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Wolverhampton Intellectual Repository and E-Theses > Research Institutes > Research Institute in Healthcare Science > Cancer Research Group > Abnormal gene expression can be linked to chromosomal gains and losses in paediatric astrocytoma

Please use this identifier to cite or link to this item: http://hdl.handle.net/2436/29973
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Title: Abnormal gene expression can be linked to chromosomal gains and losses in paediatric astrocytoma
Other Titles: In: Abstracts for the Eleventh Annual Meeting of the Society for Neuro-Oncology: November 16–19, 2006. PE-16
Authors: Potter, N.
Poh, R.
Ward, Samantha
Phipps, Kim
Hayward, Richard
Harkness, William
Thompson, Dominic
Thomas, David G.
Rees, J.
Darling, John L.
Warr, Tracy
Citation: Neuro-oncology, 8(4): 468
Publisher: Society for Neuro-Oncology and Duke University Press
Journal: Neuro-oncology
Issue Date: 2006
URI: http://hdl.handle.net/2436/29973
Additional Links: http://neuro-oncology.dukejournals.org/
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1871956
Abstract: Brain tumors are the most frequently found solid tumor in children, 40% of which are astrocytomas. These are graded according to the WHO classification into the more common low-grade (I and II) and high-grade (III and IV) tumors. Little is known about the genetic basis underlying the development of pediatric astrocytomas. In this study, we have studied the correlation between abnormal gene expression in pediatric astrocytoma with genomic copy number changes. We used the Affymetrix HGU133A array to identify differentially expressed genes in a group of pediatric astrocytoma short-term cell cultures comprising 9 grade I, 11 grade II and 12 grade IV tumors. Data analysis was carried out using Genespring version 6.0 software. In addition, we used the Spectral Chip 2600 to generate array-comparative genomic hybridization (aCGH) profiles of each short-term cell culture. Chromosome regions of gain and loss were then compared with differential gene expression using Formatter software. Hierarchical clustering of the short-term cultures according to expression profile similarity showed that the tumors clustered into 3 clear groups that were independent of grade. Two groups were predominantly low-grade tumors, comprised of a mixture of grade I and II tumors with 3 grade IV tumors, and the third group contained predominantly high-grade tumors with 2 low-grade tumors. Genes involved in the phosphatidylinositol signaling system, the cell cycle pathway, and the regulation of the actin cytoskeleton, were significantly differentially expressed between the 3 groups. Differential disruption of these cell pathways may be associated with subtypes of pediatric astrocytoma. Most tumors in the third group (including the low-grade tumors) showed copy number changes that can be correlated with changes in gene expression. In specific tumors, the downregulation of TSB1 (thrombospondin-1) correlated with loss at 15q15. This gene has previously been found to be downregulated in astrocytoma and is involved in cell adhesion. This finding suggests that gene expression in a subset of pediatric astrocytomas is influenced by gene dosage.
Type: Meetings & Proceedings
Language: en
Description: Abstracts from Neuro-Oncology are provided here courtesy of Society for Neuro-Oncology and Duke University Press
Keywords: Brain Tumours
Malignant tumours
Astrocytoma
Oncology
Genomics
HGU133A
Cell Line, Tumor
Cell Culture
Gene Expression
Paediatric tumours
Cancer genetics
Tumor Cells, Cultured
Cancer progression
Children
Chromosome Disorders
Chromosomal Aberrations
In Situ Hybridization
Gene Dosage
ISSN: 1522-8517
Appears in Collections: Cancer Research Group

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