Evidence map›Paper›PMID 19371356›Full record

ArticleBrain pathology (Zurich, Switzerland)2010

Pi3K-mTOR signaling and AMOG expression in epilepsy-associated glioneuronal tumors.

Karin Boer, Dirk Troost, Wendy Timmermans, Peter C van Rijen, Wim G M Spliet, Eleonora Aronica

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Glioma genetic profiles associated with electrophysiologic hyperexcitability.medRxiv : the preprint server for health sciences · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. What is New in the Management of Epilepsy in Gliomas?Current treatment options in neurology · 2015
    Article
  17. Malformations of cortical development and epilepsy.Cold Spring Harbor perspectives in medicine · 2015
    Review
  18. Review
  19. Review
  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

6 authors at 3 institutions in 1 country.

Karin BoerDepartment of (Neuro)Pathology, Academic Medical Center, University of Amsterdam, The Netherlands.
Dirk Troost
Wendy Timmermans
Peter C van Rijen
Wim G M Spliet
Eleonora Aronica
University of Amsterdam · NLAcademic Medical Center · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gangliogliomas (GGs) and dysembryoplastic neuroepithelial tumors (DNTs) represent the most frequent type of neoplasms in pediatric medically intractable epilepsy. Several data suggest a pathogenetic relationship between GGs and other glioneuronal malformations of cortical development (MCDs), including activation of the Pi3K-mTOR signaling pathway. To further reveal these pathogenetic similarities, we investigated immunocytochemically the expression of phosphorylated (p)-PDK1, p-AKT, p-mTOR, p-4E-BP1, p-eIF4G, p-p70S6K and p-S6, the effector proteins ERM (ezrin/radixin/moesin) and the pathway regulator AMOG (adhesion molecule on glia) in both GGs and DNTs. Components of the Pi3K-mTOR signaling pathway were observed in a higher percentage of neuronal cells in GGs compared with control cortex. In DNTs, the expression of these components was low and comparable with the expression in control samples. Strong immunoreactivity for ERM was observed in GGs, but not in DNTs. Additionally, AMOG was strongly expressed within GGs (but not in DNTs) in CD34-positive precursor cells. These findings support the previously suggested pathogenic relationship between GG and MCDs concerning activation of the Pi3K-mTOR signaling pathway and suggest a different pathogenetic origin for DNTs. The strong expression of AMOG within the precursor cells of GG may represent an additional marker for the diagnostic evaluation of these glioneuronal lesions.

Indexed as

Adenosine TriphosphatasesAdultAgedAntigens, CD34AutopsyBrain NeoplasmsCation Transport ProteinsCell Adhesion Molecules, NeuronalCerebral CortexChildCytoskeletal ProteinsDrug ResistanceEpilepsyEzrinFemaleGangliogliomaAdenosine TriphosphatasesAntigens, CD34ATP1B2 protein, humanCation Transport ProteinsCell Adhesion Molecules, NeuronalCytoskeletal ProteinsEzrinIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicrofilament ProteinsmoesinMTOR protein, humanPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesradixinRibosomal Protein S6TOR Serine-Threonine Kinases

Identifiers

PMID19371356
PMCPMC8094642
OpenAlexW1531802145

What OpenQuestion holds

Textmetadata
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.