MYC, a downstream target of BRD-NUT, is necessary and sufficient for the blockade of differentiation in NUT midline carcinoma. - Wikidata - awgldk - TriplyDB

MYC, a downstream target of BRD-NUT, is necessary and sufficient for the blockade of differentiation in NUT midline carcinoma.

MYC, a downstream target of BRD-NUT, is necessary and sufficient for the blockade of differentiation in NUT midline carcinoma.

http://www.wikidata.org/entity/Q37617063

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KATs in cancer: functions and therapies Acetylation Reader Proteins: Linking Acetylation Signaling to Genome Maintenance and Cancer Brd4 activates P-TEFb for RNA polymerase II CTD phosphorylation Targeting BET bromodomains for cancer treatment NSD3-NUT fusion oncoprotein in NUT midline carcinoma: implications for a novel oncogenic mechanism.Clinical Response of Carcinomas Harboring the BRD4-NUT Oncoprotein to the Targeted Bromodomain Inhibitor OTX015/MK-8628 Inhibition of BRD4 attenuates tumor cell self-renewal and suppresses stem cell signaling in MYC driven medulloblastoma.Activation of SOX2 expression by BRD4-NUT oncogenic fusion drives neoplastic transformation in NUT midline carcinoma.Inducible in vivo silencing of Brd4 identifies potential toxicities of sustained BET protein inhibition Mechanistic analysis of the role of bromodomain-containing protein 4 (BRD4) in BRD4-NUT oncoprotein-induced transcriptional activation.Primary Pulmonary NUT Midline Carcinoma: Clinical, Radiographic, and Pathologic Characterizations Rare childhood cancers--an increasing entity requiring the need for global consensus and collaboration.The oncogenic BRD4-NUT chromatin regulator drives aberrant transcription within large topological domains.BET inhibitor OTX015 targets BRD2 and BRD4 and decreases c-MYC in acute leukemia cells Exploiting the Epigenome to Control Cancer-Promoting Gene-Expression Programs.Concurrent nuclear ERG and MYC protein overexpression defines a subset of locally advanced prostate cancer: Potential opportunities for synergistic targeted therapeutics.Targeting BET bromodomain proteins in solid tumors Comparative drug screening in NUT midline carcinoma.Complex chromosomal rearrangements by single catastrophic pathogenesis in NUT midline carcinoma Marked for death: targeting epigenetic changes in cancer.Biological function and histone recognition of family IV bromodomain-containing proteins.Intensive treatment and survival outcomes in NUT midline carcinoma of the head and neck.NUT midline carcinoma of the larynx: an international series and review of the literature.Targeting Cancer Cells with BET Bromodomain Inhibitors.Family matters: How MYC family oncogenes impact small cell lung cancer.Re-engineering the Pancreas Tumor Microenvironment: A "Regenerative Program" Hacked.Systematic Kinase Inhibitor Profiling Identifies CDK9 as a Synthetic Lethal Target in NUT Midline Carcinoma.A novel BRD4-NUT fusion in an undifferentiated sinonasal tumor highlights alternative splicing as a contributing oncogenic factor in NUT midline carcinoma.Ectopic protein interactions within BRD4-chromatin complexes drive oncogenic megadomain formation in NUT midline carcinoma.Uncovering BRD4 hyperphosphorylation associated with cellular transformation in NUT midline carcinoma.NUT midline carcinoma as a primary lung tumor: a case report.Molecular-genetic profiling and high-throughput in vitro drug screening in NUT midline carcinoma-an aggressive and fatal disease.miR-3140 suppresses tumor cell growth by targeting BRD4 via its coding sequence and downregulates the BRD4-NUT fusion oncoprotein.Discovery of BET bromodomain inhibitors and their role in target validation Development and evaluation of a novel series of Nitroxoline-derived BET inhibitors with antitumor activity in renal cell carcinoma

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MYC, a downstream target of BRD-NUT, is necessary and sufficient for the blockade of differentiation in NUT midline carcinoma.

http://www.wikidata.org/entity/Q37617063

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 22 April 2013

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

MYC, a downstream target of BR ...... tion in NUT midline carcinoma.

@en

MYC, a downstream target of BR ...... tion in NUT midline carcinoma.

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type

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MYC, a downstream target of BR ...... tion in NUT midline carcinoma.

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MYC, a downstream target of BR ...... tion in NUT midline carcinoma.

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MYC, a downstream target of BR ...... tion in NUT midline carcinoma.

@en

MYC, a downstream target of BR ...... tion in NUT midline carcinoma.

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MYC, a downstream target of BR ...... tion in NUT midline carcinoma.

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Adlai R Grayson

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Alexandra B Aserlind

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Christopher A French

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Erica M Walsh

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Gerard Evan

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Hongfang Wang

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James E Bradner

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Jernej Godec

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Jessica M Ambrose

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Jon C Aster

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P2860

Selective inhibition of BET bromodomains

Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.

myc maintains embryonic stem cell pluripotency and self-renewal

BRD4-NUT fusion oncogene: a novel mechanism in aggressive carcinoma

BET bromodomain inhibition as a therapeutic strategy to target c-Myc

Targeting MYC dependence in cancer by inhibiting BET bromodomains

RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia

Clinicopathologic features and long-term outcomes of NUT midline carcinoma.

Diagnosis of NUT midline carcinoma using a NUT-specific monoclonal antibody.

NUT rearrangement in undifferentiated carcinomas of the upper aerodigestive tract.

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1736-1742

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scholarly article

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10.1038/ONC.2013.126

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13

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33

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2013-04-22T00:00:00Z

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1009312387

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23604113

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3942361

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