Evidence map›Paper›PMID 20660298›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

Cooperation between cyclin E and p27(Kip1) in pituitary tumorigenesis.

Audrey Roussel-Gervais, Steve Bilodeau, Sophie Vallette, France Berthelet, André Lacroix, Dominique Figarella-Branger, Thierry Brue, Jacques Drouin

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02160730 (Treatment of Pituitary Cushing Disease With a Selective CDK Inhibitor, R-roscovitine), which is not on this map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.2field-weighted citation impact, top 8% 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.

NCT02160730 phase2terminatednot on this mapstarted 2014, after this paper: background citation

Treatment of Pituitary Cushing Disease With a Selective CDK Inhibitor, R-roscovitine

TypeinterventionalSponsorShlomo Melmed, MDRan2014 to 2018Enrolled4ConditionsCushings DiseaseArmsR-roscovitine
3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Cushing syndrome.Nature reviews. Disease primers · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. The hallmarks of cancer… in pituitary tumors?Reviews in endocrine & metabolic disorders · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. [Update on mechanisms of pituitary tumorigenesis.]Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina) · 2021
    Review
  12. Review
  13. SOX2 is required independently in both stem and differentiated cells for pituitary tumorigenesis inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Loss-of-function mutations in theEndocrine-related cancer · 2017
    Article
  20. EGFR Induces E2F1-Mediated Corticotroph Tumorigenesis.Journal of the Endocrine Society · 2017
    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

8 authors at 3 institutions in 2 countries.

Audrey Roussel-GervaisLaboratoire de génétique moléculaire, Institut de recherches cliniques de Montréal, 110 avenue des Pins Ouest, Montréal, Quebec, Canada H2W 1R7.
Steve Bilodeau
Sophie Vallette
France Berthelet
André Lacroix
Dominique Figarella-Branger
Thierry Brue
Jacques Drouin
Montreal Clinical Research Institute · CACentre Hospitalier de l’Université de Montréal · CAInstitut de Neurobiologie de la Méditerranée · FR

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Cushing's disease is caused by glucocorticoid-resistant pituitary corticotroph adenomas. We have previously identified the loss of nuclear Brg1 as one mechanism that may lead to partial glucocorticoid resistance: this loss is observed in about 33% of human corticotroph adenomas. We now show that Brg1 loss of function correlates with cyclin E expression in corticotroph adenomas and with loss of the cell cycle inhibitor p27(Kip1) expression. Because Brg1 is thought to have tumor suppressor activity, the present study was undertaken to understand the putative contribution of cyclin E derepression produced by loss of Brg1 expression on adenoma development. Overexpression of cyclin E in pituitary proopiomelanocortin cells leads to abnormal reentry into cell cycle of differentiated proopiomelanocortin cells and to centrosome instability. These alterations are consistent with the intermediate lobe hyperplasia and anterior lobe adenomas that were observed in these pituitaries. When combined with the p27(Kip1) knockout, overexpression of cyclin E increased the incidence of pituitary tumors, their size, and their proliferation index. These results suggest that cyclin E up-regulation and p27(Kip1) loss-of-function act cooperatively on pituitary adenoma development.

Indexed as

AnimalsBiomarkersCell DifferentiationCell ProliferationCentrosomeCyclin-Dependent Kinase Inhibitor p27Cyclin EDNA HelicasesGene Knockdown TechniquesHyperplasiaMiceMice, TransgenicNuclear ProteinsPhenotypePituitary ACTH HypersecretionPituitary GlandBiomarkersCyclin-Dependent Kinase Inhibitor p27Cyclin EDNA HelicasesNuclear ProteinsPro-OpiomelanocortinRepressor ProteinsSmarca4 protein, mouseTranscription Factors

Identifiers

PMID20660298
PMCPMC5417399
OpenAlexW2083397128

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.