Genome-wide allelic imbalance analysis of pediatric gliomas by single nucleotide polymorphic allele array
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 a...
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Published in | Cancer research (Chicago, Ill.) Vol. 66; no. 23; pp. 11172 - 11178 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Philadelphia, PA
American Association for Cancer Research
01.12.2006
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Abstract | 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 alpha (PDGFRalpha) in a few of the 13 cases of glioblastoma multiforme analyzed. Interestingly, the amplified EGFR and PDGFRalpha 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 PDGFRalpha was lost but the remaining allele was amplified. This may represent a new molecular mechanism underlying tumor progression. |
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AbstractList | 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 alpha (PDGFRalpha) in a few of the 13 cases of glioblastoma multiforme analyzed. Interestingly, the amplified EGFR and PDGFRalpha 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 PDGFRalpha was lost but the remaining allele was amplified. This may represent a new molecular mechanism underlying tumor progression. Abstract 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. (Cancer Res 2006; 66(23): 11172-8) 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 alpha (PDGFR alpha ) in a few of the 13 cases of glioblastoma multiforme analyzed. Interestingly, the amplified EGFR and PDGFR alpha 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 alpha 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) |
Author | LAU, Ching C DI FRANCESCO, Angela M WONG, Kwong-Kwok TSANG, Yvonne T. M BHATTACHARJEE, Meenakshi ADESINA, Adekunle MECO, Daniela CHANG, Yi-Mieng RICCARDI, Riccardo PERLAKY, Laszlo DAUSER, Robert C CHINTAGUMPALA, Murali SU, Jack |
Author_xml | – sequence: 1 givenname: Kwong-Kwok surname: WONG fullname: WONG, Kwong-Kwok organization: Department of Gynecologic Oncology, The University of Texas M.D. Anderson Cancer Center, United States – sequence: 2 givenname: Yvonne T. M surname: TSANG fullname: TSANG, Yvonne T. M organization: Department of Gynecologic Oncology, The University of Texas M.D. Anderson Cancer Center, United States – sequence: 3 givenname: Meenakshi surname: BHATTACHARJEE fullname: BHATTACHARJEE, Meenakshi organization: Department of Pathology, Baylor College of Medicine, Houston, Texas, United States – sequence: 4 givenname: Murali surname: CHINTAGUMPALA fullname: CHINTAGUMPALA, Murali organization: Texas Children's Cancer Center, United States – sequence: 5 givenname: Ching C surname: LAU fullname: LAU, Ching C organization: Texas Children's Cancer Center, United States – sequence: 6 givenname: Yi-Mieng surname: CHANG fullname: CHANG, Yi-Mieng organization: Texas Children's Cancer Center, United States – sequence: 7 givenname: Jack surname: SU fullname: SU, Jack organization: Texas Children's Cancer Center, United States – sequence: 8 givenname: Angela M surname: DI FRANCESCO fullname: DI FRANCESCO, Angela M organization: Department of Pediatrics, Catholic University of Rome, Italy – sequence: 9 givenname: Daniela surname: MECO fullname: MECO, Daniela organization: Department of Pediatrics, Catholic University of Rome, Italy – sequence: 10 givenname: Riccardo surname: RICCARDI fullname: RICCARDI, Riccardo organization: Department of Pediatrics, Catholic University of Rome, Italy – sequence: 11 givenname: Laszlo surname: PERLAKY fullname: PERLAKY, Laszlo organization: Texas Children's Cancer Center, United States – sequence: 12 givenname: Robert C surname: DAUSER fullname: DAUSER, Robert C organization: Department of Neurosurgery, Baylor College of Medicine, Houston, Texas, United States – sequence: 13 givenname: Adekunle surname: ADESINA fullname: ADESINA, Adekunle organization: Department of Pathology, Baylor College of Medicine, Houston, Texas, United States |
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Keywords | Human Pediatrics Nervous system diseases Allelic imbalance DNA chip Infant Allele Glioma Central nervous system disease Loss of heterozygosity Nucleotide Tumor Genetics Genome Child Polymorphism |
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Snippet | 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... Abstract Using single nucleotide polymorphic (SNP) allele arrays, we analyzed 28 pediatric gliomas consisting of 14 high-grade gliomas and 14 low-grade... |
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SubjectTerms | Alleles Antineoplastic agents Base Sequence Biological and medical sciences Cell Cycle - genetics Child DNA Mutational Analysis Gene Amplification Gene Expression Regulation, Neoplastic - genetics Genome, Human - genetics Genotype Glioblastoma - genetics Glioblastoma - pathology Glioma - genetics Glioma - pathology Humans Loss of Heterozygosity Medical sciences Neurology Pharmacology. Drug treatments Polymorphism, Single Nucleotide - genetics Receptor, Epidermal Growth Factor - genetics Receptor, Platelet-Derived Growth Factor alpha - genetics Reverse Transcriptase Polymerase Chain Reaction Tumors Tumors of the nervous system. Phacomatoses |
Title | Genome-wide allelic imbalance analysis of pediatric gliomas by single nucleotide polymorphic allele array |
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