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Neuro-Oncology 2005 7(1):20-31; doi:10.1215/S1152851704000596
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© 2005 by the Society forNeuro-Oncology

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

Blanca Suarez-Merino, Mike Hubank, Tamas Revesz, William Harkness, Richard Hayward, Dominic Thompson, John L. Darling, David G.T. Thomas and Tracy J. Warr3

Department of Molecular Neuroscience (B.S.-M., T.R.,T.J.W.) and Division of Neurosurgery (D.G.T.T.),Institute of Neurology, National Hospital for Neurology and Neurosurgery,and Department of Molecular Haematology, Institute ofChild Health (M.H.), University College London, London; Department of Neurosurgery, Great Ormond Street Hospitalfor Sick Children NHS Trust, London (W.H., R.H., D.T.); Research Institute in Healthcare Science, University ofWolverhampton, Wolverhampton (J.L.D.); UK

3 Address correspondence to Tracy J. Warr, Department of Molecular Neuroscience,Neuro-Oncology Group, Institute of Neurology, Queen Square, London WC1N 3BG,UK(T.Warr{at}ion.ucl.ac.uk).


  Abstract

Ependymomas are glial cell-derived tumors characterized by varying degreesof chromosomal abnormalities and variability in clinical behavior. Cytogeneticanaly-sis of pediatric ependymoma has failed to identify consistent patternsof abnormalities, with the exception of monosomy of 22 or structuralabnormalities of 22q. In this study, a total of 19 pediatric ependymomasamples were used in a series of expression profiling, quantitative real-timePCR (Q-PCR), and loss of heterozygosity experiments to identify candidategenes involved in the development of this type of pediatric malignancy. Of the12,627 genes analyzed, a subset of 112 genes emerged as being abnormallyexpressed when compared to three normal brain controls. Genes with increasedexpression included the oncogene WNT5A; the p53 homologuep63; and several cell cycle, cell adhesion, and proliferation genes.Underexpressed genes comprised the NF2 interact-ing geneSCHIP-1 and the adenomatous polyposis coli (APC)-associatedgene EB1 among others. We validated the abnormal expression of six ofthese genes by Q-PCR. The subset of differentially expressed genes alsoincluded four underexpressed transcripts mapping to 22q12.3-13.3. By Q-PCR weshow that one of these genes, CBX7 (22q13.1), was deleted in 55% ofcases. Other genes mapping to cytogenetic hot spots included two overexpressedand three underexpressed genes mapping to 1q31-41 and 6q21-q24.3,respectively. These genes represent candidate genes involved in ependymomatumorigenesis. To the authors' knowledge, this is the first time microarrayanalysis and Q-PCR have been linked to identify heterozygous/homozygousdeletions.

Received June 14, 2004; Accepted September 2, 2004


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