Evidence map›Paper›PMID 22102868›Full record

ArticlePloS one2011

Deep sequencing of MYC DNA-binding sites in Burkitt lymphoma.

Volkhard Seitz, Peter Butzhammer, Burkhard Hirsch, Jochen Hecht, Ines Gütgemann, Anke Ehlers, Dido Lenze, Elisabeth Oker, Anke Sommerfeld, Edda von der Wall and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

72 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. TCF3 and ID3 Regulate TSPAN32 Expression in Burkitt Lymphoma.Scandinavian journal of immunology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. MYC-an emerging player in mitochondrial diseases.Frontiers in cell and developmental biology · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Co-Operativity between MYC and BCL-2 Pro-Survival Proteins in Cancer.International journal of molecular sciences · 2021
    Review
  20. Article

12 more citing papers are in PubMed but not listed here.

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

14 authors at 5 institutions in 1 country.

Volkhard SeitzInstitute of Pathology, Charité-University Medicine, Campus Benjamin Franklin, Berlin, Germany.
Peter Butzhammer
Burkhard Hirsch
Jochen Hecht
Ines Gütgemann
Anke Ehlers
Dido Lenze
Elisabeth Oker
Anke Sommerfeld
Edda von der Wall
Christoph König
Christian Zinser
Rainer Spang
Michael Hummel
Charité - Universitätsmedizin Berlin · DEUniversity of Regensburg · DEBerlin-Brandenburger Centrum für Regenerative Therapien · DESoftware (Germany) · DEUniversity Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMYC is a key transcription factor involved in central cellular processes such as regulation of the cell cycle, histone acetylation and ribosomal biogenesis. It is overexpressed in the majority of human tumors including aggressive B-cell lymphoma. Especially Burkitt lymphoma (BL) is a highlight example for MYC overexpression due to a chromosomal translocation involving the c-MYC gene. However, no genome-wide analysis of MYC-binding sites by chromatin immunoprecipitation (ChIP) followed by next generation sequencing (ChIP-Seq) has been conducted in BL so far. METHODOLOGY/PRINCIPAL

findingsChIP-Seq was performed on 5 BL cell lines with a MYC-specific antibody giving rise to 7,054 MYC-binding sites after bioinformatics analysis of a total of approx. 19 million sequence reads. In line with previous findings, binding sites accumulate in gene sets known to be involved in the cell cycle, ribosomal biogenesis, histone acetyltransferase and methyltransferase complexes demonstrating a regulatory role of MYC in these processes. Unexpectedly, MYC-binding sites also accumulate in many B-cell relevant genes. To assess the functional consequences of MYC binding, the ChIP-Seq data were supplemented with siRNA- mediated knock-downs of MYC in BL cell lines followed by gene expression profiling. Interestingly, amongst others, genes involved in the B-cell function were up-regulated in response to MYC silencing. CONCLUSION/SIGNIFICANCE: The 7,054 MYC-binding sites identified by our ChIP-Seq approach greatly extend the knowledge regarding MYC binding in BL and shed further light on the enormous complexity of the MYC regulatory network. Especially our observations that (i) many B-cell relevant genes are targeted by MYC and (ii) that MYC down-regulation leads to an up-regulation of B-cell genes highlight an interesting aspect of BL biology.

Indexed as

High-Throughput Nucleotide SequencingBinding SitesBiomarkers, TumorBurkitt LymphomaChromatin ImmunoprecipitationDNA, NeoplasmGene Expression ProfilingGene Expression Regulation, NeoplasticGenome, HumanHumansOligonucleotide Array Sequence AnalysisProto-Oncogene Proteins c-mycRNA, Small InterferingTumor Cells, CulturedBiomarkers, TumorDNA, NeoplasmMYC protein, humanProto-Oncogene Proteins c-mycRNA, Small Interfering

Identifiers

PMID22102868
PMCPMC3213110
OpenAlexW2084635342

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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.