title: Gliosarcoma: an immunohistochemical, ultrastructural and fluorescence in situ hybridization study.
abstract: Three cases of primary gliosarcoma (GS) were studied by immunohistochemical, ultrastructural and fluorescence in situ hybridization (FISH) methods. All tumors occurred in the supratentorial regions of the body. No patient had a prior history of irradiation to the brain. All patients died of tumor within 1 year, and autopsies were performed in two cases. Microscopically, each of the three tumors showed a mixture of glioblastoma (GBM) and a sarcomatous component (SC), which resembled fibrosarcoma with various histological features. Numerous collagen and reticulin fibers were seen in the SC of all tumors. Glial fibrillary acidic protein (GFAP) was immunoreactive only in the gliomatous component (GC). Factor VIII-related antigen was negative except for endothelial cells. One tumor exhibited alpha-smooth muscle actin positivity in the SC. Expression of MIB-1 and p53 protein was demonstrated in both components for all tumors. Labeling indices (LI) for MIB-1 ranged from 7.7 to 36.1%, and LI for p53 protein ranged from 2.9 to 57.0%. Ultrastructurally, astrocytic cells were characterized by a polygonal configuration with many cytoplasmic projections and occasional filaments. Spindle-shaped fibroblasts in the SC contained well-developed rough endoplasmic reticulum. Fluorescence in situ hybridization (FISH) performed on fresh materials or paraffin-embedded tissue demonstrated single signals for chromosome 10 in 40.6-58.3% of cells and for chromosome 17 in 37.9-48.6% of cells. Two tumors were regarded as containing losses of both chromosomes 10 and 17, while the third showed a substantial loss only of chromosome 10. As similar aberrations have been reported in GBM, these chromosomal abnormalities suggest a common pathogenesis in GS and GBM.
authors.affiliation: Department of Pathology, University of Tokushima School of Medicine, Japan. hide@basic.med.tokushima-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Horiguchi
authors.forename: T
authors.initials: T
authors.lastname: Hirose
authors.forename: S
authors.initials: S
authors.lastname: Kannuki
authors.forename: S
authors.initials: S
authors.lastname: Nagahiro
authors.forename: T
authors.initials: T
authors.lastname: Sano
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D034961:Antigens, Nuclear; D014408:Biomarkers, Tumor / Q000378:metabolism*; D001932:Brain Neoplasms / Q000235:genetics / Q000378:metabolism / Q000648:ultrastructure*; D002879:Chromosomes, Human, Pair 10 / Q000235:genetics; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics; D017809:Fatal Outcome; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D018316:Gliosarcoma / Q000235:genetics / Q000378:metabolism / Q000648:ultrastructure*; D006801:Humans; D007124:Immunoenzyme Techniques; D017404:In Situ Hybridization, Fluorescence / Q000379:methods; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D000199:Actins; D034961:Antigens, Nuclear; D014408:Biomarkers, Tumor; D005904:Glial Fibrillary Acidic Protein; D019394:Ki-67 Antigen; D009687:Nuclear Proteins; D016159:Tumor Suppressor Protein p53; D014841:von Willebrand Factor