Evidence map›Paper›PMID 23196783›Full record

ArticleMolecular medicine (Cambridge, Mass.)2013

Glucocorticoid receptor and molecular chaperones in the pathogenesis of adrenal incidentalomas: potential role of reduced sensitivity to glucocorticoids.

Svetozar S Damjanovic, Jadranka A Antic, Bojana B Ilic, Bojana Beleslin Cokic, Miomira Ivovic, Sanja I Ognjanovic, Tatjana V Isailovic, Bojana M Popovic, Ivana B Bozic, Svetislav Tatic and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Pathophysiology of Mild Hypercortisolism: From the Bench to the Bedside.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Carotid Intima-Media Thickness as the Cardiometabolic Risk Indicator in Patients with Nonfunctional Adrenal Mass and Metabolic Syndrome Screening.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  8. Article
  9. 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

13 authors at 3 institutions in 2 countries.

Svetozar S DamjanovicCentre for Endocrine Oncology and Hereditary Cancer Syndromes, Institute for Endocrinology, Diabetes and Diseases of Metabolism, Clinical Centre of Serbia, University of Belgrade, Belgrade, Serbia. sova@net.co.rs
Jadranka A Antic
Bojana B Ilic
Bojana Beleslin Cokic
Miomira Ivovic
Sanja I Ognjanovic
Tatjana V Isailovic
Bojana M Popovic
Ivana B Bozic
Svetislav Tatic
Gordana Matic
Vera N Todorovic
Ivan Paunovic
University of Belgrade · RSUniversity Clinical Centre · PLUniversity of Novi Sad · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid (GC) sensitivity depends on glucocorticoid receptor (GR) and heat shock proteins (Hsps). We investigated whether common GR genes (ER22/23EK, N363S, Bcl I, and 9β) and adrenocorticotropin receptor promoter polymorphisms influence susceptibility for unilateral adrenal incidentaloma (AI), plus GR and Hsp expression in tumorous (n = 19), peritumorous (n = 13) and normal adrenocortical (n = 11) tissues. Patients (n = 112), population-matched controls (n = 100) and tumor tissues (n = 32) were genotyped for these polymorphisms. Postdexamethasone serum cortisol was higher in patients (p < 0.001). GR gene variants, larger allele of Bcl I (odds ratio [OR] 2.9; 95% confidence interval [CI] 1.7-5.1; p < 0.001] and minor allele of 9β (OR 3.0; 95% CI 1.6-5.7; p < 0.001) were independent predictors of AI. In patients, the first allele is linked with larger tumors (p = 0.002) and the latter with higher postdexamethasone cortisol levels (p = 0.025). Both allele carriers had lesser waist circumference (p = 0.02), similar adrenocorticotropin and higher basal (p = 0.024) and postdexamethasone cortisol concentrations (p < 0.001). Tumorous and constitutional genotypes were similar. GR-D is the major receptor isoform in normal adrenal cortex by Western blotting. Loss of other receptor isoforms, decrease in immunostaining for GR (p < 0.0001), underexpression of chaperones (p ≤ 0.01) and the presence of inducible Hsp70 were found in adenomas. In conclusion, GR gene variants, C allele of Bcl I and minor allele of 9β, are associated with AIs. Their concurrent presence in patients reduces GC sensitivity. Normal adrenal cortex preferentially expresses GR-D. In adenomas, the lack of other GR isoforms and underexpression of heat shock proteins perhaps permanently impair GC signaling, which could promote dysregulated cortisol production and tumor growth. The innate GC sensitivity probably modifies these effects.

Indexed as

Adrenal CortexAdrenal Gland NeoplasmsAdultAgedAged, 80 and overBlotting, WesternCase-Control StudiesCell ExtractsFemaleGenetic Predisposition to DiseaseGlucocorticoidsHaplotypesHeat-Shock ProteinsHumansIntracellular SpaceMaleCell ExtractsGlucocorticoidsHeat-Shock ProteinsMolecular ChaperonesReceptors, CorticotropinReceptors, Glucocorticoid

Identifiers

PMID23196783
PMCPMC3563706
OpenAlexW1485800213

What OpenQuestion holds

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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.