Evidence map›Paper›PMID 18670637›Full record

ArticleNeoplasia (New York, N.Y.)2008

Genomic deletions correlate with underexpression of novel candidate genes at six loci in pediatric pilocytic astrocytoma.

Nicola Potter, Aikaterini Karakoula, Kim P Phipps, William Harkness, Richard Hayward, Dominic N P Thompson, Thomas S Jacques, Brian Harding, David G T Thomas, Rodger W Palmer and 3 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. The protein interactome of the Neuron Specific Gene family (NSG1-3).bioRxiv : the preprint server for biology · 2025
    Article
  2. Review
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  4. Article
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  6. BCL7A as a novel prognostic biomarker for glioma patients.Journal of translational medicine · 2021
    Article
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  12. SWI/SNF chromatin remodeling complexes and cancer.American journal of medical genetics. Part C, Seminars in medical genetics · 2014
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. MAPK pathway activation in pilocytic astrocytoma.Cellular and molecular life sciences : CMLS · 2012
    Review
  18. Article
  19. Article
  20. Review
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

13 authors at 4 institutions in 1 country.

Nicola PotterDepartment of Molecular Neuroscience, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, London, UK. n.potter@ion.ucl.ac.uk
Aikaterini Karakoula
Kim P Phipps
William Harkness
Richard Hayward
Dominic N P Thompson
Thomas S Jacques
Brian Harding
David G T Thomas
Rodger W Palmer
Jeremy Rees
John Darling
Tracy J Warr
University College London · GBGreat Ormond Street Hospital · GBNational Hospital for Neurology and Neurosurgery · GBUniversity of Wolverhampton · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular pathogenesis of pediatric pilocytic astrocytoma (PA) is not well defined. Previous cytogenetic and molecular studies have not identified nonrandom genetic aberrations. To correlate differential gene expression and genomic copy number aberrations (CNAs) in PA, we have used Affymetrix GeneChip HG_U133A to generate gene expression profiles of 19 pediatric patients and the SpectralChip 2600 to investigate CNAs in 11 of these tumors. Hierarchical clustering according to expression profile similarity grouped tumors and controls separately. We identified 1844 genes that showed significant differential expression between tumor and normal controls, with a large number clearly influencing phosphatidylinositol and mitogen-activated protein kinase signaling in PA. Most CNAs identified in this study were single-clone alterations. However, a small region of loss involving up to seven adjacent clones at 7q11.23 was observed in seven tumors and correlated with the underexpression of BCL7B. Loss of four individual clones was also associated with reduced gene expression including SH3GL2 at 9p21.2-p23, BCL7A (which shares 90% sequence homology with BCL7B) at 12q24.33, DRD1IP at 10q26.3, and TUBG2 and CNTNAP1 at 17q21.31. Moreover, the down-regulation of FOXG1B at 14q12 correlated with loss within the gene promoter region in most tumors. This is the first study to correlate differential gene expression with CNAs in PA.

Indexed as

Adaptor Proteins, Signal TransducingAdultAstrocytomaBrain NeoplasmsCell Adhesion Molecules, NeuronalChildChild, PreschoolChromosome AberrationsChromosomes, Human, Pair 10Chromosomes, Human, Pair 12Chromosomes, Human, Pair 17Chromosomes, Human, Pair 7Chromosomes, Human, Pair 9Cluster AnalysisFemaleForkhead Transcription FactorsAdaptor Proteins, Signal TransducingBCL7A protein, humanBCL7B protein, humanCell Adhesion Molecules, NeuronalCNTNAP1 protein, humanForkhead Transcription FactorsFOXG1 protein, humanMicrofilament ProteinsNerve Tissue ProteinsOncogene ProteinsProteinsReceptors, Dopamine D1SH3GL2 protein, human

Identifiers

PMID18670637
PMCPMC2481566
OpenAlexW1263789922

What OpenQuestion holds

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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.