title: Olig2 expression, GFAP, p53 and 1p loss analysis contribute to glioma subclassification.
abstract: The expression of Olig2, a basic helix-loop-helix (bHLH) transcription factor involved in oligodendroglial specification, was investigated by immunohistochemistry in a series of 146 tumours and control samples. Olig2 expression was restricted to glial tumours and nontumoral oligodendrocytes. It was higher in oligodendrogliomas as compared to astrocytomas and oligoastrocytomas, and in grade III as compared to grade II tumours. Olig 2 was absent or weakly expressed in glioblastoma (GBM), whereas strong expression was found in the oligodendroglial foci of GBM with oligodendroglial component (GBMO). Double labelling was performed on a subset of the most typical tumours, according to the WHO classification. It showed a mutual exclusion, at cell level, of Olig2 and GFAP expression. In pure oligodendrogliomas, tumour cells were Olig2+/GFAP-. In contrast, two main tumour populations, Olig2+/GFAP- and Olig2-/GFAP+, were found in both oligoastrocytomas and astrocytomas. Based on these data from selected samples, two separate entities can be established, corresponding to 'pure oligodendrogliomas' and 'astrocytomas and oligoastrocytomas'. The relevance of this subdivision is further supported by the association with 1p loss and a trend to better survival for pure oligodendrogliomas and with p53 expression and a trend to shorter survival for astrocytomas and oligoastrocytomas. Combined testing of Olig2, 1p status, GFAP and p53 expression may therefore be helpful in refining current classification and providing more homogeneous sets of gliomas for clinical studies.
authors.affiliation: Laboratoire de neuropathologie R Escourolle (Pr Hauw), Universite Pierre et Marie Curie, Paris, France.
authors.forename: K
authors.initials: K
authors.lastname: Mokhtari
authors.forename: S
authors.initials: S
authors.lastname: Paris
authors.forename: L
authors.initials: L
authors.lastname: Aguirre-Cruz
authors.forename: N
authors.initials: N
authors.lastname: Privat
authors.forename: E
authors.initials: E
authors.lastname: Crinière
authors.forename: Y
authors.initials: Y
authors.lastname: Marie
authors.forename: J-J
authors.initials: JJ
authors.lastname: Hauw
authors.forename: M
authors.initials: M
authors.lastname: Kujas
authors.forename: D
authors.initials: D
authors.lastname: Rowitch
authors.forename: K
authors.initials: K
authors.lastname: Hoang-Xuan
authors.forename: J-Y
authors.initials: JY
authors.lastname: Delattre
authors.forename: M
authors.initials: M
authors.lastname: Sanson
mesh_terms: D051792:Basic Helix-Loop-Helix Proteins; D001932:Brain Neoplasms / Q000145:classification* / Q000378:metabolism / Q000473:pathology; D002878:Chromosomes, Human, Pair 1; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism*; D005910:Glioma / Q000145:classification* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D019656:Loss of Heterozygosity; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D000076104:Oligodendrocyte Transcription Factor 2; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D000076104:Oligodendrocyte Transcription Factor 2; D016159:Tumor Suppressor Protein p53; C405708:OLIG2 protein, human