Evidence map›Paper›PMID 17420284›Full record

ArticleBlood2007

Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders.

John M Joslin, Anthony A Fernald, Thelma R Tennant, Elizabeth M Davis, Scott C Kogan, John Anastasi, John D Crispino, Michelle M Le Beau

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
10.6field-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

107 citing papers in PubMed, 210 citations in OpenAlex.

  1. Trial
  2. Mutational Spectrum, Copy Number Changes, and Outcome: Results of a Sequencing Study of Patients With Newly Diagnosed Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015
    Trial
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  5. Article
  6. Review
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  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
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  14. Article
  15. EGR1 Addiction in Diffuse Large B-cell Lymphoma.Molecular cancer research : MCR · 2021
    Article
  16. The Role of Somatic Mutations in Acute Myeloid Leukemia Pathogenesis.Cold Spring Harbor perspectives in medicine · 2021
    Review
  17. Article
  18. Review
  19. Review
  20. Article

47 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

8 authors at 3 institutions in 1 country.

John M JoslinSection of Hematology/Oncology and the Cancer Research Center, University of Chicago, IL 60637, USA.
Anthony A Fernald
Thelma R Tennant
Elizabeth M Davis
Scott C Kogan
John Anastasi
John D Crispino
Michelle M Le Beau
University of Chicago · USCancer Research Center · USUniversity of California, San Francisco · US

Funding

UCCRC--ETIOLOGY OF TREATMENT-INDUCED SECONDARY LEUKEMIAP01CA040046 · NCI · UNIVERSITY OF CHICAGO · PI LE BEAU, MICHELLE M · 1985 to 2012
$19.9M
MOUSE MODELS OF MYELOID LEUKEMIAU01CA084221 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHANNON, KEVIN M. · 1999 to 2009
$8.7M
Mechanisms of Leukemogenesis in Down SyndromeR01CA101774 · NCI · UNIVERSITY OF CHICAGO · PI CRISPINO, JOHN D · 2003 to 2021
$6.1M
NCI NIH HHS CA40046NCI NIH HHS CA84221NCI NIH HHS P01 CA040046NCI NIH HHS R01 CA101774NCI NIH HHS U01 CA084221
6 · The paper itself

Abstract

Loss of a whole chromosome 5 or a deletion of the long arm, del(5q), is a recurring abnormality in myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML). To identify a leukemia-related gene on chromosome 5, we previously delineated a 970-kb segment of 5q31 that is deleted in all patients examined, and prepared a transcript map of this region. EGR1 is a candidate tumor suppressor gene within the commonly deleted segment of 5q, and encodes a zinc finger transcription factor. To test the hypothesis that loss of function of Egr1 is an initiating event in the pathogenesis of AML/MDS, Egr1-deficient mice were treated with a potent DNA alkylating agent, N-ethyl-nitrosourea (ENU), to induce secondary cooperating mutations. Egr1(+/-) and Egr1(-/-) mice treated with ENU developed immature T-cell lymphomas (CD4(+), CD8(+)) or a myeloproliferative disorder (MPD) at increased rates and with shorter latencies than that of wild-type littermates. The MPD was characterized by an elevated white blood cell count, anemia, and thrombocytopenia with ineffective erythropoiesis. Biallelic mutations of Egr1 were not observed in MPDs in Egr1(+/-) mice. Our data suggest that haploinsufficiency for Egr1 plays a role in murine leukemogenesis, and in the development of AML/MDS characterized by abnormalities of chromosome 5.

Indexed as

Chromosomes, Human, Pair 5Sequence DeletionAnimalsBone Marrow CellsCell DifferentiationChromosome MappingEarly Growth Response Protein 1HumansLeukemia, MyeloidMiceMice, KnockoutMutagenesisMyelodysplastic SyndromesPolymorphism, Single-Stranded ConformationalStem CellsEarly Growth Response Protein 1EGR1 protein, humanEgr1 protein, mouse

Identifiers

PMID17420284
PMCPMC1924479
OpenAlexW2034477988

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.