Microarray analysis of pediatric ependymoma identifies a cluster of 112 candidate genes including four transcripts at 22q12.1-q13.3.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Darling, John L.
Thomas, David G.
MetadataShow full item record
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.
CitationNeuro-oncology, 7(1): 20-31
PublisherDuke University Press
DescriptionMetadata only. Full text available at links above.
- Real-time quantitative PCR analysis of pediatric ependymomas identifies novel candidate genes including TPR at 1q25 and CHIBBY at 22q12-q13.
- Authors: Karakoula K, Suarez-Merino B, Ward S, Phipps KP, Harkness W, Hayward R, Thompson D, Jacques TS, Harding B, Beck J, Thomas DG, Warr TJ
- Issue date: 2008 Nov
- Identification of tumor-specific molecular signatures in intracranial ependymoma and association with clinical characteristics.
- Authors: Modena P, Lualdi E, Facchinetti F, Veltman J, Reid JF, Minardi S, Janssen I, Giangaspero F, Forni M, Finocchiaro G, Genitori L, Giordano F, Riccardi R, Schoenmakers EF, Massimino M, Sozzi G
- Issue date: 2006 Nov 20
- Loss of heterozygosity on chromosome 22 in human ependymomas.
- Authors: Huang B, Starostik P, Kühl J, Tonn JC, Roggendorf W
- Issue date: 2002 Apr
- Molecular genetic alterations on chromosomes 11 and 22 in ependymomas.
- Authors: Lamszus K, Lachenmayer L, Heinemann U, Kluwe L, Finckh U, Höppner W, Stavrou D, Fillbrandt R, Westphal M
- Issue date: 2001 Mar 15
- Cytogenetic evidence for a chromosome 22 tumor suppressor gene in ependymoma.
- Authors: Weremowicz S, Kupsky WJ, Morton CC, Fletcher JA
- Issue date: 1992 Jul 15