TY - JOUR
T1 - Genome-wide allelic imbalance analysis of pediatric gliomas by single nucleotide polymorphic allele array
AU - Wong, Kwong Kwok
AU - Tsang, Yvonne T.M.
AU - Chang, Yi Mieng
AU - Su, Jack
AU - Di Francesco, Angela M.
AU - Meco, Daniela
AU - Riccardi, Riccardo
AU - Perlaky, Laszlo
AU - Dauser, Robert C.
AU - Adesina, Adekunle
AU - Bhattacharjee, Meenakshi
AU - Chintagumpala, Murali
AU - Lau, Ching C.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2006/12/1
Y1 - 2006/12/1
N2 - 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 α (PDGFRα) in a few of the 13 cases of glioblastoma multiforme analyzed. Interestingly, the amplified EGFR and PDGFRα 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 PDGFRα was lost but the remaining allele was amplified. This may represent a new molecular mechanism underlying tumor progression.
AB - 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 α (PDGFRα) in a few of the 13 cases of glioblastoma multiforme analyzed. Interestingly, the amplified EGFR and PDGFRα 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 PDGFRα was lost but the remaining allele was amplified. This may represent a new molecular mechanism underlying tumor progression.
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U2 - 10.1158/0008-5472.CAN-06-2438
DO - 10.1158/0008-5472.CAN-06-2438
M3 - Article
C2 - 17145861
AN - SCOPUS:33845774308
SN - 0008-5472
VL - 66
SP - 11172
EP - 11178
JO - Cancer research
JF - Cancer research
IS - 23
ER -