title: Loss of chromosome 10 in glioblastoma: relation to proliferation and angiogenesis.
abstract: Loss of chromosome 10 was assessed in 17 specimens of glioblastoma (GBM) by fluorescence in situ hybridization (FISH) technique using the centromere probe for chromosome 10. Cytospinned smear specimens were prepared from paraffin-embedded specimens. The percentage of nuclei containing a single fluorescent signal ranged from 19.2 to 88. 0% (mean, 49.3%). Thirteen tumors (76.5%) were designated as monosomy 10 because the proportion of single-signal nuclei exceeded the cut-off value (31.5%: mean of five control materials +3 standard deviations). The results confirmed the importance of the loss of chromosome 10 for the development of GBM, although no significant correlation was demonstrated between the loss of chromosome 10 and survival. In addition, proliferation potential and angiogenesis of GBM were immunohistochemically analyzed using antibodies against Ki-67 antigen (MIB-1), factor VIII-related antigen (FVIII R/Ag) and vascular endothelial growth factor (VEGF), respectively. The labeling indices of MIB-1 (1.5-57.8%) and the number of blood vessels immunoreactive for FVIII R/Ag (18-279/10 high-power fields) were not significantly related to the loss of chromosome 10. Vascular endothelial growth factor immunoreactivity in areas microvessels were counted was seen in 12 cases. However, neither the loss of chromosome 10 nor number of vessels was not correlated with VEGF expression. Other genetic abnormalities as well as loss of chromosome 10 may be involved in the cell proliferation and angiogenesis of GBM.
authors.affiliation: Department of Pathology, University of Tokushima, School of Medicine, Japan. hide@medbasic.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: T
authors.initials: T
authors.lastname: Sano
authors.forename: S
authors.initials: S
authors.lastname: Nagahiro
mesh_terms: D000328:Adult; D000368:Aged; D001932:Brain Neoplasms / Q000098:blood supply / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002455:Cell Division; D002872:Chromosome Deletion; D002879:Chromosomes, Human, Pair 10; D016228:Endothelial Growth Factors / Q000378:metabolism; D005260:Female; D005909:Glioblastoma / Q000098:blood supply / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D019394:Ki-67 Antigen / Q000378:metabolism; D008222:Lymphokines / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000209:etiology; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D016228:Endothelial Growth Factors; D019394:Ki-67 Antigen; D008222:Lymphokines; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors