Evidence map›Paper›PMID 25043018›Full record

ArticleNature2014

Activation and repression by oncogenic MYC shape tumour-specific gene expression profiles.

Susanne Walz, Francesca Lorenzin, Jennifer Morton, Katrin E Wiese, Björn von Eyss, Steffi Herold, Lukas Rycak, Hélène Dumay-Odelot, Saadia Karim, Marek Bartkuhn and 9 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 338 papers.

0numbers the graph read from it
0cells of the map it votes in
338citing papers in PubMed
21.8field-weighted citation impact, top 1% 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

338 citing papers in PubMed, 523 citations in OpenAlex.

  1. Article
  2. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. HUWE1 in Skeletal Muscle Prevents Muscle Fatigue via Maintaining Iron and Calcium Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 7 institutions in 4 countries.

Susanne Walz1] Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany [2].
Francesca Lorenzin1] Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany [2].
Jennifer MortonCRUK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK.
Katrin E WieseTheodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Björn von EyssTheodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Steffi HeroldTheodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Lukas RycakInstitute for Molecular Biology and Tumor Research (IMT), Emil-Mannkopff-Str.2, 35033 Marburg, Germany.
Hélène Dumay-OdelotUniversity of Bordeaux, IECB, ARNA laboratory, Equipe Labellisée Contre le Cancer, 33600 Pessac, France.
Saadia KarimCRUK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK.
Marek BartkuhnInstitute for Genetics, Justus-Liebig-University, Heinrich-Buff-Ring 58, 35390 Giessen, Germany.
Frederik RoelsUniversity Children's Hospital of Cologne, and Cologne Center for Molecular Medicine (CMMC), University of Cologne, Kerpener Str. 62, 50924 Cologne, Germany.
Torsten WüstefeldUniversity Hospital Tübingen, Division of Translational Gastrointestinal Oncology, Department of Internal Medicine I, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany.
Matthias FischerUniversity Children's Hospital of Cologne, and Cologne Center for Molecular Medicine (CMMC), University of Cologne, Kerpener Str. 62, 50924 Cologne, Germany.
Martin TeichmannUniversity of Bordeaux, IECB, ARNA laboratory, Equipe Labellisée Contre le Cancer, 33600 Pessac, France.
Lars Zender1] University Hospital Tübingen, Division of Translational Gastrointestinal Oncology, Department of Internal Medicine I, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany [2] Translational Gastrointestinal Oncology Group within the German Center for Translational Cancer Research (DKTK), German Cancer Research Center (DKFZ), 69121 Heidelberg, Germany.
Chia-Lin WeiDOE Joint Genome Institute, 2800 Mitchell Drive, Walnut Creek, California 94598, USA.
Owen SansomCRUK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK.
Elmar Wolf1] Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany [2] Rudolf Virchow Center/DFG Research Center for Experimental Biomedicine, University of Würzburg, Josef-Schneider-Str.2, 97080 Würzburg, Germany [3].
Martin Eilers1] Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany [2] Comprehensive Cancer Center Mainfranken, University of Würzburg, Josef-Schneider-Str. 6, 97080 Würzburg, Germany [3].
University of Würzburg · DECancer Research UK Scotland Institute · GBUniversité de Bordeaux · FRUniversity of Cologne · DEInstitute of Molecular Biology · DEJoint Genome Institute · USJustus-Liebig-Universität Gießen · DE

Funding

Cancer Research UK 12481Cancer Research UK A11650Cancer Research UK A12481Cancer Research UK A7130European Research Council 311301
6 · The paper itself

Abstract

In mammalian cells, the MYC oncoprotein binds to thousands of promoters. During mitogenic stimulation of primary lymphocytes, MYC promotes an increase in the expression of virtually all genes. In contrast, MYC-driven tumour cells differ from normal cells in the expression of specific sets of up- and downregulated genes that have considerable prognostic value. To understand this discrepancy, we studied the consequences of inducible expression and depletion of MYC in human cells and murine tumour models. Changes in MYC levels activate and repress specific sets of direct target genes that are characteristic of MYC-transformed tumour cells. Three factors account for this specificity. First, the magnitude of response parallels the change in occupancy by MYC at each promoter. Functionally distinct classes of target genes differ in the E-box sequence bound by MYC, suggesting that different cellular responses to physiological and oncogenic MYC levels are controlled by promoter affinity. Second, MYC both positively and negatively affects transcription initiation independent of its effect on transcriptional elongation. Third, complex formation with MIZ1 (also known as ZBTB17) mediates repression of multiple target genes by MYC and the ratio of MYC and MIZ1 bound to each promoter correlates with the direction of response.

Indexed as

TranscriptomeAnimalsBinding SitesCell Line, TumorDown-RegulationE-Box ElementsGene Expression Regulation, NeoplasticGenes, mycHumansKruppel-Like Transcription FactorsMiceNeoplasmsNuclear ProteinsPromoter Regions, GeneticProtein Inhibitors of Activated STATProto-Oncogene Proteins c-mycKruppel-Like Transcription FactorsMiz1 protein, mouseMYC protein, humanMyc protein, mouseNuclear ProteinsProtein Inhibitors of Activated STATProto-Oncogene Proteins c-mycRNA Polymerase IIUbiquitin-Protein LigasesZBTB17 protein, human

Identifiers

PMID25043018
PMCPMC6879323
OpenAlexW2004071564

What OpenQuestion holds

Textmetadata
LicenceTDM
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.