Linked Life Data

9736406

Source:http://linkedlifedata.com/resource/pubmed/id/9736406

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1998-11-12
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1320-5463
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
595-602
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9736406-Actins, pubmed-meshheading:9736406-Adult, pubmed-meshheading:9736406-Antigens, Nuclear, pubmed-meshheading:9736406-Brain Neoplasms, pubmed-meshheading:9736406-Chromosomes, Human, Pair 10, pubmed-meshheading:9736406-Chromosomes, Human, Pair 17, pubmed-meshheading:9736406-Fatal Outcome, pubmed-meshheading:9736406-Female, pubmed-meshheading:9736406-Glial Fibrillary Acidic Protein, pubmed-meshheading:9736406-Gliosarcoma, pubmed-meshheading:9736406-Humans, pubmed-meshheading:9736406-Immunoenzyme Techniques, pubmed-meshheading:9736406-In Situ Hybridization, Fluorescence, pubmed-meshheading:9736406-Ki-67 Antigen, pubmed-meshheading:9736406-Male, pubmed-meshheading:9736406-Middle Aged, pubmed-meshheading:9736406-Nuclear Proteins, pubmed-meshheading:9736406-Tumor Markers, Biological, pubmed-meshheading:9736406-Tumor Suppressor Protein p53, pubmed-meshheading:9736406-von Willebrand Factor
pubmed:year
1998
pubmed:articleTitle
Gliosarcoma: an immunohistochemical, ultrastructural and fluorescence in situ hybridization study.
pubmed:affiliation
Department of Pathology, University of Tokushima School of Medicine, Japan. hide@basic.med.tokushima-u.ac.jp
pubmed:publicationType
Journal Article, Case Reports, Research Support, Non-U.S. Gov't