Evidence map›Paper›PMID 30139767›Full record

ArticleEndocrine-related cancer2019

Non-secreting pituitary tumours characterised by enhanced expression of YAP/TAZ.

Paraskevi Xekouki, Emily J Lodge, Jakob Matschke, Alice Santambrogio, John R Apps, Ariane Sharif, Thomas S Jacques, Simon Aylwin, Vincent Prevot, Ran Li and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Endocrine-related cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Pituitary Tumorigenesis-Implications for Management.Medicina (Kaunas, Lithuania) · 2023
    Review
  6. Article
  7. Cellular interactions in the pituitary stem cell niche.Cellular and molecular life sciences : CMLS · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. 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

14 authors at 10 institutions in 4 countries.

Paraskevi XekoukiCentre for Craniofacial and Regenerative Biology, King's College London, London, UK.
Emily J LodgeCentre for Craniofacial and Regenerative Biology, King's College London, London, UK.
Jakob MatschkeInstitute of Neuropathology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
Alice SantambrogioCentre for Craniofacial and Regenerative Biology, King's College London, London, UK.
John R AppsBirth Defects Research Centre, Developmental Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, University College London, London, UK.
Ariane SharifLaboratory of Development and Plasticity of the Neuroendocrine Brain, Inserm U1172, Jean-Pierre Aubert Research Centre, Lille, France.
Thomas S JacquesBirth Defects Research Centre, Developmental Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, University College London, London, UK.
Simon AylwinDepartment of Endocrinology, King's College Hospital NHS Foundation Trust, London, UK.
Vincent PrevotLaboratory of Development and Plasticity of the Neuroendocrine Brain, Inserm U1172, Jean-Pierre Aubert Research Centre, Lille, France.
Ran LiDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Jörg FlitschDepartment of Neurosurgery, Hamburg University Medical Center, Hamburg, Germany.
Stefan R BornsteinDepartment of Endocrinology and Diabetes, King's College London, London, UK.
Marily TheodoropoulouMedizinische Klinik und Poliklinik IV, Ludwig-Maximilians-Universität München, Munich, Germany.
Cynthia L AndoniadouCentre for Craniofacial and Regenerative Biology, King's College London, London, UK.
King's College London · GBUniversität Hamburg · DECentre de Recherche Jean Pierre Aubert · FRGreat Ormond Street Hospital · GBHuazhong University of Science and Technology · CNInserm · FRKing's College Hospital NHS Foundation Trust · GBLudwig-Maximilians-Universität München · DEUniversity College London · GBUniversity Hospital Carl Gustav Carus · DE

Funding

Medical Research Council G0701018Medical Research Council G1100578Medical Research Council MR/L016729/1Medical Research Council MR/N004272/1Wellcome Trust
6 · The paper itself

Abstract

Tumours of the anterior pituitary can manifest from all endocrine cell types but the mechanisms for determining their specification are not known. The Hippo kinase cascade is a crucial signalling pathway regulating growth and cell fate in numerous organs. There is mounting evidence implicating this in tumour formation, where it is emerging as an anti-cancer target. We previously demonstrated activity of the Hippo kinase cascade in the mouse pituitary and nuclear association of its effectors YAP/TAZ with SOX2-expressing pituitary stem cells. Here, we sought to investigate whether these components are expressed in the human pituitary and if they are deregulated in human pituitary tumours. Analysis of pathway components by immunofluorescence reveals pathway activity during normal human pituitary development and in the adult gland. Poorly differentiated pituitary tumours (null-cell adenomas, adamantinomatous craniopharyngiomas (ACPs) and papillary craniopharyngiomas (PCPs)), displayed enhanced expression of pathway effectors YAP/TAZ. In contrast, differentiated adenomas displayed lower or absent levels. Knockdown of the kinase-encoding Lats1 in GH3 rat mammosomatotropinoma cells suppressed Prl and Gh promoter activity following an increase in YAP/TAZ levels. In conclusion, we have demonstrated activity of the Hippo kinase cascade in the human pituitary and association of high YAP/TAZ with repression of the differentiated state both in vitro and in vivo. Characterisation of this pathway in pituitary tumours is of potential prognostic value, opening up putative avenues for treatments.

Indexed as

Adaptor Proteins, Signal TransducingAgedAged, 80 and overAnimalsApoptosis Regulatory ProteinsCell Line, TumorFemaleHumansIntracellular Signaling Peptides and ProteinsMalePituitary GlandPituitary NeoplasmsProtein Serine-Threonine KinasesRatsRNA InterferenceTrans-ActivatorsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsIntracellular Signaling Peptides and ProteinsLats1 protein, ratProtein Serine-Threonine KinasesTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humanWWTR1 protein, ratYAP1 protein, humanYap1 protein, ratYAP-Signaling ProteinsHippo signallingpituitary tumourTAZYAP

Identifiers

PMID30139767
PMCPMC6215911
OpenAlexW2889032866

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.