ArrayExpress Uploader0human5.8 yearsnot specifiedGlioblastoma16.5 yearsnot specifiedGlioblastoma6.3 yearsnot specifiedGlioblastoma16.5 yearsnot specifiedGlioblastoma17.8 yearsnot specifiedGlioblastoma7 yearsnot specifiedGlioblastoma13.8 yearsPost-ALLGlioblastoma9.9 yearsnot specifiedGlioblastoma19.8 yearsPost-ALLGlioblastoma9.7 yearsPost-ALLGlioblastoma19.8 yearsPost-GerminomaGlioblastoma1.2 yearsnot specifiedGlioblastoma1 month yearsnot specifiedGlioblastoma7.3 yearsDiffuse pontine gliomaGlioblastoma10.9 yearsnot specifiedGlioblastoma4.7 yearsnot specifiedGlioblastoma14.3 yearsnot specifiedGlioblastoma14.08 yearsnot specifiedGlioblastoma4 yearsDiffuse pontine gliomaGlioblastoma1 yearsnot specifiedGlioblastoma10 yearsnot specifiedGlioblastoma11.25 yearsnot specifiedGlioblastoma3 yearsnot specifiedGlioblastoma19 yearsnot specifiedGlioblastoma14 yearsnot specifiedGlioblastoma12 yearsnot specifiedGlioblastoma8.9 yearsPost-EpendymomaGlioblastoma13.1 yearsnot specifiedGlioblastoma3.8 yearsnot specifiedGlioblastoma14.8 yearsnot specifiedGlioblastoma10.7 yearsnot specifiedGlioblastoma13.1 yearsPost-medulloblastomaGlioblastoma13.5 yearsnot specifiedGlioblastoma3.6 yearsnot specifiedGlioblastoma variant9.2 yearsPost-ALLGlioblastoma variant8 yearsnot specifiedGlioblastoma variant14.3 yearsnot specifiedGlioblastoma variant7.5 yearsnot specifiedanaplastic astrocytoma5 days oldnot specifiedanaplastic astrocytoma2.75 yearsnot specifiedanaplastic astrocytoma2 yearsnot specifiedanaplastic astrocytoma6 yearsnot specifiedanaplastic astrocytoma23 yearsPost-ALLanaplastic astrocytoma12 yearsnot specifiedanaplastic astrocytoma5 yearsnot specifiedanaplastic astrocytoma9 yearsnot specifiedanaplastic astrocytoma16.7 yearsPost-ALLanaplastic oligodendroglioma22.7 yearsnot specifiedanaplastic oligodendroglioma10.7 yearsnot specifiedanaplastic oligodendroglioma1.6 yearsnot specifiedanaplastic oligodendroglioma6.2 yearsnot specifiedanaplastic oligodendroglioma7 yearsnot specifiedAnaplastic PXA19 yearsnot specifiedAnaplastic PXA3527arrayexpress_sid4Purpose: To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG). Patients and...E-GEOD-19578/profile/8773/arrayexpressuploader353cancerchromosomecranialdiseasegliomaDec.12, 2014Falseintegrated-molecular-genetic-profiling-of-pediatriE-GEOD-19578_A-AFFY-44Integrated molecular genetic profiling of pediatric-high grade gliomas reveals key differences with adult diseaseSep.15, 2014Purpose: To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG). Patients and Methods: We conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGG, including 7 diffuse intrinsic pontine gliomas, and 10 HGG cases arising in children who received cranial irradiation for a previous cancer, using Affymetrix 500K GeneChips. Gene expression signatures for 53 tumors were analyzed with Affymetrix U133v2 arrays. Results were compared with publicly available data from adult tumors. Results: Pediatric and adult glioblastoma were clearly distinguished by frequent gain of chromosome 1q (30% vs 9%) and lower frequency of chromosome 7 gain (13% vs 74%), respectively. The most common focal amplifications also differed, with PDGFRA and EGFR predominant in childhood and adult populations respectively. These common alterations in pediatric HGG were detected at higher frequency in irradiation-induced tumors, suggesting that these are initiating events in childhood gliomagenesis. CDKN2A was the most common tumor suppressor gene targeted by homozygous deletion in pediatric HGG. No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences in pathogenesis between childhood HGG and adult secondary glioblastoma. Integrated copy number and gene expression data indicated that deregulated PDGFRA signaling plays a major role in pediatric HGG. Conclusions: Integrated molecular profiling showed substantial differences in the molecular features underlying pediatric and adult HGG, indicating that findings in adult tumors cannot be simply extrapolated to younger patients. PDGFRA may be a useful target for pediatric HGG including diffuse pontine gliomas. Keywords: disease state analysis 78 samples for SNP analysis, including 10 samples arising in children who received cranial irradiation for a previous cancer and 7 diffuse pontine gliomas; 53 of them with gene expression analysis; 2 tumor grades To have access to SNP CEL files, please contact Dr. Suzanne Baker (suzzane.baker@stjude.org).http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-19578http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-19578/samples/