title: Utility of in situ demonstration of 1p loss and p53 overexpression in pathologic diagnosis of oligodendroglial tumors.
abstract: To improve the diagnostic accuracy of oligodendroglial tumors and to find more convenient parameters that could predict the cytogenetic status, oligodendroglial and astrocytic tumors were cytogenetically and immunohistochemically investigated. Materials included 22 oligodendroglial tumors (15 oligodendrogliomas and 7 oligoastrocytomas) and 20 astrocytic tumors. 1p loss was examined with the fluorescence in situ hybridization (FISH) method. Expression of GFAP, Olig2 and p53 was immunohistochemically investigated and co-localization of GFAP and Olig2 was evaluated on double-immunostained sections. Furthermore, TP53 mutation analyses were carried out on three oligodendroglial tumors showing p53 protein overexpression with a direct sequence analysis. Our FISH studies demonstrated 1p loss in 73% of oligodendroglial tumors (80% oligodendrogliomas and 57% oligoastrocytomas) and in only 10% of astrocytic tumors. There were no clear-cut morphologic differences between 1p-deleted and 1p-intact oligodendroglial tumors. GFAP and Olig2 were expressed in most oligodendroglial and astrocytic tumors, and their cellular localization was almost independent of each other. Overexpression of p53 was observed in five oligodendroglial tumors, all of which were 1p-intact. In comparison, 16 oligodendroglial tumors with 1p deletion showed no overexpression of p53. TP53 missense mutations were detected in three of the p53 overexpressed oligodendroglial tumors studied. Our results suggest that 1p loss is almost specific to oligodendroglial tumors. Although the prediction of 1p status based solely on the morphologic features seems to be difficult, the immunohistochemistry for p53 is a useful tool in that p53 overexpression is closely related to the 1p-intact status in oligodendroglial tumors.
authors.affiliation: Department of Pathology, Saitama Medical School, Moroyama, Iruma-gun, Saitama, Japan. thirose@tph.gr.jp
authors.forename: Takanori
authors.initials: T
authors.lastname: Hirose
authors.forename: Keisuke
authors.initials: K
authors.lastname: Ishizawa
authors.forename: Shio
authors.initials: S
authors.lastname: Shimada
mesh_terms: D000328:Adult; D000368:Aged; D001254:Astrocytoma / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism; D051792:Basic Helix-Loop-Helix Proteins / Q000096:biosynthesis; D001932:Brain Neoplasms / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism; D002878:Chromosomes, Human, Pair 1 / Q000235:genetics*; D005260:Female; D017353:Gene Deletion; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D006801:Humans; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D000076104:Oligodendrocyte Transcription Factor 2; D009837:Oligodendroglioma / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis* / Q000235:genetics
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