ArticleCancer research2014
Activation of SOX2 expression by BRD4-NUT oncogenic fusion drives neoplastic transformation in NUT midline carcinoma.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Trial
- NUT Carcinoma Arising in Stensen's Duct: First Reported Case and Literature Review.Head and neck pathology · 2026Review
- Shared PRAME epitopes are T-cell targets in NUT carcinoma.Journal for immunotherapy of cancer · 2026Article
- SOX2 is a dispensable modulator of NUT carcinoma oncogenesis in mice.Life science alliance · 2026Article
- International guidelines on the diagnosis and treatment of NUT carcinoma.Innovation (Cambridge (Mass.)) · 2026Review
- Immune biomarker landscape and fusion partner-phenotype associations in thoracic and head-and-neck NUT carcinoma.Frontiers in immunology · 2026Article
- Magnifying Glass on Sinonasal NUT Carcinoma Heterogeneity via Spatial Transcriptomics.Head & neck · 2026Article
- Hiding in plain sight: NUT carcinoma is an unrecognized subtype of squamous cell carcinoma of the lungs and head and neck.Nature reviews. Clinical oncology · 2025Review
- Article
- [Research Progress on Pathogenesis and Treatment of NUT Carcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- Top IHC/ISH Hacks for and Molecular Surrogates of Poorly Differentiated Sinonasal Small Round Cell Tumors.Head and neck pathology · 2024Review
- NovelJTO clinical and research reports · 2024Article
- The BRD4-NUT Fusion Alone Drives Malignant Transformation of NUT Carcinoma.Cancer research · 2023Article
- EZH2 synergizes with BRD4-NUT to drive NUT carcinoma growth through silencing of key tumor suppressor genes.bioRxiv : the preprint server for biology · 2023Article
- Characterization of molecular mechanisms driving Merkel cell polyomavirus oncogene transcription and tumorigenic potential.PLoS pathogens · 2023Article
- Nuclear protein in testis carcinoma of the lung.Translational oncology · 2023Review
- NUT Carcinoma of the Submandibular Gland: A Case at This Uncommon Site with Review of the Literature.Head and neck pathology · 2022Review
- Update from the 5th Edition of the World Health Organization Classification of Head and Neck Tumors: Nasal Cavity, Paranasal Sinuses and Skull Base.Head and neck pathology · 2022Review
- NUT Carcinoma: Clinicopathologic Features, Molecular Genetics and Epigenetics.Frontiers in oncology · 2022Review
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
BRD4 is implicated in the pathogenesis of a number of different cancers. It is also the target of translocation t(15;19) that accounts for the highly aggressive NUT midline carcinoma (NMC). We discovered that t(15;19) NMC cells display the ability to grow into stem cell-like spheres and express an exceptionally high level of the stem cell marker, SOX2. The BRD4-NUT fusion oncogene resulting from t(15;19) translocation is required for the abnormal activation of SOX2, which drives the stem cell-like proliferation and cellular transformation in NMC cells. SOX2 knockdown phenocopies the effects of BRD4-NUT inhibition, whereas ectopic SOX2 expression rescues the phenotype. The BRD4-NUT-induced abnormal SOX2 activation was observed in multiple NMC cell lines as well as in NMC primary tumors. We further demonstrate that BRD4-NUT oncoprotein recruits p300 to stimulate transcription activation and that inhibition of p300 represses SOX2 transcription in NMC cells. These studies identify this stem cell marker as a novel BRD4-NUT target that supports the highly aggressive transforming activity of t(15;19) carcinomas. Our study provides new mechanistic insights for understanding how alteration of BRD4 function by BRD4-NUT oncogene leads to the highly malignant NMC carcinoma. Because abnormal stem cell self-renewal is frequently observed during tumor formation and metastasis, the aberrant stem cell-like proliferation associated with BRD4 dysregulation observed in NMC carcinoma may have implications for studying the oncogenic mechanism of other BRD4-associated tumors.
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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.