Evidence map›Paper›PMID 25486484›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Analysis of STAT4 expression in cutaneous T-cell lymphoma (CTCL) patients and patient-derived cell lines.

Ivan V Litvinov, Brendan Cordeiro, Simon Fredholm, Niels Ødum, Hanieh Zargham, Yuanshen Huang, Youwen Zhou, Kevin Pehr, Thomas S Kupper, Anders Woetmann and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
5.9field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

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  20. The Role of Tumor Microenvironment in the Pathogenesis of Sézary Syndrome.International journal of molecular sciences · 2022
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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

11 authors at 6 institutions in 4 countries.

Ivan V Litvinova Division of Dermatology ; McGill University Health Centre ; Montréal , QC Canada.
Brendan Cordeiro
Simon Fredholm
Niels Ødum
Hanieh Zargham
Yuanshen Huang
Youwen Zhou
Kevin Pehr
Thomas S Kupper
Anders Woetmann
Denis Sasseville
McGill University Health Centre · CAUniversity of Copenhagen · DKHarvard University Press · USQuest University Canada · CAUniversity of British Columbia · CAZero to Three · US

Funding

Targeting Raf in Melanoma: Mechanisms for Effect & Resistance & Opportunities forP50CA093683 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI KUPPER, THOMAS S. · 2001 to 2012
$25.8M
Canadian Institutes of Health ResearchNCI NIH HHS P50 CA093683NCI NIH HHS P50CA093683
6 · The paper itself

Abstract

Deregulation of STAT signaling has been implicated in the pathogenesis for a variety of cancers, including CTCL. Recent reports indicate that loss of STAT4 expression is an important prognostic marker for CTCL progression and is associated with the acquisition of T helper 2 cell phenotype by malignant cells. However, little is known about the molecular mechanism behind the downregulation of STAT4 in this cancer. In the current work we test the expression of STAT4 and STAT6 via RT-PCR and/or Western Blot in CTCL lesional skin samples and in immortalized patient-derived cell lines. In these malignant cell lines we correlate the expression of STAT4 and STAT6 with the T helper (Th) phenotype markers and test the effect of Histone Deacetylase (HDAC) inhibitors and siRNA-mediated knock down of miR-155 on STAT4 expression. Our findings demonstrate that STAT4 expression correlates with Th1 phenotype, while STAT6 is associated with the Th2 phenotype. Our results further document that STAT4 and STAT6 genes are inversely regulated in CTCL. Treatment with HDAC inhibitors upregulates STAT4 expression, while at the same time decreases STAT6 expression in MyLa cells. Also, siRNA-mediated knock down of miR-155 leads to upregulation in STAT4 expression in MyLa cells. In summary, our results suggest that loss of STAT4 expression and associated switch to Th2 phenotype during Mycosis Fungoides progression may be driven via aberrant histone acetylation and/or upregulation of oncogenic miR-155 microRNA.

Indexed as

Cell Line, TumorDepsipeptidesGene Expression Regulation, NeoplasticGene Knockdown TechniquesHealthy VolunteersHistone Deacetylase InhibitorsHumansHydroxamic AcidsInflammationLymphoma, T-Cell, CutaneousMicroRNAsPhenotypeRNA, MessengerRNA, Small InterferingSkinSkin DiseasesDepsipeptidesHistone Deacetylase InhibitorsHydroxamic AcidsMicroRNAsMIRN155 microRNA, humanRNA, MessengerRNA, Small InterferingromidepsinSTAT4 protein, humanSTAT4 Transcription FactorSTAT6 protein, humanSTAT6 Transcription FactorVorinostatAbbreviations: CTCLCutaneous T-Cell Lymphoma (CTCL)cutaneous T-cell lymphoma; MFhistone deacetylase; STATmi-R155Mycosis Fungoides (MF)mycosis fungoides; SSsézary syndrome; HDACSézary Syndrome (SS)signal transducers and activators of transcription.STAT6 and STAT4

Identifiers

PMID25486484
PMCPMC4614388
OpenAlexW2032152255

What OpenQuestion holds

Textmetadata
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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.