Evidence map›Paper›PMID 33972799›Full record

ArticleNature genetics2021

Histone acetylation dynamics modulates chromatin conformation and allele-specific interactions at oncogenic loci.

Stephanie Sungalee, Yuanlong Liu, Ruxandra A Lambuta, Natalya Katanayeva, Maria Donaldson Collier, Daniele Tavernari, Sandrine Roulland, Giovanni Ciriello, Elisa Oricchio

Abstract read
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In one paragraph

Article in Nature genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
–field-weighted citation impact
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

57 citing papers in PubMed.

  1. Review
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  9. Article
  10. H3K27ac Is Essential for Human Naive Pluripotency Modulated by m6A-Driven EP300 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  11. Targeting the 3D genome by anthracyclines for chemotherapeutic effects.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
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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

9 authors.

Stephanie Sungalee *Swiss Institute for Experimental Cancer Research, School of Life Sciences, EPFL, Lausanne, Switzerland.ORCID http://orcid.org/0000-0001-5633-8826
Yuanlong Liu *Swiss Cancer Center Leman, Lausanne, Switzerland.
Ruxandra A LambutaSwiss Institute for Experimental Cancer Research, School of Life Sciences, EPFL, Lausanne, Switzerland.
Natalya KatanayevaSwiss Institute for Experimental Cancer Research, School of Life Sciences, EPFL, Lausanne, Switzerland.ORCID http://orcid.org/0000-0002-4240-1254
Maria Donaldson CollierSwiss Institute for Experimental Cancer Research, School of Life Sciences, EPFL, Lausanne, Switzerland.
Daniele TavernariSwiss Cancer Center Leman, Lausanne, Switzerland.ORCID http://orcid.org/0000-0001-5981-7363
Sandrine RoullandAix-Marseille University, CNRS, INSERM, Centre d'Immunologie de Marseille-Luminy, Marseille, France.
Giovanni CirielloSwiss Cancer Center Leman, Lausanne, Switzerland.ORCID http://orcid.org/0000-0003-2021-8683
Elisa OricchioSwiss Institute for Experimental Cancer Research, School of Life Sciences, EPFL, Lausanne, Switzerland. elisa.oricchio@epfl.ch.ORCID http://orcid.org/0000-0002-1690-0447

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In cancer cells, enhancer hijacking mediated by chromosomal alterations and/or increased deposition of acetylated histone H3 lysine 27 (H3K27ac) can support oncogene expression. However, how the chromatin conformation of enhancer-promoter interactions is affected by these events is unclear. In the present study, by comparing chromatin structure and H3K27ac levels in normal and lymphoma B cells, we show that enhancer-promoter-interacting regions assume different conformations according to the local abundance of H3K27ac. Genetic or pharmacological depletion of H3K27ac decreases the frequency and the spreading of these interactions, altering oncogene expression. Moreover, enhancer hijacking mediated by chromosomal translocations influences the epigenetic status of the regions flanking the breakpoint, prompting the formation of distinct intrachromosomal interactions in the two homologous chromosomes. These interactions are accompanied by allele-specific gene expression changes. Overall, our work indicates that H3K27ac dynamics modulates interaction frequency between regulatory regions and can lead to allele-specific chromatin configurations to sustain oncogene expression.

Indexed as

AllelesGenetic LociNucleic Acid ConformationOncogenesAcetylationBase PairingCell Line, TumorChromatinEnhancer Elements, GeneticEpigenesis, GeneticGene DosageHistonesHumansLysinePromoter Regions, GeneticChromatinHistonesLysine

Identifiers

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Read underepoch 390

Registered trials

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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.