Evidence map›Paper›PMID 31118277›Full record

ArticleMolecular systems biology2019

Linking aberrant chromatin features in chronic lymphocytic leukemia to transcription factor networks.

Jan-Philipp Mallm, Murat Iskar, Naveed Ishaque, Lara C Klett, Sabrina J Kugler, Jose M Muino, Vladimir B Teif, Alexandra M Poos, Sebastian Großmann, Fabian Erdel and 12 more

Open access · goldAbstract read
In one paragraph

Article in Molecular systems biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 60 citations in OpenAlex.

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  15. Enhancing sensitivity and versatility of Tn5-based single cell omics.Frontiers in epigenetics and epigenomics · 2023
    Article
  16. Review
  17. Article
  18. Towards precision medicine in lymphoid malignancies.Journal of internal medicine · 2022
    Review
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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

22 authors at 6 institutions in 3 countries.

Jan-Philipp MallmDivision of Chromatin Networks, German Cancer Research Center (DKFZ) and Bioquant, Heidelberg, Germany.
Murat IskarDivision of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Naveed IshaqueDivision of Theoretical Bioinformatics and Heidelberg Center for Personalized Oncology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Lara C KlettDivision of Chromatin Networks, German Cancer Research Center (DKFZ) and Bioquant, Heidelberg, Germany.
Sabrina J KuglerMechanisms of Leukemogenesis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Jose M MuinoDepartment of Computational Molecular Biology, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID 0000-0002-6403-7262
Vladimir B TeifSchool of Biological Sciences, University of Essex, Colchester, UK.ORCID 0000-0002-5931-7534
Alexandra M PoosDivision of Chromatin Networks, German Cancer Research Center (DKFZ) and Bioquant, Heidelberg, Germany.
Sebastian GroßmannDivision of Chromatin Networks, German Cancer Research Center (DKFZ) and Bioquant, Heidelberg, Germany.
Fabian ErdelDivision of Chromatin Networks, German Cancer Research Center (DKFZ) and Bioquant, Heidelberg, Germany.ORCID 0000-0003-2888-7777
Daniele TavernariDivision of Chromatin Networks, German Cancer Research Center (DKFZ) and Bioquant, Heidelberg, Germany.ORCID 0000-0001-5981-7363
Sandra D KoserDivision of Applied Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Sabrina SchumacherDivision of Chromatin Networks, German Cancer Research Center (DKFZ) and Bioquant, Heidelberg, Germany.
Benedikt BrorsDivision of Applied Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Rainer KönigIntegrated Research and Treatment Center, Center for Sepsis Control and Care (CSCC), Jena University Hospital, Jena, Germany.
Daniel RemondiniDepartment of Physics and Astronomy, Bologna University, Bologna, Italy.ORCID 0000-0003-3185-7456
Martin VingronDepartment of Computational Molecular Biology, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Stephan StilgenbauerDepartment of Internal Medicine III, University Hospital Ulm, Ulm, Germany.
Peter LichterDivision of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Marc ZapatkaDivision of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0001-8287-5967
Daniel MertensMechanisms of Leukemogenesis, German Cancer Research Center (DKFZ), Heidelberg, Germany daniel.mertens@uniklinik-ulm.de karsten.rippe@dkfz.de.ORCID 0000-0003-0227-7188
Karsten RippeDivision of Chromatin Networks, German Cancer Research Center (DKFZ) and Bioquant, Heidelberg, Germany daniel.mertens@uniklinik-ulm.de karsten.rippe@dkfz.de.ORCID 0000-0001-9951-9395
German Cancer Research Center · DEMax Planck Institute for Molecular Genetics · DECentre National de la Recherche Scientifique · FRJena University Hospital · DEUniversity Hospital Ulm · DEUniversity of Essex · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

In chronic lymphocytic leukemia (CLL), a diverse set of genetic mutations is embedded in a deregulated epigenetic landscape that drives cancerogenesis. To elucidate the role of aberrant chromatin features, we mapped DNA methylation, seven histone modifications, nucleosome positions, chromatin accessibility, binding of EBF1 and CTCF, as well as the transcriptome of B cells from CLL patients and healthy donors. A globally increased histone deacetylase activity was detected and half of the genome comprised transcriptionally downregulated partially DNA methylated domains demarcated by CTCF CLL samples displayed a H3K4me3 redistribution and nucleosome gain at promoters as well as changes of enhancer activity and enhancer linkage to target genes. A DNA binding motif analysis identified transcription factors that gained or lost binding in CLL at sites with aberrant chromatin features. These findings were integrated into a gene regulatory enhancer containing network enriched for B-cell receptor signaling pathway components. Our study predicts novel molecular links to targets of CLL therapies and provides a valuable resource for further studies on the epigenetic contribution to the disease.

Indexed as

Gene Expression Regulation, LeukemicGene Regulatory NetworksAgedAmino Acid MotifsBinding SitesCCCTC-Binding FactorChromatinDNADNA MethylationDown-RegulationEnhancer Elements, GeneticHistone DeacetylasesHistonesHumansLeukemia, Lymphocytic, Chronic, B-CellMiddle AgedCCCTC-Binding FactorChromatinCTCF protein, humanDNAEBF1 protein, humanHistone Deacetylaseshistone H3 trimethyl Lys4HistonesTrans-Activatorsbivalent promoterDNA methylationenhancergene regulatory networkshistone modifications

Identifiers

PMID31118277
PMCPMC6529931
OpenAlexW2945230928

What OpenQuestion holds

Textmetadata
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.