Evidence map›Paper›PMID 34075200›Full record

ArticleLeukemia2021

STAT3 activation in large granular lymphocyte leukemia is associated with cytokine signaling and DNA hypermethylation.

Daehong Kim, Giljun Park, Jani Huuhtanen, Bishwa Ghimire, Hanna Rajala, Richard Moriggl, Wing C Chan, Matti Kankainen, Mikko Myllymäki, Satu Mustjoki

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2021. 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
2.3field-weighted citation impact, top 11% 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, 39 citations in OpenAlex.

  1. Article
  2. How Genomic and Structural Context Could Shape JAK-STAT Variant Pathogenicity.Twin research and human genetics : the official journal of the International Society for Twin Studies · 2026
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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

10 authors at 3 institutions in 3 countries.

Daehong KimHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Helsinki, Finland.ORCID http://orcid.org/0000-0002-1253-8946
Giljun ParkHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Helsinki, Finland.
Jani HuuhtanenHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Helsinki, Finland.ORCID http://orcid.org/0000-0003-2750-4033
Bishwa GhimireInstitute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland.ORCID http://orcid.org/0000-0001-5076-8366
Hanna RajalaHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Helsinki, Finland.
Richard MorigglInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0003-0918-9463
Wing C ChanDepartment of Pathology, City of Hope National Medical Center, Duarte, CA, USA.
Matti KankainenHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Helsinki, Finland.ORCID http://orcid.org/0000-0002-4714-9481
Mikko MyllymäkiHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Helsinki, Finland.
Satu MustjokiHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Helsinki, Finland. satu.mustjoki@helsinki.fi.ORCID http://orcid.org/0000-0002-0816-8241
University of Helsinki · FICity Of Hope National Medical Center · USUniversity of Veterinary Medicine Vienna · AT

Funding

Austrian Science Fund FWF I 4157
6 · The paper itself

Abstract

Large granular lymphocyte leukemia (LGLL) is characterized by somatic gain-of-function STAT3 mutations. However, the functional effects of STAT3 mutations on primary LGLL cells have not been studied in detail. In this study, we show that CD8+ T cells isolated from STAT3 mutated LGLL patients have high protein levels of epigenetic regulators, such as DNMT1, and are characterized by global hypermethylation. Correspondingly, treatment of healthy CD8+ T cells with IL-6, IL-15, and/or MCP-1 cytokines resulted in STAT3 activation, increased DNMT1, EZH2, c-MYC, l-MYC, MAX, and NFκB levels, increased DNA methylation, and increased oxidative stress. Similar results were discovered in KAI3 NK cells overexpressing gain-of-function STAT3

Indexed as

DNA MethylationGene Expression Regulation, NeoplasticMutationBiomarkers, TumorCytokinesHumansKiller Cells, NaturalLeukemia, Large Granular LymphocyticSignal TransductionSTAT3 Transcription FactorTumor Cells, CulturedBiomarkers, TumorCytokinesSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID34075200
PMCPMC8632689
OpenAlexW3165690206

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.