PMID- 11328534
OWN - NLM
STAT- MEDLINE
DCOM- 20010628
LR  - 20190915
IS  - 1320-5463 (Print)
IS  - 1320-5463 (Linking)
VI  - 51
IP  - 3
DP  - 2001 Mar
TI  - TP53 deleted cells in de novo glioblastomas using fluorescence in situ 
      hybridization.
PG  - 187-92
AB  - Glioblastoma (GBM) has been known to have two distinct genetic pathways of 
      tumorigenesis. Secondary GBM shows frequent TP53 mutation, but de novo (primary) 
      GBM is usually independent of TP53 alteration. However, the subpopulation of TP53 
      altered cells in the latter tumor is obscure. In order to assess TP53 deleted 
      cells in de novo GBM quantitatively, we performed dual color fluorescence in situ 
      hybridization (FISH) for TP53 and centromere 17 in nine cases of de novo GBM with 
      frozen surgical materials. Single TP53 signal cells indicating TP53 deletion were 
      recognized in 8.7-35.6% (mean, 21.3%) among the nine cases. In addition, 
      immunohistochemistry was performed for the Ki-67 antigen (MIB-1) and p53 protein 
      in all nine cases. Labeling indices (LI) of MIB-1 ranged from 2.8 to 46.9% (mean, 
      20.8%). Between the group with the more dense subpopulation of TP53 deleted cells 
      (15% or more) by FISH and the group with less subpopulation than the former, 
      these LI of MIB-1 demonstrated statistically significant difference (respective 
      means, 28.2% and 6.1%; P < 0.05). Conversely, LI of p53 protein shown to be 
      0-50.9% (mean, 24.9%) had no correlation with the subpopulation of TP53 deleted 
      cells by FISH. Four cases who had higher LI of p53 protein (mean, 39.7%) than the 
      subpopulation of TP53 deleted cells (mean, 12.7%), respectively, indicated the 
      presence of many p53 protein immunoreactive cells without TP53 deletion. These 
      results suggest that: (i) de novo GBM also has subpopulation of TP53 deleted 
      cells; (ii) TP53 alteration, which may not be a major event, participates in cell 
      proliferation of de novo GBM; and (iii) de novo GBM tends to have accumulation of 
      wild-type p53 protein.
FAU - Horiguchi, H
AU  - Horiguchi H
AD  - Department of Pathology, University of Tokushima School of Medicine, 3-18-15 
      Kuramoto, Tokushima 770-8503, Japan. hide@basic.med.tokushima-u.ac.jp
FAU - Sano, T
AU  - Sano T
FAU - Hirose, T
AU  - Hirose T
LA  - eng
PT  - Journal Article
PL  - Australia
TA  - Pathol Int
JT  - Pathology international
JID - 9431380
RN  - 0 (Ki-67 Antigen)
RN  - 0 (Tumor Suppressor Protein p53)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cell Count
MH  - Cell Nucleus/chemistry/genetics
MH  - Centromere/genetics
MH  - Female
MH  - Gene Deletion
MH  - Genes, p53/*genetics
MH  - Glioblastoma/chemistry/*genetics/mortality/pathology/surgery
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence
MH  - Ki-67 Antigen/analysis
MH  - Male
MH  - Middle Aged
MH  - Mutation
MH  - Neoplasm Staging
MH  - Supratentorial Neoplasms/chemistry/*genetics/mortality/pathology/surgery
MH  - Survival Rate
MH  - Tumor Suppressor Protein p53/analysis/*genetics
EDAT- 2001/05/01 10:00
MHDA- 2001/06/29 10:01
CRDT- 2001/05/01 10:00
PHST- 2001/05/01 10:00 [pubmed]
PHST- 2001/06/29 10:01 [medline]
PHST- 2001/05/01 10:00 [entrez]
AID - pin1186 [pii]
AID - 10.1046/j.1440-1827.2001.01186.x [doi]
PST - ppublish
SO  - Pathol Int. 2001 Mar;51(3):187-92. doi: 10.1046/j.1440-1827.2001.01186.x.