title: Glioblastomas with an oligodendroglial component: a pathological and molecular study.
abstract: 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.
authors.affiliation: Biologie des Interactions Neurone-Glie, INSERM U495 et Universite P. et M. Curie, Paris, France.
authors.forename: J
authors.initials: J
authors.lastname: He
authors.forename: K
authors.initials: K
authors.lastname: Mokhtari
authors.forename: M
authors.initials: M
authors.lastname: Sanson
authors.forename: Y
authors.initials: Y
authors.lastname: Marie
authors.forename: M
authors.initials: M
authors.lastname: Kujas
authors.forename: S
authors.initials: S
authors.lastname: Huguet
authors.forename: P
authors.initials: P
authors.lastname: Leuraud
authors.forename: L
authors.initials: L
authors.lastname: Capelle
authors.forename: J Y
authors.initials: JY
authors.lastname: Delattre
authors.forename: J
authors.initials: J
authors.lastname: Poirier
authors.forename: K
authors.initials: K
authors.lastname: Hoang-Xuan
mesh_terms: D000328:Adult; D000368:Aged; D001932:Brain Neoplasms / Q000235:genetics* / Q000473:pathology*; D002869:Chromosome Aberrations; D002878:Chromosomes, Human, Pair 1; D002879:Chromosomes, Human, Pair 10; D002888:Chromosomes, Human, Pair 19; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics; D066246:ErbB Receptors / Q000235:genetics; D005260:Female; D017353:Gene Deletion; D005909:Glioblastoma / Q000235:genetics* / Q000473:pathology*; D006801:Humans; D019656:Loss of Heterozygosity; D008297:Male; D008875:Middle Aged; D009836:Oligodendroglia / Q000473:pathology*; D051059:PTEN Phosphohydrolase; D010744:Phosphoric Monoester Hydrolases / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D025521:Tumor Suppressor Proteins
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D066246:ErbB Receptors; D010744:Phosphoric Monoester Hydrolases; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human