Evidence map›Paper›PMID 26593398›Full record

ArticleScientific reports2015

EZH2 is highly expressed in pituitary adenomas and associated with proliferation.

David Schult, Annett Hölsken, Sonja Siegel, Michael Buchfelder, Rudolf Fahlbusch, Ilonka Kreitschmann-Andermahr, Rolf Buslei

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. International journal of molecular sciences · 2023
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. 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 2 institutions in 1 country.

David SchultInstitute of Neuropathology, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054 Erlangen.
Annett HölskenInstitute of Neuropathology, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054 Erlangen.
Sonja SiegelDepartment of Neurosurgery, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054 Erlangen.
Michael BuchfelderDepartment of Neurosurgery, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054 Erlangen.
Rudolf FahlbuschDepartment of Neurosurgery, International Neuroscience Institute, Rudolf-Pichlmayr-Straße 4, 30625 Hannover.
Ilonka Kreitschmann-AndermahrDepartment of Neurosurgery, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054 Erlangen.
Rolf BusleiInstitute of Neuropathology, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054 Erlangen.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEInternational Neuroscience Institute · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enhancer of zeste homolog 2 (EZH2) is a core epigenetic regulator, playing a crucial role in cell cycle regulation. The protein is known to be associated with proliferation and worse outcome in several tumor entities. In this study, we immunohistochemically investigated the expression pattern of EZH2 in a large cohort of pituitary tumors. These results were correlated with clinical features and double immunofluorescence stainings (DIS) were conducted to evaluate co-expression of EZH2 and proliferation marker Ki-67. Furthermore, we analyzed the effect of EZH2 inhibition on cell proliferation in vitro using the pituitary cell line AtT-20. While in the normal anterior pituitary EZH2 was almost absent, the cohort of tumors showed enhanced expression levels (p ≤ 0.0005). This was positively associated with Ki-67 indices (r = 0.834, p ≤ 0.0005) and DIF confirmed a predominant co-expression of both markers. In vitro experiments revealed a significant (p ≤ 0.05) decrease of tumor cell proliferation using the EZH2 inhibitor GSK126. Our results further support that epigenetic events are involved in the pathogenesis and biology of pituitary adenomas (PA). Therefore, EZH2 may function as a new potential target for therapeutic interventions in PA.

Indexed as

Gene Expression Regulation, NeoplasticAdenomaAdolescentAdultAgedAged, 80 and overAntineoplastic AgentsCell Line, TumorCell ProliferationCohort StudiesEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsEpigenesis, GeneticFemaleHistonesHumansAntineoplastic AgentsEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsEZH2 protein, humanGSK-2816126HistonesIndolesKi-67 AntigenPolycomb Repressive Complex 2Pyridones

Identifiers

PMID26593398
PMCPMC4655333
OpenAlexW2415648435

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.