Evidence map›Paper›PMID 15507668›Full record

ArticleThe Journal of molecular diagnostics : JMD2004

Constitutive expression of the AP-1 transcription factors c-jun, junD, junB, and c-fos and the marginal zone B-cell transcription factor Notch2 in splenic marginal zone lymphoma.

Gunhild Trøen, Vigdis Nygaard, Tor-Kristian Jenssen, Ida Münster Ikonomou, Anne Tierens, Estella Matutes, Alicja Gruszka-Westwood, Daniel Catovsky, Ola Myklebost, Grete Lauritzsen and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of molecular diagnostics : JMD, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Lymphomagenic CARD11/BCL10/MALT1 signaling drives malignant B-cell proliferation via cooperative NF-κB and JNK activation.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

12 authors at 4 institutions in 2 countries.

Gunhild TrøenDepartment of Pathology, The Norwegian Radium Hospital, University of Oslo, Montebello N-0310, Oslo, Norway. gunhild.troen@labmed.uio.no.
Vigdis Nygaard
Tor-Kristian Jenssen
Ida Münster Ikonomou
Anne Tierens
Estella Matutes
Alicja Gruszka-Westwood
Daniel Catovsky
Ola Myklebost
Grete Lauritzsen
Eivind Hovig
Jan Delabie
Norwegian Cancer Society · NOInstitute of Cancer Research · GBPubGene (Norway) · NORoyal Marsden Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Splenic marginal zone lymphoma (SMZL) is a lymphoma type of putative marginal zone B-cell origin. No specific genetic alterations have yet been demonstrated in SMZL. Clinically, SMZL is a low-grade B-cell non-Hodgkin lymphoma. However, the presence of p53 mutation, 7q22-7q32 deletion or the absence of somatic hypermutations of immunoglobulin genes has been correlated with a worse prognosis. In this study, we analyzed genome-wide gene expression of 24 cases of SMZL using the microarray technique. The AP-1 transcription factors c-jun, junD, junB, and c-fos as well as Notch2 were found to be specifically up-regulated. These data were confirmed by real-time PCR and immunohistochemical staining of tissue sections. The absence of concordant high expression of the MAP kinases, the signaling cascade leading to AP-1 up-regulation, suggests autoregulation of the AP-1 transcription factors and an important role in SMZL oncogenesis. High expression of Notch2, a transcription factor that induces marginal zone B-cell differentiation, is highly suggestive for a marginal zone B-cell origin of SMZL. In addition, SMZL with the 7q deletion showed high expression of TGF-beta1 and low expression of the DNA helicase XPB, a crucial part of the nucleotide excision repair complex, possibly explaining the more aggressive clinical course of those cases.

Indexed as

Gene Expression Regulation, NeoplasticAllelesChromosomes, Human, Pair 7DNADown-RegulationFluorescent DyesGene DeletionGenes, junGenes, p53HumansImmunohistochemistryLymphoma, B-CellMicrosatellite RepeatsMutationNucleic Acid HybridizationOligonucleotide Array Sequence AnalysisDNAFluorescent DyesNOTCH2 protein, humanProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junReceptor, Notch2Receptors, Cell SurfaceTranscription Factor AP-1

Identifiers

PMID15507668
PMCPMC1867488
OpenAlexW2143034553

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.