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

Potter, N; Karakoula, A; Phipps, KP; Harkness, W; Hayward, R; Thompson, DNP; Jacques, TS; ... Warr, TJ; + view all (2008) Genomic deletions correlate with underexpression of novel candidate genes at six loci in pediatric pilocytic astrocytoma. NEOPLASIA , 10 (8) 757 - U37. 10.1593/neo.07914. Gold open access

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.

Type: Article
Title: Genomic deletions correlate with underexpression of novel candidate genes at six loci in pediatric pilocytic astrocytoma
Open access status: An open access publication
DOI: 10.1593/neo.07914
Publisher version: http://www.ncbi.nlm.nih.gov/pmc/ articles/PMC24815...
Keywords: COPY-NUMBER VARIATION, IDENTIFIES MOLECULAR SUBTYPES, NERVOUS-SYSTEM TUMORS, LOW-GRADE, PROMOTER HYPERMETHYLATION, GLIOBLASTOMA-MULTIFORME, MICROARRAY DATA, BRAIN-TUMORS, EPIGENETIC INACTIVATION, MALIGNANT PROGRESSION
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > UCL GOS Institute of Child Health
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > UCL GOS Institute of Child Health > ICH Development Bio and Cancer Prog
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > UCL GOS Institute of Child Health > ICH Developmental Neurosciences Prog
URI: http://discovery.ucl.ac.uk/id/eprint/114720
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