PMID- 11319800
OWN - NLM
STAT- MEDLINE
DCOM- 20010712
LR  - 20061115
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 31
IP  - 2
DP  - 2001 Jun
TI  - Identification of recurrent chromosomal rearrangements and the unique 
      relationship between low-level amplification and translocation in glioblastoma.
PG  - 125-33
AB  - To elucidate the structural abnormalities and the relationship between chromosome 
      structural disorders and DNA copy number aberrations in tumor cells, we applied 
      the techniques of spectral karyotyping (SKY), comparative genomic hybridization 
      (CGH), and fluorescence in situ hybridization (FISH), using yeast artificial 
      chromosome (YAC) probes for nine human glioblastoma cell lines. One striking 
      finding was that independently derived cell lines had the same recurrent marker 
      chromosomes. Seven recurrent chromosomes were detected by these cytogenetic 
      methods. In particular, cell lines U251, SNB-19, and U373-MG showed very similar 
      karyotypes. It is also interesting that regions of DNA amplification were found 
      translocated and/or inserted at a high rate (91.7%). In all, there were 12 
      amplified loci in five of the nine cell lines. These amplified chromosomal bands 
      were scattered on the chromosomes, including the normal chromosome, with one 
      exception (7q32-qter in U373-MG). FISH with YAC clones mapping to these 
      chromosomal regions as DNA probes often showed DNA probe signals not only at 
      original chromosomal sites but also in translocated or inserted segments. This 
      form of DNA amplification was characterized by low-level increases (four- to 
      10-fold) and by translocation or insertion of the relevant chromosomal locus. 
      These studies shed light on typical derivative chromosomes and the relationship 
      between DNA amplification and chromosomal translocation in glioblastoma.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Kubota, H
AU  - Kubota H
AD  - Department of Pathology, Yamaguchi University School of Medicine, Yamaguchi, 
      Japan.
FAU - Nishizaki, T
AU  - Nishizaki T
FAU - Harada, K
AU  - Harada K
FAU - Harada, K
AU  - Harada K
FAU - Oga, A
AU  - Oga A
FAU - Ito, H
AU  - Ito H
FAU - Suzuki, M
AU  - Suzuki M
FAU - Sasaki, K
AU  - Sasaki K
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
SB  - IM
CIN - Genes Chromosomes Cancer. 2002 Jan;33(1):103-5. PMID: 11746993
MH  - Chromosome Aberrations/*genetics
MH  - Chromosome Disorders
MH  - Gene Amplification/*genetics
MH  - Glioblastoma/*genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Male
MH  - Middle Aged
MH  - Nucleic Acid Hybridization
MH  - Translocation, Genetic/*genetics
MH  - Tumor Cells, Cultured
EDAT- 2001/04/25 10:00
MHDA- 2001/07/13 10:01
CRDT- 2001/04/25 10:00
PHST- 2001/04/25 10:00 [pubmed]
PHST- 2001/07/13 10:01 [medline]
PHST- 2001/04/25 10:00 [entrez]
AID - 10.1002/gcc.1126 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2001 Jun;31(2):125-33. doi: 10.1002/gcc.1126.