Evidence map›Paper›PMID 23039325›Full record

ArticleBMC cancer2012

Deletion of the TNFAIP3/A20 gene detected by FICTION analysis in classical Hodgkin lymphoma.

Junko Nomoto, Nobuhiro Hiramoto, Motohiro Kato, Masashi Sanada, Akiko Miyagi Maeshima, Hirokazu Taniguchi, Fumie Hosoda, Yoshitaka Asakura, Wataru Munakata, Naohiro Sekiguchi and 7 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

  1. Iranian journal of basic medical sciences · 2025
    Article
  2. Article
  3. Histologic transformation of follicular lymphoma: pathologists' viewpoint.Journal of clinical and experimental hematopathology : JCEH · 2023
    Review
  4. Genetic lesions and targeted therapy in Hodgkin lymphoma.Therapeutic advances in hematology · 2023
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. The role of aberrant proteolysis in lymphomagenesis.Current opinion in hematology · 2015
    Review
  16. 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

17 authors at 4 institutions in 1 country.

Junko NomotoHematology Division, National Cancer Center Hospital, Tokyo, Japan.
Nobuhiro Hiramoto
Motohiro Kato
Masashi Sanada
Akiko Miyagi Maeshima
Hirokazu Taniguchi
Fumie Hosoda
Yoshitaka Asakura
Wataru Munakata
Naohiro Sekiguchi
Dai Maruyama
Takashi Watanabe
Hitoshi Nakagama
Kengo Takeuchi
Kensei Tobinai
Seishi Ogawa
Yukio Kobayashi
Tokyo National Hospital · JPThe University of Tokyo · JPJapanese Foundation For Cancer Research · JPNational Cancer Centre Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe TNFAIP3 gene, which encodes a ubiquitin-modifying enzyme (A20) involved in the negative regulation of NF-κB signaling, is frequently inactivated by gene deletions/mutations in a variety of B-cell malignancies. However, the detection of this in primary Hodgkin lymphoma (HL) specimens is hampered by the scarcity of Hodgkin Reed-Sternberg (HR-S) cells even after enrichment by micro-dissection.

methodsWe used anti-CD30 immunofluorescence with fluorescence in-situ hybridization (FISH) to evaluate the relative number of TNFAIP3/CEP6 double-positive signals in CD30-positive cells.

resultsFrom a total of 47 primary classical Hodgkin lymphoma (cHL) specimens, 44 were evaluable. We found that the relative numbers of TNFAIP3/CD30 cells were distributed among three groups, corresponding to those having homozygous (11%), heterozygous (32%), and no (57%) deletions in TNFAIP3. This shows that TNFAIP3 deletions could be sensitively detected using our chosen methods.

conclusionsComparing the results with mutation analysis, TNFAIP3 inactivation was shown to have escaped detection in many samples with homozygous deletions. This suggests that TNFAIP3 inactivation in primary cHL specimens might be more frequent than previously reported.

Indexed as

Gene DeletionAdolescentAdultAgedAged, 80 and overAnalysis of VarianceDNA-Binding ProteinsFemaleFluorescent Antibody TechniqueGenotypeHodgkin DiseaseHumansIn Situ Hybridization, FluorescenceIntracellular Signaling Peptides and ProteinsKi-1 AntigenMaleDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsKi-1 AntigenNuclear ProteinsTNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID23039325
PMCPMC3519598
OpenAlexW1991780318

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LicenceCC BY
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Registered trials

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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.