Evidence map›Paper›PMID 15840692›Full record

ArticleBlood2005

Egr-1 abrogates the block imparted by c-Myc on terminal M1 myeloid differentiation.

Marianna Shafarenko, Dan A Liebermann, Barbara Hoffman

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. CDK6 Inhibition: A Novel Approach in AML Management.International journal of molecular sciences · 2020
    Review
  4. CaAdvances in cancer research · 2020
    Review
  5. Article
  6. Article
  7. The progress of early growth response factor 1 and leukemia.Intractable & rare diseases research · 2016
    Review
  8. Article
  9. Multifaceted roles of STIM proteins.Pflugers Archiv : European journal of physiology · 2013
    Review
  10. Article
  11. Article
  12. WT1/EGR1-mediated control of STIM1 expression and function in cancer cells.Frontiers in bioscience (Landmark edition) · 2011
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

3 authors at 1 institution in 1 country.

Marianna ShafarenkoFels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, 3307 N Broad St, Philadelphia, PA 19140, USA.
Dan A Liebermann
Barbara Hoffman
Temple University · US

Funding

NEGATIVE REGULATORS OF MYELOPOIESISR01CA081168 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI HOFFMAN, BARBARA · 1999 to 2009
$2.4M
SHARED RESOURCES FOR CANCER RESEARCHR24CA088261 · NCI · TEMPLE UNIVERSITY · PI REDDY, E PREMKUMAR · 2001 to 2005
$1.3M
NUCLEAR REGULATORS IN MYELOPOIESIS AND LEUKEMIAR01CA059774 · NCI · TEMPLE UNIVERSITY · PI LIEBERMANN, DAN A · 1994 to 1998
–
NCI NIH HHS 1 RO1 CA59774NCI NIH HHS 1 RO1 CA81168NCI NIH HHS CA88261-03
6 · The paper itself

Abstract

Both deregulated growth and blocks in differentiation cooperate in the multistage process of leukemogenesis. Thus, understanding functional interactions between genes that regulate normal blood cell development, including cell growth and differentiation, and how their altered expression contributes to leukemia, is important for rational drug design. Previously, we have shown that the zinc finger transcription factor Egr-1 plays a role in monocytic differentiation. Ectopic expression of Egr-1 in M1 myeloblastic leukemia cells was observed to activate the macrophage differentiation program in the absence of the differentiation inducer interleukin 6 (IL-6) and to promote terminal differentiation in its presence. In addition, we have shown that deregulated expression of the proto-oncogene c-myc blocks the myeloid terminal differentiation program. Here we show that restoring expression of Egr-1 in M1 cells that express deregulated c-Myc abrogates the c-Myc block in terminal differentiation, resulting in cells that undergo functional macrophage maturation. However, there is an absence of both growth arrest and cell adhesion. In addition, Egr-1 expression diminished M1myc leukemogenicity in vivo. These findings indicate that Egr-1 can act as a tumor suppressor gene and suggest that Egr-1 or Egr-1 targets may provide important tools for differentiation therapy in certain leukemic phenotypes.

Indexed as

Cell DifferentiationAnimalsCell AdhesionCell Line, TumorCell ProliferationDNA-Binding ProteinsEarly Growth Response Protein 1Genes, Tumor SuppressorImmediate-Early ProteinsLeukemia, Myeloid, AcuteMacrophagesMiceMice, Inbred StrainsProto-Oncogene Proteins c-mycTranscription FactorsDNA-Binding ProteinsEarly Growth Response Protein 1Egr1 protein, mouseImmediate-Early ProteinsMyc protein, mouseProto-Oncogene Proteins c-mycTranscription Factors

Identifiers

PMID15840692
PMCPMC1895156
OpenAlexW1970988683

What OpenQuestion holds

Textmetadata
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.