Evidence map›Paper›PMID 31235852›Full record

ArticleScientific reports2019

SOCS2 is part of a highly prognostic 4-gene signature in AML and promotes disease aggressiveness.

Chi Huu Nguyen, Tobias Glüxam, Angela Schlerka, Katharina Bauer, Alexander M Grandits, Hubert Hackl, Oliver Dovey, Sabine Zöchbauer-Müller, Jonathan L Cooper, George S Vassiliou and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

  1. 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

13 authors at 6 institutions in 2 countries.

Chi Huu NguyenDepartment of Medicine I, Division of Oncology, Medical University of Vienna, Vienna, Austria.
Tobias GlüxamDepartment of Medicine I, Division of Oncology, Medical University of Vienna, Vienna, Austria.
Angela SchlerkaDepartment of Medicine I, Division of Oncology, Medical University of Vienna, Vienna, Austria.
Katharina BauerDepartment of Medicine I, Division of Oncology, Medical University of Vienna, Vienna, Austria.
Alexander M GranditsDepartment of Medicine I, Division of Oncology, Medical University of Vienna, Vienna, Austria.
Hubert HacklDivision of Bioinformatics, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0003-4055-3841
Oliver DoveyWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK.
Sabine Zöchbauer-MüllerDepartment of Medicine I, Division of Oncology, Medical University of Vienna, Vienna, Austria.
Jonathan L CooperWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK.
George S VassiliouWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK.ORCID http://orcid.org/0000-0003-4337-8022
Dagmar StoiberLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Rotraud WieserDepartment of Medicine I, Division of Oncology, Medical University of Vienna, Vienna, Austria. rotraud.wieser@meduniwien.ac.at.ORCID http://orcid.org/0000-0003-4384-6658
Gerwin HellerDepartment of Medicine I, Division of Oncology, Medical University of Vienna, Vienna, Austria. gerwin.heller@meduniwien.ac.at.ORCID http://orcid.org/0000-0001-8742-5631
Comprehensive Cancer Center Vienna · ATWellcome Sanger Institute · GBInnsbruck Medical University · ATInstitute of Science and Technology Austria · ATLudwig Boltzmann Institute for Cancer Research · ATUniversity of Veterinary Medicine Vienna · AT

Funding

Austrian Science Fund FWF P 28013Austrian Science Fund FWF P 28256Cancer Research UK 23015Medical Research Council MC_PC_12009
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a heterogeneous disease with respect to its genetic and molecular basis and to patients´ outcome. Clinical, cytogenetic, and mutational data are used to classify patients into risk groups with different survival, however, within-group heterogeneity is still an issue. Here, we used a robust likelihood-based survival modeling approach and publicly available gene expression data to identify a minimal number of genes whose combined expression values were prognostic of overall survival. The resulting gene expression signature (4-GES) consisted of 4 genes (SOCS2, IL2RA, NPDC1, PHGDH), predicted patient survival as an independent prognostic parameter in several cohorts of AML patients (total, 1272 patients), and further refined prognostication based on the European Leukemia Net classification. An oncogenic role of the top scoring gene in this signature, SOCS2, was investigated using MLL-AF9 and Flt3-ITD/NPM1c driven mouse models of AML. SOCS2 promoted leukemogenesis as well as the abundance, quiescence, and activity of AML stem cells. Overall, the 4-GES represents a highly discriminating prognostic parameter in AML, whose clinical applicability is greatly enhanced by its small number of genes. The newly established role of SOCS2 in leukemia aggressiveness and stemness raises the possibility that the signature might even be exploitable therapeutically.

Indexed as

AnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansLeukemia, Myeloid, AcuteMiceNeoplastic Stem CellsPrognosisSuppressor of Cytokine Signaling ProteinsSOCS2 protein, humanSuppressor of Cytokine Signaling Proteins

Identifiers

PMID31235852
PMCPMC6591510
OpenAlexW2953867576

What OpenQuestion holds

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Registered trials

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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.