PMID- 9736406
OWN - NLM
STAT- MEDLINE
DCOM- 19981112
LR  - 20190915
IS  - 1320-5463 (Print)
IS  - 1320-5463 (Linking)
VI  - 48
IP  - 8
DP  - 1998 Aug
TI  - Gliosarcoma: an immunohistochemical, ultrastructural and fluorescence in situ 
      hybridization study.
PG  - 595-602
AB  - 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.
FAU - Horiguchi, H
AU  - Horiguchi H
AD  - Department of Pathology, University of Tokushima School of Medicine, Japan. 
      hide@basic.med.tokushima-u.ac.jp
FAU - Hirose, T
AU  - Hirose T
FAU - Kannuki, S
AU  - Kannuki S
FAU - Nagahiro, S
AU  - Nagahiro S
FAU - Sano, T
AU  - Sano T
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Pathol Int
JT  - Pathology international
JID - 9431380
RN  - 0 (Actins)
RN  - 0 (Antigens, Nuclear)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Ki-67 Antigen)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (von Willebrand Factor)
SB  - IM
MH  - Actins/metabolism
MH  - Adult
MH  - Antigens, Nuclear
MH  - Biomarkers, Tumor/*metabolism
MH  - Brain Neoplasms/genetics/metabolism/*ultrastructure
MH  - Chromosomes, Human, Pair 10/genetics
MH  - Chromosomes, Human, Pair 17/genetics
MH  - Fatal Outcome
MH  - Female
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Gliosarcoma/genetics/metabolism/*ultrastructure
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - In Situ Hybridization, Fluorescence/methods
MH  - Ki-67 Antigen/metabolism
MH  - Male
MH  - Middle Aged
MH  - Nuclear Proteins/metabolism
MH  - Tumor Suppressor Protein p53/metabolism
MH  - von Willebrand Factor/metabolism
EDAT- 1998/09/15 00:00
MHDA- 1998/09/15 00:01
CRDT- 1998/09/15 00:00
PHST- 1998/09/15 00:00 [pubmed]
PHST- 1998/09/15 00:01 [medline]
PHST- 1998/09/15 00:00 [entrez]
AID - 10.1111/j.1440-1827.1998.tb03956.x [doi]
PST - ppublish
SO  - Pathol Int. 1998 Aug;48(8):595-602. doi: 10.1111/j.1440-1827.1998.tb03956.x.