PMID- 10504534
OWN - NLM
STAT- MEDLINE
DCOM- 20000105
LR  - 20190915
IS  - 1320-5463 (Print)
IS  - 1320-5463 (Linking)
VI  - 49
IP  - 8
DP  - 1999 Aug
TI  - Loss of chromosome 10 in glioblastoma: relation to proliferation and 
      angiogenesis.
PG  - 681-6
AB  - 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.
FAU - Horiguchi, H
AU  - Horiguchi H
AD  - Department of Pathology, University of Tokushima, School of Medicine, Japan. 
      hide@medbasic.basic.med.tokushima-u.ac.jp
FAU - Hirose, T
AU  - Hirose T
FAU - Sano, T
AU  - Sano T
FAU - Nagahiro, S
AU  - Nagahiro S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Pathol Int
JT  - Pathology international
JID - 9431380
RN  - 0 (Endothelial Growth Factors)
RN  - 0 (Ki-67 Antigen)
RN  - 0 (Lymphokines)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (Vascular Endothelial Growth Factors)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Brain Neoplasms/blood supply/*genetics/metabolism/pathology
MH  - Cell Division
MH  - *Chromosome Deletion
MH  - *Chromosomes, Human, Pair 10
MH  - Endothelial Growth Factors/metabolism
MH  - Female
MH  - Glioblastoma/blood supply/*genetics/metabolism/pathology
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Ki-67 Antigen/metabolism
MH  - Lymphokines/metabolism
MH  - Male
MH  - Middle Aged
MH  - Neovascularization, Pathologic/etiology
MH  - Vascular Endothelial Growth Factor A
MH  - Vascular Endothelial Growth Factors
EDAT- 1999/10/03 00:00
MHDA- 1999/10/03 00:01
CRDT- 1999/10/03 00:00
PHST- 1999/10/03 00:00 [pubmed]
PHST- 1999/10/03 00:01 [medline]
PHST- 1999/10/03 00:00 [entrez]
AID - pin934 [pii]
AID - 10.1046/j.1440-1827.1999.00934.x [doi]
PST - ppublish
SO  - Pathol Int. 1999 Aug;49(8):681-6. doi: 10.1046/j.1440-1827.1999.00934.x.