Evidence map›Paper›PMID 28663557›Full record

ArticleNature communications2017

Disruption of the C/EBPα-miR-182 balance impairs granulocytic differentiation.

Alexander Arthur Wurm, Polina Zjablovskaja, Miroslava Kardosova, Dennis Gerloff, Daniela Bräuer-Hartmann, Christiane Katzerke, Jens-Uwe Hartmann, Touati Benoukraf, Stephan Fricke, Nadja Hilger and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

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  14. Pediatric Germline Predisposition to Myeloid Neoplasms.Current hematologic malignancy reports · 2022
    Review
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  17. Bimodal expression ofEJHaem · 2021
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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

17 authors at 4 institutions in 4 countries.

Alexander Arthur WurmDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany.
Polina ZjablovskajaInstitute of Molecular Genetics, Academy of Sciences of the Czech Republic, Videnska 1083, Prague 4, 142 20, Czech Republic.
Miroslava KardosovaInstitute of Molecular Genetics, Academy of Sciences of the Czech Republic, Videnska 1083, Prague 4, 142 20, Czech Republic.
Dennis GerloffDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany.
Daniela Bräuer-HartmannDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany.
Christiane KatzerkeDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany.
Jens-Uwe HartmannDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany.
Touati BenoukrafCancer Science Institute, National University of Singapore, 14 Medical Drive, Singapore, 117599, Singapore.
Stephan FrickeFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, Leipzig, 04103, Germany.
Nadja HilgerFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, Leipzig, 04103, Germany.
Anne-Marie MüllerFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, Leipzig, 04103, Germany.
Marius BillDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany.
Sebastian SchwindDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany.
Daniel G TenenCancer Science Institute, National University of Singapore, 14 Medical Drive, Singapore, 117599, Singapore.ORCID http://orcid.org/0000-0002-6423-3888
Dietger NiederwieserDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany.
Meritxell Alberich-JordaInstitute of Molecular Genetics, Academy of Sciences of the Czech Republic, Videnska 1083, Prague 4, 142 20, Czech Republic.
Gerhard BehreDivision of Hematology and Oncology, Leipzig University Hospital, Johannisallee 32a, Leipzig, 04103, Germany. Gerhard.Behre@medizin.uni-leipzig.de.
University Hospital Leipzig · DECzech Academy of Sciences · CZFraunhofer Institute for Cell Therapy and Immunology · DENational University of Singapore · SG

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
Transcriptional and epigenetic heterogeneity of stem/progenitor cellsP01HL131477 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI David T Scadden · 2017 to 2026
$24.6M
Mechanisms of regulation by RNA in acute myeloid leukemiaR35CA197697 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 2015 to 2021
$7.1M
Noncoding RNA-DNMT1 interactions in hematopoiesisR01DK103858 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 2015 to 2017
$783k
NCI NIH HHS P01 CA066996NCI NIH HHS R35 CA197697NHLBI NIH HHS P01 HL131477NIDDK NIH HHS R01 DK103858
6 · The paper itself

Abstract

Transcription factor C/EBPα is a master regulator of myelopoiesis and its inactivation is associated with acute myeloid leukemia. Deregulation of C/EBPα by microRNAs during granulopoiesis or acute myeloid leukemia development has not been studied. Here we show that oncogenic miR-182 is a strong regulator of C/EBPα. Moreover, we identify a regulatory loop between C/EBPα and miR-182. While C/EBPα blocks miR-182 expression by direct promoter binding during myeloid differentiation, enforced expression of miR-182 reduces C/EBPα protein level and impairs granulopoiesis in vitro and in vivo. In addition, miR-182 expression is highly elevated particularly in acute myeloid leukemia patients with C-terminal CEBPA mutations, thereby depicting a mechanism by which C/EBPα blocks miR-182 expression. Furthermore, we present miR-182 expression as a prognostic marker in cytogenetically high-risk acute myeloid leukemia patients. Our data demonstrate the importance of a controlled balance between C/EBPα and miR-182 for the maintenance of healthy granulopoiesis.C/EBPα is a critical transcription factor involved in myelopoiesis and its inactivation is associated with acute myeloid leukemia (AML). Here the authors show a negative feedback loop between C/EBPα and miR-182 and identify this miRNA as a marker of high-risk AML.

Indexed as

GranulocytesAnimalsBlotting, WesternCCAAT-Enhancer-Binding ProteinsCell DifferentiationHumansLeukemia, Myeloid, AcuteLeukopoiesisMiceMice, KnockoutMicroRNAsPrognosisReal-Time Polymerase Chain ReactionCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanCEBPA protein, mouseMicroRNAsMirn182 microRNA, humanMirn182 microRNA, mouse

Identifiers

PMID28663557
PMCPMC5491528
OpenAlexW2657974551

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.