Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease
To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG). We conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGGs, including seven diffuse intrinsic pontine gliomas, and 10 HGGs arising in children who received c...
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| Published in: | Journal of clinical oncology Vol. 28; no. 18; p. 3061 |
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| Main Authors: | , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
United States
20.06.2010
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| Subjects: | |
| ISSN: | 1527-7755, 1527-7755 |
| Online Access: | Get more information |
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| Abstract | To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG).
We conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGGs, including seven diffuse intrinsic pontine gliomas, and 10 HGGs arising in children who received cranial irradiation for a previous cancer using single nucleotide polymorphism microarray analysis. Gene expression was analyzed with gene expression microarrays for 53 tumors. Results were compared with publicly available data from adult tumors.
Significant differences in copy number alterations distinguish childhood and adult glioblastoma. PDGFRA was the predominant target of focal amplification in childhood HGG, including diffuse intrinsic pontine gliomas, and gene expression analyses supported an important role for deregulated PDGFRalpha signaling in pediatric HGG. No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma. Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively). PDGFRA amplification and 1q gain occurred at significantly higher frequency in irradiation-induced tumors, suggesting that these are initiating events in childhood gliomagenesis. A subset of pediatric HGGs showed minimal copy number changes.
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. PDGFRalpha may be a useful target for pediatric HGG, including diffuse pontine gliomas. |
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| AbstractList | To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG).
We conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGGs, including seven diffuse intrinsic pontine gliomas, and 10 HGGs arising in children who received cranial irradiation for a previous cancer using single nucleotide polymorphism microarray analysis. Gene expression was analyzed with gene expression microarrays for 53 tumors. Results were compared with publicly available data from adult tumors.
Significant differences in copy number alterations distinguish childhood and adult glioblastoma. PDGFRA was the predominant target of focal amplification in childhood HGG, including diffuse intrinsic pontine gliomas, and gene expression analyses supported an important role for deregulated PDGFRalpha signaling in pediatric HGG. No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma. Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively). PDGFRA amplification and 1q gain occurred at significantly higher frequency in irradiation-induced tumors, suggesting that these are initiating events in childhood gliomagenesis. A subset of pediatric HGGs showed minimal copy number changes.
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. PDGFRalpha may be a useful target for pediatric HGG, including diffuse pontine gliomas. To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG).PURPOSETo define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG).We conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGGs, including seven diffuse intrinsic pontine gliomas, and 10 HGGs arising in children who received cranial irradiation for a previous cancer using single nucleotide polymorphism microarray analysis. Gene expression was analyzed with gene expression microarrays for 53 tumors. Results were compared with publicly available data from adult tumors.PATIENTS AND METHODSWe conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGGs, including seven diffuse intrinsic pontine gliomas, and 10 HGGs arising in children who received cranial irradiation for a previous cancer using single nucleotide polymorphism microarray analysis. Gene expression was analyzed with gene expression microarrays for 53 tumors. Results were compared with publicly available data from adult tumors.Significant differences in copy number alterations distinguish childhood and adult glioblastoma. PDGFRA was the predominant target of focal amplification in childhood HGG, including diffuse intrinsic pontine gliomas, and gene expression analyses supported an important role for deregulated PDGFRalpha signaling in pediatric HGG. No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma. Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively). PDGFRA amplification and 1q gain occurred at significantly higher frequency in irradiation-induced tumors, suggesting that these are initiating events in childhood gliomagenesis. A subset of pediatric HGGs showed minimal copy number changes.RESULTSSignificant differences in copy number alterations distinguish childhood and adult glioblastoma. PDGFRA was the predominant target of focal amplification in childhood HGG, including diffuse intrinsic pontine gliomas, and gene expression analyses supported an important role for deregulated PDGFRalpha signaling in pediatric HGG. No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma. Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively). PDGFRA amplification and 1q gain occurred at significantly higher frequency in irradiation-induced tumors, suggesting that these are initiating events in childhood gliomagenesis. A subset of pediatric HGGs showed minimal copy number changes.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. PDGFRalpha may be a useful target for pediatric HGG, including diffuse pontine gliomas.CONCLUSIONIntegrated 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. PDGFRalpha may be a useful target for pediatric HGG, including diffuse pontine gliomas. |
| Author | Zhao, Wei Paugh, Barbara S Liu, Zhaoli Coyle, Beth Gajjar, Amar Jones, Chris Baker, Suzanne J Adamowicz-Brice, Martyna Grundy, Richard G Lowe, James Broniscer, Alberto Qu, Chunxu Zhang, Junyuan Hargrave, Darren Ellison, David W Bax, Dorine A Barrow, Jennifer |
| Author_xml | – sequence: 1 givenname: Barbara S surname: Paugh fullname: Paugh, Barbara S organization: St Jude Children's Research Hospital, Memphis, TN 38105, USA – sequence: 2 givenname: Chunxu surname: Qu fullname: Qu, Chunxu – sequence: 3 givenname: Chris surname: Jones fullname: Jones, Chris – sequence: 4 givenname: Zhaoli surname: Liu fullname: Liu, Zhaoli – sequence: 5 givenname: Martyna surname: Adamowicz-Brice fullname: Adamowicz-Brice, Martyna – sequence: 6 givenname: Junyuan surname: Zhang fullname: Zhang, Junyuan – sequence: 7 givenname: Dorine A surname: Bax fullname: Bax, Dorine A – sequence: 8 givenname: Beth surname: Coyle fullname: Coyle, Beth – sequence: 9 givenname: Jennifer surname: Barrow fullname: Barrow, Jennifer – sequence: 10 givenname: Darren surname: Hargrave fullname: Hargrave, Darren – sequence: 11 givenname: James surname: Lowe fullname: Lowe, James – sequence: 12 givenname: Amar surname: Gajjar fullname: Gajjar, Amar – sequence: 13 givenname: Wei surname: Zhao fullname: Zhao, Wei – sequence: 14 givenname: Alberto surname: Broniscer fullname: Broniscer, Alberto – sequence: 15 givenname: David W surname: Ellison fullname: Ellison, David W – sequence: 16 givenname: Richard G surname: Grundy fullname: Grundy, Richard G – sequence: 17 givenname: Suzanne J surname: Baker fullname: Baker, Suzanne J |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20479398$$D View this record in MEDLINE/PubMed |
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| Snippet | To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG).
We conducted a high-resolution analysis of... To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG).PURPOSETo define copy number alterations and gene... |
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| SubjectTerms | Adolescent Adult Biomarkers, Tumor - genetics Brain Neoplasms - genetics Brain Neoplasms - pathology Child Child, Preschool Chromosomes, Human, Pair 1 - genetics Cranial Irradiation Gene Expression Profiling Glioma - genetics Glioma - pathology Humans Infant Oligonucleotide Array Sequence Analysis Polymorphism, Single Nucleotide - genetics Prognosis Receptor, Platelet-Derived Growth Factor alpha - genetics Young Adult |
| Title | Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease |
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