Evidence map›Paper›PMID 18924150›Full record

ArticleInternational journal of cancer2009

Defining a role for Sonic hedgehog pathway activation in desmoplastic medulloblastoma by identifying GLI1 target genes.

Joon Won Yoon, Richard Gilbertson, Stephen Iannaccone, Philip Iannaccone, David Walterhouse

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  13. A highlight on Sonic hedgehog pathway.Cell communication and signaling : CCS · 2018
    Review
  14. Review
  15. Article
  16. Article
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  19. Sonic hedgehog patterning during cerebellar development.Cellular and molecular life sciences : CMLS · 2016
    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

5 authors at 2 institutions in 1 country.

Joon Won YoonDevelopmental Biology Program, Children's Memorial Research Center, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Richard Gilbertson
Stephen Iannaccone
Philip Iannaccone
David Walterhouse
Northwestern University · USSt. Jude Children's Research Hospital · US

Funding

Physiology Core - Interdepartmental Two-photon Imaging CenterP30NS054850 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SURMEIER, DALTON JAMES · 2007 to 2012
$3.3M
An Investigation of Radial Glia as the Source of Ependymoma Stem CellsR01CA129541 · NCI · UNIVERSITY OF CAMBRIDGE · PI GILBERTSON, RICHARD · 2007 to 2016
$3.0M
NCI NIH HHS R01 CA129541NINDS NIH HHS P30 NS054850
6 · The paper itself

Abstract

A subgroup of medulloblastomas shows constitutive activation of the Sonic hedgehog pathway with expression of GLI1. We identified the subset of GLI1 transforming target genes specifically expressed in medulloblastomas by comparing GLI1 targets in RK3E cells transformed by GLI1 with the gene expression profile of Sonic hedgehog signature medulloblastomas. We identified 1,823 genes whose expression was altered more than 2-fold in 2 independent RK3E + GLI1 cell lines. We identified 25 whose expression was altered similarly in medulloblastomas expressing GLI1. We identified potential GLI binding elements in the regulatory regions of 10 of these genes, confirmed that GLI1 binds the regulatory regions and activates transcription of select genes, and showed that GLI1 directly represses transcription of Krox-20. We identified upregulation of CXCR4, a chemokine receptor that plays roles in the proliferation and migration of granule cell neuron precursors during development, supporting the concept that reinitiation of developmental programs may contribute to medulloblastoma tumorigenesis. In addition, the targets suggest a pathway through which GLI1 may ultimately affect medulloblastoma cell proliferation, survival and genomic stability by converging on p53, SGK1, MGMT and NTRK2. We identify a p53 mutation in RK3E + GLI1 cells, suggesting that p53 mutations may sometimes shift the balance toward dysregulated tumor cell survival.

Indexed as

AnimalsCerebellar NeoplasmsDNA Modification MethylasesDNA Repair EnzymesEpithelial CellsHedgehog ProteinsHeLa CellsHumansImmediate-Early ProteinsKidneyMedulloblastomaProtein Serine-Threonine KinasesRatsReceptors, CXCR4Receptor, trkBSerum-Glucocorticoid Regulated KinasesCXCR4 protein, humanDNA Modification MethylasesDNA Repair EnzymesGLI1 protein, humanHedgehog ProteinsImmediate-Early ProteinsMGMT protein, humanProtein Serine-Threonine KinasesReceptors, CXCR4Receptor, trkBSerum-Glucocorticoid Regulated KinasesTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor ProteinsZinc Finger Protein GLI1

Identifiers

PMID18924150
PMCPMC3889649
OpenAlexW2078505529

What OpenQuestion holds

Textmetadata
LicenceTDM
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.