
| BRD4-NUT fusion oncogene: a novel mechanism in aggressive carcinoma. | None |
| Abrogation of the interaction between P-TEFb and Brd4 thus provides a mechanism for E2-mediated repression of the viral oncogenes from the integrated viral genomes in cancer cells. | None |
| Genome-wide siRNA screen identifies SMCX, EP400, and Brd4 as E2-dependent regulators of human papillomavirus oncogene expression. | 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 |
| 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 |
| Mechanistic analysis of the role of bromodomain-containing protein 4 (BRD4) in BRD4-NUT oncoprotein-induced transcriptional activation. | None |
| The oncogenic BRD4-NUT chromatin regulator drives aberrant transcription within large topological domains. | None |
| A novel BRD4-NUT fusion in an undifferentiated sinonasal tumor highlights alternative splicing as a contributing oncogenic factor in NUT midline carcinoma. | None |
| This study reveals how cells undergoing oncogene-induced senescence acquire a distinctive enhancer landscape that includes formation of super-enhancers adjacent to immune-modulatory genes required for paracrine immune activation. This process links BRD4 and super-enhancers to a tumor-suppressive immune surveillance program that can be disrupted by small molecule inhibitors of the bromo and extra terminal domain family of | None |
| Thus, Brd4 activates human papillomavirus 16 transcription at this integration site, and strong selection for E6/E7 expression can drive the formation of a super-enhancer-like element to promote oncogenesis. | None |
| The BRD4-KDM5C-PTEN may be a new oncogenic pathway in CRPC development. | None |