Evidence map›Paper›PMID 31286998›Full record

ArticleJournal of hematology & oncology2019

Nuclear factor of activated T-cells, NFATC1, governs FLT3

Maria Solovey, Ying Wang, Christian Michel, Klaus H Metzeler, Tobias Herold, Joachim R Göthert, Volker Ellenrieder, Elisabeth Hessmann, Stefan Gattenlöhner, Andreas Neubauer and 4 more

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

Article in Journal of hematology & oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  6. Zebrafish models of acute leukemias: Current models and future directions.Wiley interdisciplinary reviews. Developmental biology · 2021
    Review
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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

14 authors at 5 institutions in 1 country.

Maria SoloveyDepartment of Hematology, Oncology and Immunology, University Hospital Giessen and Marburg, Campus Marburg, Philipps University Marburg, Marburg, Germany.
Ying WangDepartment of Hematology, Oncology and Immunology, University Hospital Giessen and Marburg, Campus Marburg, Philipps University Marburg, Marburg, Germany.
Christian MichelDepartment of Hematology, Oncology and Immunology, University Hospital Giessen and Marburg, Campus Marburg, Philipps University Marburg, Marburg, Germany.
Klaus H MetzelerLaboratory for Leukemia Diagnostics, Department of Medicine III, University Hospital, LMU Munich, Munich, Germany.
Tobias HeroldLaboratory for Leukemia Diagnostics, Department of Medicine III, University Hospital, LMU Munich, Munich, Germany.
Joachim R GöthertDepartment of Hematology, University Hospital Essen, Essen, Germany.
Volker EllenriederDepartment of Gastroenterology, University Hospital Goettingen, Goettingen, Germany.
Elisabeth HessmannDepartment of Gastroenterology, University Hospital Goettingen, Goettingen, Germany.
Stefan GattenlöhnerInstitute of Pathology, Justus-Liebig-University, Giessen, Germany.
Andreas NeubauerDepartment of Hematology, Oncology and Immunology, University Hospital Giessen and Marburg, Campus Marburg, Philipps University Marburg, Marburg, Germany.
Dinko PavlinicGenomics Core Facility, EMBL Heidelberg , Heidelberg, Germany.
Vladimir BenesGenomics Core Facility, EMBL Heidelberg , Heidelberg, Germany.
Oliver RuppDepartment of Bioinformatics and Systems Biology, University Giessen, Giessen, Germany.
Andreas BurchertDepartment of Hematology, Oncology and Immunology, University Hospital Giessen and Marburg, Campus Marburg, Philipps University Marburg, Marburg, Germany. burchert@staff.uni-marburg.de.
Universitätsklinikum Gießen und Marburg · DEEssen University Hospital · DELMU Klinikum · DEMunich Leukemia Laboratory (Germany) · DEUniversity of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) patients with a high allelic burden of an internal tandem duplication (ITD)-mutated FMS-like Tyrosine Kinase-3 (FLT3) have a dismal outcome. FLT3

methodsWe generated a triple transgenic mouse model, in which tamoxifen-inducible Cre-recombinase targets expression of a constitutively nuclear transcription factor NFATC1 to FLT3

resultsWe find that NFATC1 governs FLT3

conclusionsNFATC1 expression causes FLT3

Indexed as

AnimalsCell Transformation, Neoplasticfms-Like Tyrosine Kinase 3Hematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteMiceMice, Inbred C57BLMice, TransgenicNFATC Transcription FactorsPrognosisFlt3 protein, mousefms-Like Tyrosine Kinase 3Nfatc1 protein, mouseNFATC Transcription FactorsAcute myeloid leukemiaDrug resistanceFLT3ITDHematopoietic stem cellsNFATC1

Identifiers

PMID31286998
PMCPMC6615262
OpenAlexW2959180713

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.