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dc.contributor.authorSuarez-Merino, Blanca
dc.contributor.authorHubank, Mike
dc.contributor.authorRevesz, Tamas
dc.contributor.authorHarkness, William
dc.contributor.authorHayward, Richard
dc.contributor.authorThompson, Dominic
dc.contributor.authorDarling, John L.
dc.contributor.authorThomas, David G.
dc.contributor.authorWarr, Tracy
dc.date.accessioned2008-01-23T14:59:53Z
dc.date.available2008-01-23T14:59:53Z
dc.date.issued2005
dc.identifier.citationNeuro-oncology, 7(1): 20-31
dc.identifier.issn1522-8517
dc.identifier.pmid15701279
dc.identifier.doi10.1215/S1152851704000596
dc.identifier.urihttp://hdl.handle.net/2436/16695
dc.descriptionMetadata only. Full text available at links above.
dc.description.abstractEpendymomas 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.
dc.language.isoen
dc.publisherDuke University Press
dc.relation.urlhttp://neuro-oncology.dukejournals.org/cgi/content/abstract/7/1/20
dc.subject.meshBrain Neoplasms
dc.subject.meshChildren
dc.subject.meshChild, Preschool
dc.subject.meshChromosomes, Human, Pair 22
dc.subject.meshEpendymoma
dc.subject.meshFemale
dc.subject.meshHumans
dc.subject.meshInfant
dc.subject.meshLoss of Heterozygosity
dc.subject.meshMale
dc.subject.meshOligonucleotide Array Sequence Analysis
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction
dc.titleMicroarray analysis of pediatric ependymoma identifies a cluster of 112 candidate genes including four transcripts at 22q12.1-q13.3.
dc.typeArticle
html.description.abstractEpendymomas 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.


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