Evidence map›Paper›PMID 33323974›Full record

ArticleOncogene2021

STAT3 promotes melanoma metastasis by CEBP-induced repression of the MITF pathway.

Alexander Swoboda, Robert Soukup, Oliver Eckel, Katharina Kinslechner, Bettina Wingelhofer, David Schörghofer, Christina Sternberg, Ha T T Pham, Maria Vallianou, Jaqueline Horvath and 17 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 64 citations in OpenAlex.

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  18. Dormancy of cutaneous melanoma.Cancer cell international · 2024
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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

27 authors at 9 institutions in 6 countries.

Alexander Swoboda *Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Robert Soukup *Center for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria.
Oliver EckelInstitute of Animal Breeding and Genetics, University of Veterinary Medicine, Vienna, Austria.
Katharina KinslechnerCenter for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria.
Bettina WingelhoferLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
David SchörghoferCenter for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria.
Christina SternbergDepartment of Biosciences, Cancer Cluster Salzburg, University of Salzburg, Salzburg, Austria.
Ha T T PhamLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Maria VallianouCenter for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria.
Jaqueline HorvathLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Dagmar StoiberLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Lukas KennerLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.ORCID http://orcid.org/0000-0003-2184-1338
Lionel LarueInstitute Curie, Normal and Pathological Development of Melanocytes, CNRS UMR3347, INSERM U1021 Equipe labellisée, Orsay, France.ORCID http://orcid.org/0000-0002-2010-6107
Valeria PoliDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Turin, Italy.ORCID http://orcid.org/0000-0002-3739-3966
Friedrich BeermannISREC, Swiss Federal Institute of Technology in Lausanne, Lausanne, Switzerland.
Takashi YokotaDepartment of Stem Cell Biology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan.
Stefan KubicekCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0003-0855-8343
Thomas KrausgruberCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0002-1374-0329
André F RendeiroCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0001-9362-5373
Christoph BockCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0001-6091-3088
Rainer ZenzInstitute of Cancer Research, Medical University of Vienna, Vienna, Austria.
Boris KovacicCenter for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria.
Fritz AbergerDepartment of Biosciences, Cancer Cluster Salzburg, University of Salzburg, Salzburg, Austria.ORCID http://orcid.org/0000-0003-2009-6305
Markus HengstschlägerCenter for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria.
Peter PetzelbauerDepartment of Dermatology, Skin and Endothelium Research Division (SERD), Medical University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0001-7080-5259
Mario MikulaCenter for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria. mario.mikula@meduniwien.ac.at.ORCID http://orcid.org/0000-0001-5782-0681
Richard MorigglLudwig Boltzmann Institute for Cancer Research, Vienna, Austria. richard.moriggl@vetmeduni.ac.at.ORCID http://orcid.org/0000-0003-0918-9463
Medical University of Vienna · ATUniversity of Veterinary Medicine Vienna · ATAustrian Academy of Sciences · ATLudwig Boltzmann Institute for Cancer Research · ATUniversity of Salzburg · ATCentre National de la Recherche Scientifique · FRÉcole Polytechnique Fédérale de Lausanne · CHKanazawa University · JPUniversity of Turin · IT

Funding

Austrian Science Fund FWF F 4707Austrian Science Fund FWF F 6105Austrian Science Fund FWF P 25336
6 · The paper itself

Abstract

Metastatic melanoma is hallmarked by its ability of phenotype switching to more slowly proliferating, but highly invasive cells. Here, we tested the impact of signal transducer and activator of transcription 3 (STAT3) on melanoma progression in association with melanocyte inducing transcription factor (MITF) expression levels. We established a mouse melanoma model for deleting Stat3 in melanocytes with specific expression of human hyperactive NRAS

Indexed as

AnimalsCCAAT-Enhancer-Binding Protein-betaCell Line, TumorCell ProliferationDisease Models, AnimalGene Expression Regulation, NeoplasticHumansMelanocytesMelanomaMiceMicrophthalmia-Associated Transcription FactorNeoplasm MetastasisSignal TransductionSTAT3 Transcription FactorCCAAT-Enhancer-Binding Protein-betaCebpb protein, mouseMicrophthalmia-Associated Transcription FactorMitf protein, mouseStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID33323974
PMCPMC7116782
OpenAlexW3111302247

What OpenQuestion holds

Textmetadata
LicenceTDM
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.