Glioblastomas with an Oligodendroglial Component: A Pathological and Molecular Study
Glioblastoma (GBM) is considered by the WHO classification to represent the most malignant grade of the astrocytic tumors. However, a subset of GBM includes recognizable areas with oligodendroglial features, suggesting that some GBM may also have an oligodendroglial origin. The aim of this study was...
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| Veröffentlicht in: | Journal of neuropathology and experimental neurology 2001-09, Vol.60 (9), p.863-871 |
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| container_title | Journal of neuropathology and experimental neurology |
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| creator | HE, J MOKHTARI, K SANSON, M MARIE, Y KUJAS, M HUGUET, S LEURAUD, P CAPELLE, L DELATTRE, J Y POIRIER, J HOANG-XUAN, K |
| description | Glioblastoma (GBM) is considered by the WHO classification to represent the most malignant grade of the astrocytic tumors. However, a subset of GBM includes recognizable areas with oligodendroglial features, suggesting that some GBM may also have an oligodendroglial origin. The aim of this study was to analyze the molecular profile of GBM associated with an oligodendroglial component (GBMO). We analyzed a series of 25 GBMO. Loss of heterozygosity (LOH) on 1p and 19q, known as common markers of oligodendroglial tumors, were observed in 40% and 60% of cases, respectively; 72% of the tumors displayed one or both of these markers. All but 4 tumors (84%) showed alterations known to be preferentially involved in the progression of astrocytic tumors to GBM, such as EGFR amplification (44%), P16 deletion (48%), LOH on 10q (64%), PTEN (20%), and TP53 (24%) mutations. Therefore, GBMO displayed all the genetic aberrations found in “standard” GBM with a comparable incidence, but differed from GBM by having a higher rate of LOH on 1p and 19q. These results suggest that GBMO might represent a subgroup of tumors of oligodendroglial origin that is distinct from the “standard” GBM in terms of tumorigenesis pathway. |
| doi_str_mv | 10.1093/jnen/60.9.863 |
| format | Article |
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However, a subset of GBM includes recognizable areas with oligodendroglial features, suggesting that some GBM may also have an oligodendroglial origin. The aim of this study was to analyze the molecular profile of GBM associated with an oligodendroglial component (GBMO). We analyzed a series of 25 GBMO. Loss of heterozygosity (LOH) on 1p and 19q, known as common markers of oligodendroglial tumors, were observed in 40% and 60% of cases, respectively; 72% of the tumors displayed one or both of these markers. All but 4 tumors (84%) showed alterations known to be preferentially involved in the progression of astrocytic tumors to GBM, such as EGFR amplification (44%), P16 deletion (48%), LOH on 10q (64%), PTEN (20%), and TP53 (24%) mutations. Therefore, GBMO displayed all the genetic aberrations found in “standard” GBM with a comparable incidence, but differed from GBM by having a higher rate of LOH on 1p and 19q. These results suggest that GBMO might represent a subgroup of tumors of oligodendroglial origin that is distinct from the “standard” GBM in terms of tumorigenesis pathway.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1093/jnen/60.9.863</identifier><identifier>PMID: 11556543</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>Hagerstown, MD: American Association of Neuropathologists, Inc</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Brain Neoplasms - genetics ; Brain Neoplasms - pathology ; Chromosome Aberrations ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 10 ; Chromosomes, Human, Pair 19 ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; ErbB Receptors - genetics ; Female ; Gene Deletion ; Glioblastoma - genetics ; Glioblastoma - pathology ; Humans ; Loss of Heterozygosity ; Male ; Medical sciences ; Middle Aged ; Neurology ; Oligodendroglia - pathology ; Phosphoric Monoester Hydrolases - genetics ; PTEN Phosphohydrolase ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Proteins ; Tumors of the nervous system. 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However, a subset of GBM includes recognizable areas with oligodendroglial features, suggesting that some GBM may also have an oligodendroglial origin. The aim of this study was to analyze the molecular profile of GBM associated with an oligodendroglial component (GBMO). We analyzed a series of 25 GBMO. Loss of heterozygosity (LOH) on 1p and 19q, known as common markers of oligodendroglial tumors, were observed in 40% and 60% of cases, respectively; 72% of the tumors displayed one or both of these markers. All but 4 tumors (84%) showed alterations known to be preferentially involved in the progression of astrocytic tumors to GBM, such as EGFR amplification (44%), P16 deletion (48%), LOH on 10q (64%), PTEN (20%), and TP53 (24%) mutations. Therefore, GBMO displayed all the genetic aberrations found in “standard” GBM with a comparable incidence, but differed from GBM by having a higher rate of LOH on 1p and 19q. These results suggest that GBMO might represent a subgroup of tumors of oligodendroglial origin that is distinct from the “standard” GBM in terms of tumorigenesis pathway.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - pathology</subject><subject>Chromosome Aberrations</subject><subject>Chromosomes, Human, Pair 1</subject><subject>Chromosomes, Human, Pair 10</subject><subject>Chromosomes, Human, Pair 19</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>ErbB Receptors - genetics</subject><subject>Female</subject><subject>Gene Deletion</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - pathology</subject><subject>Humans</subject><subject>Loss of Heterozygosity</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Oligodendroglia - pathology</subject><subject>Phosphoric Monoester Hydrolases - genetics</subject><subject>PTEN Phosphohydrolase</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Proteins</subject><subject>Tumors of the nervous system. 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However, a subset of GBM includes recognizable areas with oligodendroglial features, suggesting that some GBM may also have an oligodendroglial origin. The aim of this study was to analyze the molecular profile of GBM associated with an oligodendroglial component (GBMO). We analyzed a series of 25 GBMO. Loss of heterozygosity (LOH) on 1p and 19q, known as common markers of oligodendroglial tumors, were observed in 40% and 60% of cases, respectively; 72% of the tumors displayed one or both of these markers. All but 4 tumors (84%) showed alterations known to be preferentially involved in the progression of astrocytic tumors to GBM, such as EGFR amplification (44%), P16 deletion (48%), LOH on 10q (64%), PTEN (20%), and TP53 (24%) mutations. Therefore, GBMO displayed all the genetic aberrations found in “standard” GBM with a comparable incidence, but differed from GBM by having a higher rate of LOH on 1p and 19q. These results suggest that GBMO might represent a subgroup of tumors of oligodendroglial origin that is distinct from the “standard” GBM in terms of tumorigenesis pathway.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>11556543</pmid><doi>10.1093/jnen/60.9.863</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Adult Aged Biological and medical sciences Brain Neoplasms - genetics Brain Neoplasms - pathology Chromosome Aberrations Chromosomes, Human, Pair 1 Chromosomes, Human, Pair 10 Chromosomes, Human, Pair 19 Cyclin-Dependent Kinase Inhibitor p16 - genetics ErbB Receptors - genetics Female Gene Deletion Glioblastoma - genetics Glioblastoma - pathology Humans Loss of Heterozygosity Male Medical sciences Middle Aged Neurology Oligodendroglia - pathology Phosphoric Monoester Hydrolases - genetics PTEN Phosphohydrolase Tumor Suppressor Protein p53 - genetics Tumor Suppressor Proteins Tumors of the nervous system. Phacomatoses |
| title | Glioblastomas with an Oligodendroglial Component: A Pathological and Molecular Study |
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