Evidence map›Paper›PMID 15385932›Full record

ArticleLeukemia2004

Suppressor of cytokine signaling 3 expression in anaplastic large cell lymphoma.

J H Cho-Vega, G Z Rassidakis, H M Amin, P Tsioli, K Spurgers, Y K Remache, F Vega, A H Goy, F Gilles, L Jeffrey Medeiros

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Obesity and Risk for Lymphoma: Possible Role of Leptin.International journal of molecular sciences · 2022
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. SOCS regulation of the JAK/STAT signalling pathway.Seminars in cell & developmental biology · 2008
    Review
  10. Loss of protein inhibitors of activated STAT-3 expression in glioblastoma multiforme tumors: implications for STAT-3 activation and gene expression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008
    Article
  11. Review
  12. Review
  13. JunB expression is a common feature of CD30+ lymphomas and lymphomatoid papulosis.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2005
    Article
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 1 institution in 1 country.

J H Cho-VegaDepartment of Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
G Z Rassidakis
H M Amin
P Tsioli
K Spurgers
Y K Remache
F Vega
A H Goy
F Gilles
L Jeffrey Medeiros
The University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Using a cDNA microarray, we found that suppressor of cytokine signaling 3 (SOCS3) is highly expressed in anaplastic lymphoma kinase (ALK)+ anaplastic large cell lymphoma (ALCL) cell lines. As SOCS3 is induced by activated signal transducer and activator of transcription 3 (STAT3), and ALK activates STAT3, we hypothesized that SOCS3 may play a role in ALK+ ALCL pathogenesis via the Janus kinase 3 (JAK3)-STAT3 pathway. Using ALCL cell lines, we show by coimmunoprecipitation experiments that SOCS3 physically binds with JAK3 in vitro, and that JAK3 inhibition by WHI-P154 downregulates SOCS3 expression. Western blot analysis confirmed expression of SOCS3 and also showed coexpression of phosphorylated (activated) STAT3 (pSTAT3). Direct sequencing of the SOCS3 gene showed no mutations or alternative splicing. In ALCL tumors that were assessed by immunohistochemistry, nine of 12 (75%) ALK+ tumors were SOCS3 positive and eight (67%) coexpressed pSTAT3. In comparison, 18 of 25 (72%) ALK-- tumors were SOCS3 positive and seven (28%) coexpressed pSTAT3. These results show that SOCS3 is overexpressed in ALCL, attributable to JAK3-STAT3 activation and likely related to ALK in ALK+ tumors. However, SOCS3 is also expressed in tumors that lack STAT3 and ALK suggesting alternative mechanisms of upregulation.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionAlternative SplicingAnaplastic Lymphoma KinaseDNA-Binding ProteinsGene Expression ProfilingHumansImmunoprecipitationJanus Kinase 3Lymphoma, Large-Cell, AnaplasticMutationOligonucleotide Array Sequence AnalysisPhosphorylationProtein-Tyrosine KinasesQuinazolinesReceptor Protein-Tyrosine KinasesALK protein, humanAnaplastic Lymphoma KinaseDNA-Binding ProteinsJAK3 protein, humanJanus Kinase 3Protein-Tyrosine KinasesQuinazolinesReceptor Protein-Tyrosine KinasesRepressor ProteinsSOCS3 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTrans-ActivatorsTranscription FactorsWHI P154

Identifiers

PMID15385932
OpenAlexW2064038593

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.