Evidence map›Paper›PMID 28692055›Full record

ArticleOncogene2017

Cellular prion protein (PrP

L Provenzano, Y Ryan, D A Hilton, J Lyons-Rimmer, F Dave, E A Maze, C L Adams, R Rigby-Jones, S Ammoun, C O Hanemann

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Emerging roles of the cellular prion protein (PrPCellular and molecular life sciences : CMLS · 2023
    Review
  8. Review
  9. Article
  10. The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. The Cellular Prion Protein: A Promising Therapeutic Target for Cancer.International journal of molecular sciences · 2020
    Review
  18. Article
  19. Article
  20. Prion Protein in Glioblastoma Multiforme.International journal of molecular sciences · 2019
    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

10 authors at 1 institution in 1 country.

L ProvenzanoInstitute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, UK.
Y RyanInstitute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, UK.
D A HiltonDepartment of Cellular and Anatomical Pathology, Derriford Hospital, Plymouth, UK.
J Lyons-RimmerInstitute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, UK.
F DaveInstitute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, UK.
E A MazeInstitute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, UK.
C L AdamsInstitute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, UK.
R Rigby-JonesDepartment of Cellular and Anatomical Pathology, Derriford Hospital, Plymouth, UK.
S AmmounInstitute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, UK.
C O HanemannInstitute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, Plymouth, UK.
Derriford Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of function mutations in the neurofibromatosis Type 2 (NF2) gene, coding for a tumour suppressor, Merlin, cause multiple tumours of the nervous system such as schwannomas, meningiomas and ependymomas. These tumours may occur sporadically or as part of the hereditary condition neurofibromatosis Type 2 (NF2). Current treatment is confined to (radio) surgery and no targeted drug therapies exist. NF2 mutations and/or Merlin inactivation are also seen in other cancers including some mesothelioma, breast cancer, colorectal carcinoma, melanoma and glioblastoma. To study the relationship between Merlin deficiency and tumourigenesis, we have developed an in vitro model comprising human primary schwannoma cells, the most common Merlin-deficient tumour and the hallmark for NF2. Using this model, we show increased expression of cellular prion protein (PrP

Indexed as

CarcinogenesisCell ProliferationHumansMeningiomaMesotheliomaMutationNeurilemmomaNeurofibromatosis 2Neurofibromin 2Primary Cell CulturePrion ProteinsReceptors, LamininRibosomal ProteinsSignal TransductionNeurofibromin 2Prion ProteinsReceptors, LamininRibosomal ProteinsRPSA protein, human

Identifiers

PMID28692055
OpenAlexW2735599880

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.