Evidence map›Paper›PMID 25485578›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Deregulation in STAT signaling is important for cutaneous T-cell lymphoma (CTCL) pathogenesis and cancer progression.

Elena Netchiporouk, Ivan V Litvinov, Linda Moreau, Martin Gilbert, Denis Sasseville, Madeleine Duvic

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 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
9.9field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Immunopathogenesis of itch: an integrative framework for chronic pruritus.JID innovations : skin science from molecules to population health · 2026
    Review
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  8. Review
  9. Article
  10. Article
  11. Review
  12. Tumors in the setting of dupilumab use: A review of the literature.The World Allergy Organization journal · 2025
    Review
  13. HDAC10 and its implications in Sézary syndrome pathogenesis.Frontiers in cell and developmental biology · 2025
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. NewCells · 2023
    Article
  20. Article

12 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

6 authors at 3 institutions in 2 countries.

Elena Netchiporouka Division of Dermatology ; McGill University Health Centre ; Montréal , QC Canada.
Ivan V Litvinov
Linda Moreau
Martin Gilbert
Denis Sasseville
Madeleine Duvic
McGill University Health Centre · CAThe University of Texas MD Anderson Cancer Center · USUniversité Laval · CA

Funding

PERCEPTION OF SUPPORT IN PARENTS OF CHILDREN WITH CANCERF31CA008681 · NCI · UNIVERSITY OF FLORIDA · PI WILLIAMS, HOLLY A · 1988 to 1993
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MARKERS OF RESPONSE IN CUTANEOUS T-CELL LYMPHOMAR21CA074117 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI DUVIC, MADELEINE · 1998 to 1999
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NCI NIH HHS K24CA08681NCI NIH HHS R21CA074117
6 · The paper itself

Abstract

Deregulation of STAT signaling has been implicated in the pathogenesis for a variety of cancers, including CTCL. Constitutive activation of STAT5 and STAT3 was observed in early and late stages of CTCL, respectively. In early stages, IL-2, IL-7 and IL-15 signaling via JAK1 and JAK3 kinases is believed to be responsible for activating STAT5, while in advanced stages development of IL-21 autocrine signaling is thought to be important for STAT3 activation. Recent molecular evidence further suggests that upregulation of STAT5 in early disease stages results in increased expression of oncogenic miR-155 microRNA that subsequently targets STAT4 expression on mRNA level. STAT4 signaling is known to be critical for T helper (Th) 1 phenotype differentiation and its loss results in a switch from Th1 to Th2 phenotype in malignant T cells. During this switch the expression of STAT6 is often upregulated in CTCL. In advanced stages, activation of STAT3 and STAT5 may become completely cytokine-independent and be driven only via constitutively active JAK1 and JAK3 kinases. Further research into the molecular pathogenesis of JAK/STAT signaling in this cancer may enable us to develop effective therapies for our patients.

Indexed as

Signal TransductionDisease ProgressionHumansInterleukin-15Interleukin-2Interleukin-7Janus Kinase 1Janus Kinase 2Lymphoma, T-Cell, CutaneousMicroRNAsRNA, MessengerSTAT3 Transcription FactorSTAT4 Transcription FactorSTAT5 Transcription FactorSTAT6 Transcription FactorSTAT Transcription FactorsInterleukin-15Interleukin-2Interleukin-7Janus Kinase 1Janus Kinase 2MicroRNAsRNA, MessengerSTAT3 Transcription FactorSTAT4 Transcription FactorSTAT5 Transcription FactorSTAT6 Transcription FactorSTAT Transcription Factorsand STAT6Cutaneous T-Cell Lymphoma (CTCL)Mycosis FungoidesSézary SyndromeSTAT3STAT4STAT5

Identifiers

PMID25485578
PMCPMC4612117
OpenAlexW2162357150

What OpenQuestion holds

Textmetadata
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.