Evidence map›Paper›PMID 31591386›Full record

ArticleOncogenesis2019

Loss of CYLD accelerates melanoma development and progression in the Tg(Grm1) melanoma mouse model.

Miriam Martha de Jel, Mandy Schott, Susanne Lamm, Winfried Neuhuber, Silke Kuphal, Anja-Katrin Bosserhoff

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 27 citations in OpenAlex.

  1. Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Deubiquitylating Enzymes in Cancer and Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  9. CYLD in health and disease.Disease models & mechanisms · 2023
    Review
  10. Review
  11. Review
  12. Review
  13. Impact ofInternational journal of molecular medicine · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Miriam Martha de JelInstitute for Biochemistry, University of Erlangen-Nürnberg (FAU), Erlangen, Germany.
Mandy SchottInstitute for Biochemistry, University of Erlangen-Nürnberg (FAU), Erlangen, Germany.
Susanne LammInstitute for Biochemistry, University of Erlangen-Nürnberg (FAU), Erlangen, Germany.
Winfried NeuhuberInstitute for Anatomy, University of Erlangen-Nürnberg (FAU), Erlangen, Germany.
Silke KuphalInstitute for Biochemistry, University of Erlangen-Nürnberg (FAU), Erlangen, Germany.
Anja-Katrin BosserhoffInstitute for Biochemistry, University of Erlangen-Nürnberg (FAU), Erlangen, Germany. anja.bosserhoff@fau.de.ORCID http://orcid.org/0000-0001-8147-394X
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) FOR2172
6 · The paper itself

Abstract

The deubiquitinase cylindromatosis (CYLD) is a well-known tumor suppressor, found to be down regulated in many cancer types including breast cancer, colon carcinoma and malignant melanoma. CYLD is suppressed in human melanoma cells by the transcriptional repressor SNAIL1 leading to an increase of their proliferative, invasive and migratory potential. To gain additional insights into the distinct function of this tumor suppressor gene a new mouse model Tg(Grm1)Cyld

Identifiers

PMID31591386
PMCPMC6779913
OpenAlexW2978831269

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.