Evidence map›Paper›PMID 20133820›Full record

ArticleThe American journal of pathology2010

Novel proteins regulated by mTOR in subependymal giant cell astrocytomas of patients with tuberous sclerosis complex and new therapeutic implications.

Magdalena Ewa Tyburczy, Katarzyna Kotulska, Piotr Pokarowski, Jakub Mieczkowski, Joanna Kucharska, Wieslawa Grajkowska, Maciej Roszkowski, Sergiusz Jozwiak, Bozena Kaminska

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
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  6. Review
  7. iScience · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Subependymal giant cell astrocytomas are characterized by mTORC1 hyperactivation, a very low somatic mutation rate, and a unique gene expression profile.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021
    Article
  14. TheFrontiers in molecular neuroscience · 2021
    Article
  15. Article
  16. New frontiers in modeling tuberous sclerosis with human stem cell-derived neurons and brain organoids.Developmental dynamics : an official publication of the American Association of Anatomists · 2020
    Review
  17. Review
  18. Article
  19. Article
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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

9 authors at 3 institutions in 1 country.

Magdalena Ewa TyburczyThe Nencki Institute of Experimental Biology, Warsaw, Poland.
Katarzyna Kotulska
Piotr Pokarowski
Jakub Mieczkowski
Joanna Kucharska
Wieslawa Grajkowska
Maciej Roszkowski
Sergiusz Jozwiak
Bozena Kaminska
Children's Memorial Health Institute · PLInstytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLUniversity of Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subependymal giant cell astrocytomas (SEGAs) are rare brain tumors associated with tuberous sclerosis complex (TSC), a disease caused by mutations in TSC1 or TSC2, resulting in enhancement of mammalian target of rapamycin (mTOR) activity, dysregulation of cell growth, and tumorigenesis. Signaling via mTOR plays a role in multifaceted genomic responses, but its effectors in the brain are largely unknown. Therefore, gene expression profiling on four SEGAs was performed with Affymetrix Human Genome arrays. Of the genes differentially expressed in TSC, 11 were validated by real-time PCR on independent tumor samples and 3 SEGA-derived cultures. Expression of several proteins was confirmed by immunohistochemistry. The differentially-regulated proteins were mainly involved in tumorigenesis and nervous system development. ANXA1, GPNMB, LTF, RND3, S100A11, SFRP4, and NPTX1 genes were likely to be mTOR effector genes in SEGA, as their expression was modulated by an mTOR inhibitor, rapamycin, in SEGA-derived cells. Inhibition of mTOR signaling affected size of cultured SEGA cells but had no influence on their proliferation, morphology, or migration, whereas inhibition of both mTOR and extracellular signal-regulated kinase signaling pathways led to significant alterations of these processes. For the first time, we identified genes related to the occurrence of SEGA and regulated by mTOR and demonstrated an effective modulation of SEGA growth by pharmacological inhibition of both mTOR and extracellular signal-regulated kinase signaling pathways, which could represent a novel therapeutic approach.

Indexed as

Gene Expression Regulation, NeoplasticAstrocytesAstrocytomaBromodeoxyuridineGene Expression ProfilingGiant CellsHumansImmunohistochemistryModels, BiologicalOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionRNASignal TransductionTOR Serine-Threonine KinasesTuberous SclerosisBromodeoxyuridineMTOR protein, humanRNATOR Serine-Threonine Kinases

Identifiers

PMID20133820
PMCPMC2843477
OpenAlexW2156198853

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.