Evidence map›Paper›PMID 27698495›Full record

ArticlePloS one2016

The Oncoprotein BRD4-NUT Generates Aberrant Histone Modification Patterns.

Barry M Zee, Amy B Dibona, Artyom A Alekseyenko, Christopher A French, Mitzi I Kuroda

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. NUTM1-rearranged neoplasia: a multi-institution experience yields novel fusion partners and expands the histologic spectrum.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019
    Article
  11. Review
  12. Ectopic protein interactions within BRD4-chromatin complexes drive oncogenic megadomain formation in NUT midline carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  13. G3 (Bethesda, Md.) · 2017
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Barry M ZeeDepartment of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America.
Amy B DibonaDepartment of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, United States of America.
Artyom A AlekseyenkoDepartment of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America.
Christopher A FrenchDepartment of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, United States of America.
Mitzi I KurodaDepartment of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America.
Harvard University · USBrigham and Women's Hospital · US

Funding

VASCULAR, PULMONARY AND RENAL INJURYT32HL007627 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GIMBRONE, MICHAEL A, MITCHELL, RICHARD N · 1985 to 2019
$12.7M
Pathogenesis of NUT-Rearranged CarcinomaR01CA124633 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI Christopher A French · 2007 to 2026
$7.0M
Comprehensive analysis of epigenetic regulators in their native chromatin contextR01GM101958 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI KURODA, MITZI I · 2012 to 2018
$2.4M
NCI NIH HHS R01 CA124633NHLBI NIH HHS T32 HL007627NIGMS NIH HHS R01 GM101958
6 · The paper itself

Abstract

Defects in chromatin proteins frequently manifest in diseases. A striking case of a chromatin-centric disease is NUT-midline carcinoma (NMC), which is characterized by expression of NUT as a fusion partner most frequently with BRD4. ChIP-sequencing studies from NMC patients revealed that BRD4-NUT (B4N) covers large genomic regions and elevates transcription within these domains. To investigate how B4N modulates chromatin, we performed affinity purification of B4N when ectopically expressed in 293-TREx cells and quantified the associated histone posttranslational modifications (PTM) using proteomics. We observed significant enrichment of acetylation particularly on H3 K18 and of combinatorial patterns such as H3 K27 acetylation paired with K36 methylation. We postulate that B4N complexes override the preexisting histone code with new PTM patterns that reflect aberrant transcription and that epigenetically modulate the nucleosome environment toward the NMC state.

Indexed as

AcetylationCarcinoma, Squamous CellCell DifferentiationCell Line, TumorChromatinDNA MethylationGenome, HumanHistone CodeHistonesHumansNuclear ProteinsNucleosomesOncogene Proteins, FusionProteomicsTranscription, GeneticBRD4-NUT fusion oncogene protein, humanChromatinHistonesNuclear ProteinsNucleosomesOncogene Proteins, Fusion

Identifiers

PMID27698495
PMCPMC5047744
OpenAlexW2529805434

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.