Evidence map›Paper›PMID 12568298›Full record

ReviewInternational journal of hematology2003

Hodgkin's lymphoma and CD30 signal transduction.

Ryouichi Horie, Masaaki Higashihara, Toshiki Watanabe

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Immunotherapies for Hodgkin's lymphoma.Critical reviews in oncology/hematology · 2008
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Marek's disease is a natural model for lymphomas overexpressing Hodgkin's disease antigen (CD30).Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  12. Prognostic factors in pediatric Hodgkin disease.Current oncology reports · 2003
    Review
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

3 authors.

Ryouichi HorieFourth Department of Internal Medicine, Kitasato University, School of Medicine, Kanagawa, Japan. rhorie@med.kitasato-u.ac.jp
Masaaki Higashihara
Toshiki Watanabe

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advances in molecular biology have shed light on the biological basis of Hodgkin's lymphoma (HL). Knowledge of the biological basis has enabled us to understand that most Hodgkin and Reed-Sternberg (H-RS) cells are derived from germinal center B-cells and constitutive nuclear factor kappaB (NF-kappaB) activation is a common molecular feature. Molecular mechanisms responsible for constitutive NF-kappaB activation, Epstein Barr virus latent membrane protein 1, and defective IkappaBalpha and IkappaB kinase activation have been clarified in the past several years. A recent study revealed the biological link between 2 characteristic features of H-RS cells: CD30 overexpression and constitutive NF-kappaB activation. Ligand-independent signaling by overexpressed CD3O was shown to be a common mechanism that induced constitutive NF-kappaB activation in these cells. These results suggest the self-growth-promoting potential of H-RS cells and redefine the biology of HL composed of H-RS cells and lymphocytes.

Indexed as

Hodgkin DiseaseHumansKi-1 AntigenNF-kappa BReed-Sternberg CellsSignal TransductionKi-1 AntigenNF-kappa B

Identifiers

PMID12568298

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.