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Genome-Wide Allelic Imbalance Analysis of Pediatric Gliomas by Single Nucleotide Polymorphic Allele Array

¹ Department of Gynecologic Oncology, The University of Texas M.D. Anderson Cancer Center; ² Texas Children's Cancer Center and Departments of ³ Pediatrics, ⁴ Neurosurgery, and ⁵ Pathology, Baylor College of Medicine, Houston, Texas; and ⁶ Department of Pediatrics, Catholic University of Rome, Italy

Requests for reprints: Kwong-Kwok Wong, Department of Gynecologic Oncology, The University of Texas M.D. Anderson Cancer Center, Unit 1362, 1515 Holcombe Boulevard, Houston, Texas 77030. Phone: 713-792-0229; Fax: 713-745-5099; E-mail: kkwong{at}mdanderson.org.

Using single nucleotide polymorphic (SNP) allele arrays, we analyzed 28 pediatric gliomas consisting of 14 high-grade gliomas and 14 low-grade gliomas. Most of the low-grade gliomas had no detectable loss of heterozygosity (LOH) in any of the 11,562 SNP loci; exceptions were two gangliogliomas (3q and 9p), one astrocytoma (6q), and two subependymal giant cell astrocytomas (16p and 21q). On the other hand, all high-grade gliomas had various degrees of LOH affecting 52 to 2,168 SNP loci on various chromosomes. LOH occurred most frequently in regions located at 4q (54%), 6q (46%), 9p (38%), 10q (38%), 11p (38%), 12 (38%), 13q (69%), 14q (54%), 17 (38%), 18p (46%), and 19q (38%). We also detected amplifications of epidermal growth factor receptor (EGFR) or platelet-derived growth factor receptor (PDGFR) in a few of the 13 cases of glioblastoma multiforme analyzed. Interestingly, the amplified EGFR and PDGFR were located within regions of LOH. SNP loci with LOH and copy number changes were validated by sequencing and quantitative PCR, respectively. Our results indicate that, in some pediatric glioblastoma multiforme, one allele each of EGFR and PDGFR was lost but the remaining allele was amplified. This may represent a new molecular mechanism underlying tumor progression. (Cancer Res 2006; 66(23): 11172-8)

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