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    Microarray analysis of pediatric ependymoma identifies a cluster of 112 candidate genes including four transcripts at 22q12.1-q13.3.

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    Authors
    Suarez-Merino, Blanca
    Hubank, Mike
    Revesz, Tamas
    Harkness, William
    Hayward, Richard
    Thompson, Dominic
    Darling, John L.
    Thomas, David G.
    Warr, Tracy
    Issue Date
    2005
    
    Metadata
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    Abstract
    Ependymomas are glial cell-derived tumors characterized by varying degrees of chromosomal abnormalities and variability in clinical behavior. Cytogenetic analysis of pediatric ependymoma has failed to identify consistent patterns of abnormalities, with the exception of monosomy of 22 or structural abnormalities of 22q. In this study, a total of 19 pediatric ependymoma samples were used in a series of expression profiling, quantitative real-time PCR (Q-PCR), and loss of heterozygosity experiments to identify candidate genes involved in the development of this type of pediatric malignancy. Of the 12,627 genes analyzed, a subset of 112 genes emerged as being abnormally expressed when compared to three normal brain controls. Genes with increased expression included the oncogene WNT5A; the p53 homologue p63; and several cell cycle, cell adhesion, and proliferation genes. Underexpressed genes comprised the NF2 interacting gene SCHIP-1 and the adenomatous polyposis coli (APC)-associated gene EB1 among others. We validated the abnormal expression of six of these genes by Q-PCR. The subset of differentially expressed genes also included four underexpressed transcripts mapping to 22q12.313.3. By Q-PCR we show that one of these genes, 7 CBX7(22q13.1), was deleted in 55% of cases. Other genes mapping to cytogenetic hot spots included two overexpressed and three underexpressed genes mapping to 1q31-41 and 6q21-q24.3, respectively. These genes represent candidate genes involved in ependymoma tumorigenesis. To the authors' knowledge, this is the first time microarray analysis and Q-PCR have been linked to identify heterozygous/homozygous deletions.
    Citation
    Neuro-oncology, 7(1): 20-31
    Publisher
    Duke University Press
    URI
    http://hdl.handle.net/2436/16695
    DOI
    10.1215/S1152851704000596
    PubMed ID
    15701279
    Additional Links
    http://neuro-oncology.dukejournals.org/cgi/content/abstract/7/1/20
    Type
    Journal article
    Language
    en
    Description
    Metadata only. Full text available at links above.
    ISSN
    1522-8517
    ae974a485f413a2113503eed53cd6c53
    10.1215/S1152851704000596
    Scopus Count
    Collections
    Research Institute in Healthcare Science

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