Identification of differentially expressed genes in paediatric ependymoma
Suarez-Merino, Blanca Hubank, Mike Hayward, Richard Harkness, William Thompson, Dominic Phipps, Kim Revesz, Tamas Darling, John L. Thomas, David G. Warr, Tracy
Suarez-Merino, Blanca
Hubank, Mike
Hayward, Richard
Harkness, William
Thompson, Dominic
Phipps, Kim
Revesz, Tamas
Darling, John L.
Thomas, David G.
Warr, Tracy
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2003
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In: Abstracts from the Fifteenth International Conference on Brain Tumor Research and Therapy, May 24–27, 2003, Sorrento, Italy. No.124
Abstract
To date, the genetic events that contribute to the pathogenesis of ependymoma are essentially unknown. Furthermore, previous cytogenetic studies have demonstrated that approximately 50% of tumors have no detectable chromosome abnormalities. In this study, we used the Affymetrix GeneChip U95Av2 microarrays to generate gene expression profiles in 11 pediatric ependymoma, comprising 6 fresh frozen samples and 5 short-term cultures. A total of 107 genes were differentially expressed in both the biopsies and cell cultures compared with normal control tissue derived from corpus callosum. The 84 genes with increased expression included many encoding adhesion and extracellular matrix proteins; genes involved in the cell cycle, such as cyclin D1, CDK2, CDK4, and Wee1; transcription factors such as Zic1; and known oncogenes such as c-myc, WNT5A, JUN, TC21, RAB36, and FOP. An interesting group also found to be overexpressed comprises the insulin-like growth factor binding proteins IGFBP2, IGFBP3, and IGFBP4, which may be responsible for the autostimulation of cell growth in these tumors. Of the 23 genes that were underexpressed by 5-fold or less, 6 were of unknown function. Others included the apoptotic control gene ATIP the DAAM1 gene associated with the Wnt/frz oncogenic pathway, and genes involved in vesicle trafficking and recycling within and across cells, such as NPC1, RAB40B, TJP2, and SH3GL3. We have identified a number of candidate genes and genetic pathways that have not previously been associated with the pathogenesis of pediatric ependymoma. Further evaluation of the expression or mutation status of these genes will elucidate their roles in ependymoma development.
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Neuro-oncology, 5(4): 399
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en
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Abstracts from Neuro-Oncology are provided here courtesy of Society for Neuro-Oncology and Duke University Press.
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1522-8517