Evidence map›Paper›PMID 30953469›Full record

ArticleBMC cancer2019

Identification of ADGRE5 as discriminating MYC target between Burkitt lymphoma and diffuse large B-cell lymphoma.

Karsten Kleo, Lora Dimitrova, Elisabeth Oker, Nancy Tomaszewski, Erika Berg, Franziska Taruttis, Julia C Engelmann, Philipp Schwarzfischer, Jörg Reinders, Rainer Spang and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. CD97/Cells · 2026
    Review
  2. Article
  3. Review
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  5. Article
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  7. Article
  8. Heterogeneity of childhood acute leukemia with mature B-cell immunophenotype.Journal of cancer research and clinical oncology · 2019
    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

13 authors at 4 institutions in 2 countries.

Karsten KleoCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pathology, D-10117, Berlin, Germany. karsten.kleo@charite.de.
Lora DimitrovaCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pathology, D-10117, Berlin, Germany.
Elisabeth OkerCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pathology, D-10117, Berlin, Germany.
Nancy TomaszewskiCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pathology, D-10117, Berlin, Germany.
Erika BergCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pathology, D-10117, Berlin, Germany.
Franziska TaruttisStatistical Bioinformatics, Institute of Functional Genomics, University of Regensburg, D-93053, Regensburg, Germany.
Julia C EngelmannStatistical Bioinformatics, Institute of Functional Genomics, University of Regensburg, D-93053, Regensburg, Germany.
Philipp SchwarzfischerFunctional Genomics, Institute of Functional Genomics, University of Regensburg, D-93053, Regensburg, Germany.
Jörg ReindersFunctional Genomics, Institute of Functional Genomics, University of Regensburg, D-93053, Regensburg, Germany.
Rainer SpangStatistical Bioinformatics, Institute of Functional Genomics, University of Regensburg, D-93053, Regensburg, Germany.
Wolfram GronwaldFunctional Genomics, Institute of Functional Genomics, University of Regensburg, D-93053, Regensburg, Germany.
Peter J OefnerFunctional Genomics, Institute of Functional Genomics, University of Regensburg, D-93053, Regensburg, Germany.
Michael HummelCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pathology, D-10117, Berlin, Germany.
University of Regensburg · DECharité - Universitätsmedizin Berlin · DEHumboldt-Universität zu Berlin · DEFreie Universität Berlin · DE

Funding

MMML-MYC-SYS 0316166H
6 · The paper itself

Abstract

backgroundMYC is a heterogeneously expressed transcription factor that plays a multifunctional role in many biological processes such as cell proliferation and differentiation. It is also associated with many types of cancer including the malignant lymphomas. There are two types of aggressive B-cell lymphoma, namely Burkitt lymphoma (BL) and a subgroup of diffuse large cell lymphoma (DLBCL), which both carry MYC translocations and overexpress MYC but both differ significantly in their clinical outcome. In DLBCL, MYC translocations are associated with an aggressive behavior and poor outcome, whereas MYC-positive BL show a superior outcome.

methodsTo shed light on this phenomenon, we investigated the different modes of actions of MYC in aggressive B-cell lymphoma cell lines subdivided into three groups: (i) MYC-positive BL, (ii) DLBCL with MYC translocation (DLBCLpos) and (iii) DLBCL without MYC translocation (DLBCLneg) for control. In order to identify genome-wide MYC-DNA binding sites a chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-Seq) was performed. In addition, ChIP-Seq for H3K4me3 was used for determination of genomic regions accessible for transcriptional activity. These data were supplemented with gene expression data derived from RNA-Seq.

resultsBioinformatics integration of all data sets revealed different MYC-binding patterns and transcriptional profiles in MYC-positive BL and DLBCL cell lines indicating different functional roles of MYC for gene regulation in aggressive B-cell lymphomas. Based on this multi-omics analysis we identified ADGRE5 (alias CD97) - a member of the EGF-TM7 subfamily of adhesion G protein-coupled receptors - as a MYC target gene, which is specifically expressed in BL but not in DLBCL regardless of MYC translocation.

conclusionOur study describes a diverse genome-wide MYC-DNA binding pattern in BL and DLBCL cell lines with and without MYC translocations. Furthermore, we identified ADREG5 as a MYC target gene able to discriminate between BL and DLBCL irrespectively of the presence of MYC breaks in DLBCL. Since ADGRE5 plays an important role in tumor cell formation, metastasis and invasion, it might also be instrumental to better understand the different pathobiology of BL and DLBCL and help to explain discrepant clinical characteristics of BL and DLBCL.

Indexed as

Gene Expression Regulation, NeoplasticAntigens, CDBurkitt LymphomaCell Line, TumorComputational BiologyDatasets as TopicGene Expression ProfilingHumansLymphoma, Large B-Cell, DiffuseProto-Oncogene Proteins c-mycReceptors, G-Protein-CoupledSequence Analysis, RNATranslocation, GeneticADGRE5 protein, humanAntigens, CDMYC protein, humanProto-Oncogene Proteins c-mycReceptors, G-Protein-CoupledADGRE5BLCD97ChIP-SeqDLBCLLymphomaMYCRNA-Seq

Identifiers

PMID30953469
PMCPMC6451309
OpenAlexW2946122087

What OpenQuestion holds

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LicenceCC BY
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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.