Evidence map›Paper›PMID 24584857›Full record

ArticleScientific reports2014

CEBPA-dependent HK3 and KLF5 expression in primary AML and during AML differentiation.

Elena A Federzoni, Magali Humbert, Bruce E Torbett, Gerhard Behre, Martin F Fey, Mario P Tschan

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

Article in Scientific reports, 2014. 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
2.1field-weighted citation impact, top 12% 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, 36 citations in OpenAlex.

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  15. Loss of Pax5 Exploits Sca1-BCR-ABLCancer research · 2018
    Article
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  19. C/EBPα in normal and malignant myelopoiesis.International journal of hematology · 2015
    Review
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

6 authors at 3 institutions in 3 countries.

Elena A Federzoni1] Experimental Oncology/Hematology, Department of Clinical Research, University of Bern, Bern, Switzerland [2] Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland [3] Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA [4].
Magali Humbert1] Experimental Oncology/Hematology, Department of Clinical Research, University of Bern, Bern, Switzerland [2] Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland [3].
Bruce E TorbettDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA.
Gerhard BehreDepartment for Hematology and Oncology, University Hospital of Leipzig, Leipzig, Germany.
Martin F Fey1] Experimental Oncology/Hematology, Department of Clinical Research, University of Bern, Bern, Switzerland [2] Department of Medical Oncology, Inselspital, Bern University Hospital, Bern, Switzerland.
Mario P Tschan1] Experimental Oncology/Hematology, Department of Clinical Research, University of Bern, Bern, Switzerland [2] Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland [3] Department of Medical Oncology, Inselspital, Bern University Hospital, Bern, Switzerland [4] Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
University of Bern · CHScripps Research Institute · USUniversity Hospital Leipzig · DE

Funding

Anti-HIV Gene Delivery to Human Hematopoietic CellsR01HL091219 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI TORBETT, BRUCE EDWARD · 2007 to 2010
$1.6M
NHLBI NIH HHS NIH R01HL091219NHLBI NIH HHS R01 HL091219
6 · The paper itself

Abstract

The basic leucine zipper transcription factor CCAAT/enhancer binding protein alpha (CEBPA) codes for a critical regulator during neutrophil differentiation. Aberrant expression or function of this protein contributes to the development of acute myeloid leukemia (AML). In this study, we identified two novel unrelated CEBPA target genes, the glycolytic enzyme hexokinase 3 (HK3) and the krüppel-like factor 5 (KLF5) transcription factor, by comparing gene profiles in two cohorts of CEBPA wild-type and mutant AML patients. In addition, we found CEBPA-dependent activation of HK3 and KLF5 transcription during all-trans retinoic acid (ATRA) mediated neutrophil differentiation of acute promyelocytic leukemia (APL) cells. Moreover, we observed direct regulation of HK3 by CEBPA, whereas our data suggest an indirect regulation of KLF5 by this transcription factor. Altogether, our data provide an explanation for low HK3 and KLF5 expression in particular AML subtype and establish these genes as novel CEBPA targets during neutrophil differentiation.

Indexed as

CCAAT-Enhancer-Binding ProteinsCell DifferentiationCell Line, TumorCell Transformation, NeoplasticHexokinaseHumansKruppel-Like Transcription FactorsLeukemia, Myeloid, AcuteNeutrophilsCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanHexokinaseKLF5 protein, humanKruppel-Like Transcription Factors

Identifiers

PMID24584857
PMCPMC3939455
OpenAlexW2162764200

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.