Evidence map›Paper›PMID 28566736›Full record

ArticleLeukemia2018

Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling.

M Hahn, J-P Bürckert, C A Luttenberger, S Klebow, M Hess, M Al-Maarri, M Vogt, S Reißig, M Hallek, A Wienecke-Baldacchino and 6 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. CYLD in health and disease.Disease models & mechanisms · 2023
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. The role of deubiquitinating enzymes in cancer drug resistance.Cancer chemotherapy and pharmacology · 2020
    Review
  13. Article
  14. Article
  15. Ubiquitination regulation of inflammatory responses through NF-κB pathway.American journal of translational research · 2018
    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

16 authors at 6 institutions in 3 countries.

M HahnInstitute for Molecular Medicine, University Medical Centre of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
J-P BürckertDepartment of Infection and Immunity, Luxembourg Institute of Health, Strassen, Luxembourg.
C A LuttenbergerInstitute for Molecular Medicine, University Medical Centre of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
S KlebowInstitute for Molecular Medicine, University Medical Centre of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
M HessInstitute of Medical Biostatistics, Epidemiology and Informatics, University Medical Centre of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
M Al-MaarriMax Planck Institute for Metabolism Research, CECAD, CMMC, Institute for Genetics, Cologne, Germany.
M VogtMax Planck Institute for Metabolism Research, CECAD, CMMC, Institute for Genetics, Cologne, Germany.
S ReißigInstitute for Molecular Medicine, University Medical Centre of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
M HallekDepartment I of Internal Medicine, CMMC, CECAD, University of Cologne, Cologne, Germany.
A Wienecke-BaldacchinoLife Science Research Unit (LSRU), University of Luxembourg, Esch-sur-Alzette, Luxembourg.
T BuchInstitute of Laboratory Animal Science, University of Zürich, Zürich, Switzerland.
C P MullerDepartment of Infection and Immunity, Luxembourg Institute of Health, Strassen, Luxembourg.
C P PallaschDepartment I of Internal Medicine, CMMC, CECAD, University of Cologne, Cologne, Germany.
F T WunderlichMax Planck Institute for Metabolism Research, CECAD, CMMC, Institute for Genetics, Cologne, Germany.
A WaismanInstitute for Molecular Medicine, University Medical Centre of the Johannes Gutenberg-University of Mainz, Mainz, Germany.ORCID 0000-0003-4304-8234
N HövelmeyerInstitute for Molecular Medicine, University Medical Centre of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Johannes Gutenberg University Mainz · DEMax Planck Institute for Metabolism Research · DELuxembourg Institute of Health · LUUniversity of Cologne · DEUniversity of Luxembourg · LUUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-κB activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-κB and tumor suppressor gene CYLD regulates the pool of CD5

Indexed as

AnimalsB-LymphocytesCD5 AntigensCell ProliferationCell SurvivalDeubiquitinating Enzyme CYLDGenes, Tumor SuppressorHumansLeukemia, Lymphocytic, Chronic, B-CellMiceNF-kappa BRNA SplicingSignal TransductionUbiquitinationCD5 AntigensCYLD protein, humanDeubiquitinating Enzyme CYLDNF-kappa B

Identifiers

PMID28566736
OpenAlexW2618371488

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.