Evidence map›Paper›PMID 28797028›Full record

ArticleBritish journal of cancer2017

Characterisation of the cancer-associated glucocorticoid system: key role of 11β-hydroxysteroid dehydrogenase type 2.

Nicola Cirillo, David J Morgan, Maria Carmela Pedicillo, Antonio Celentano, Lorenzo Lo Muzio, Michael J McCullough, Stephen S Prime

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-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

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

7 authors at 4 institutions in 3 countries.

Nicola CirilloMelbourne Dental School, The University of Melbourne, 720 Swanston Street, Carlton, Melbourne, VIC 3053, Australia.
David J MorganSchool of Cellular &Molecular Medicine, University of Bristol, Bristol BS8 1TD, UK.
Maria Carmela PedicilloDepartment of Clinical and Experimental Medicine, University of Foggia, Foggia 71122, Italy.
Antonio CelentanoMelbourne Dental School, The University of Melbourne, 720 Swanston Street, Carlton, Melbourne, VIC 3053, Australia.
Lorenzo Lo MuzioDepartment of Clinical and Experimental Medicine, University of Foggia, Foggia 71122, Italy.
Michael J McCulloughMelbourne Dental School, The University of Melbourne, 720 Swanston Street, Carlton, Melbourne, VIC 3053, Australia.
Stephen S PrimeCentre for Clinical and Diagnostic Oral Sciences, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AD, UK.
University of Melbourne · AUUniversity of Foggia · ITQueen Mary University of London · GBUniversity of Bristol · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies have shown that production of cortisol not only takes place in several non-adrenal peripheral tissues such as epithelial cells but, also, the local inter-conversion between cortisone and cortisol is regulated by the 11β-hydroxysteroid dehydrogenases (11β-HSDs). However, little is known about the activity of this non-adrenal glucocorticoid system in cancers.

methodsThe presence of a functioning glucocorticoid system was assessed in human skin squamous cell carcinoma (SCC) and melanoma and further, in 16 epithelial cell lines from 8 different tissue types using ELISA, western blotting and immunofluorescence. 11β-HSD2 was inhibited both pharmacologically and by siRNA technology. Naïve CD8

resultsWe show that cortisol production is a common feature of malignant cells and has paracrine functions. Cortisol production correlated with the magnitude of glucocorticoid receptor (GR)-dependent inhibition of tumour-specific CD8

conclusionsThe results demonstrate evidence of a cancer-associated glucocorticoid system and show for the first time, the functional significance of cancer-derived cortisol in tumour progression.

Indexed as

11-beta-Hydroxysteroid Dehydrogenase Type 111-beta-Hydroxysteroid Dehydrogenase Type 2Adrenocorticotropic HormoneCarcinoma, Squamous CellCD8-Positive T-LymphocytesCell AdhesionCell ProliferationCortisoneCulture Media, ConditionedDown-RegulationEpithelial CellsGene SilencingGlycyrrhetinic AcidHT29 CellsHumansHydrocortisone11-beta-Hydroxysteroid Dehydrogenase Type 111-beta-Hydroxysteroid Dehydrogenase Type 218alpha-glycyrrhetinic acidAdrenocorticotropic HormoneCortisoneCulture Media, ConditionedGlycyrrhetinic AcidHydrocortisoneReceptors, Glucocorticoid

Identifiers

PMID28797028
PMCPMC5625663
OpenAlexW2744153677

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.