Evidence map›Paper›PMID 29728695›Full record

ReviewLeukemia2018

Implications of STAT3 and STAT5 signaling on gene regulation and chromatin remodeling in hematopoietic cancer.

Bettina Wingelhofer, Heidi A Neubauer, Peter Valent, Xiaonan Han, Stefan N Constantinescu, Patrick T Gunning, Mathias Müller, Richard Moriggl

Open access · hybridAbstract readReview
In one paragraph

Review in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed, 1 pooled it
9.3field-weighted citation impact, top 1% 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

168 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.

  1. Pooled it
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  6. Oxidative Phosphorylation and Fatty Acid Oxidation Are Central to Mitochondrial Metabolism Rewiring in CML Stem/Progenitor Cell Survival.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
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108 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 5 countries.

Bettina WingelhoferInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Heidi A NeubauerInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Peter ValentDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Ludwig Boltzmann-Cluster Oncology, Medical University of Vienna, Vienna, Austria.
Xiaonan HanDivision of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center (CCHMC), Cincinnati, OH, USA.
Stefan N ConstantinescuLudwig Institute for Cancer Research Brussels, Brussels, Belgium.ORCID http://orcid.org/0000-0002-8599-2699
Patrick T GunningDepartment of Chemical & Physical Sciences, University of Toronto Mississauga, Mississauga, ON, Canada.
Mathias MüllerInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Richard MorigglInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria. richard.moriggl@vetmeduni.ac.at.ORCID http://orcid.org/0000-0003-0918-9463
University of Veterinary Medicine Vienna · ATCincinnati Children's Hospital Medical Center · USLudwig Boltzmann Institute for Cardiovascular Research · ATLudwig Cancer Research · BEUniversity of Toronto · CA

Funding

Regulation of adult stem cell homeostatic response to inflammatory injuryR21AI103388 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI HAN, XIAONAN · 2013 to 2014
$423k
CIHRNIAID NIH HHS R21 AI103388
6 · The paper itself

Abstract

STAT3 and STAT5 proteins are oncogenic downstream mediators of the JAK-STAT pathway. Deregulated STAT3 and STAT5 signaling promotes cancer cell proliferation and survival in conjunction with other core cancer pathways. Nuclear phosphorylated STAT3 and STAT5 regulate cell-type-specific transcription profiles via binding to promoter elements and exert more complex functions involving interaction with various transcriptional coactivators or corepressors and chromatin remodeling proteins. The JAK-STAT pathway can rapidly reshape the chromatin landscape upon cytokine, hormone, or growth factor stimulation and unphosphorylated STAT proteins also appear to be functional with respect to regulating chromatin accessibility. Notably, cancer genome landscape studies have implicated mutations in various epigenetic modifiers as well as the JAK-STAT pathway as underlying causes of many cancers, particularly acute leukemia and lymphomas. However, it is incompletely understood how mutations within these pathways can interact and synergize to promote cancer. We summarize the current knowledge of oncogenic STAT3 and STAT5 functions downstream of cytokine signaling and provide details on prerequisites for DNA binding and gene transcription. We also discuss key interactions of STAT3 and STAT5 with chromatin remodeling factors such as DNA methyltransferases, histone modifiers, cofactors, corepressors, and other transcription factors.

Indexed as

Chromatin Assembly and DisassemblyGene Expression Regulation, NeoplasticHematologic NeoplasmsHumansSignal TransductionSTAT3 Transcription FactorSTAT5 Transcription FactorTranscription, GeneticSTAT3 protein, humanSTAT3 Transcription FactorSTAT5 Transcription Factor

Identifiers

PMID29728695
PMCPMC6087715
OpenAlexW2794594588

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.