PMID- 11241796
OWN - NLM
STAT- MEDLINE
DCOM- 20010510
LR  - 20191025
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 30
IP  - 4
DP  - 2001 Apr
TI  - Hgfr/Met oncogene acts as target for gene amplification in DMBA-induced rat 
      sarcomas: free chromatin fluorescence in situ hybridization analysis of amplicon 
      arrays in homogeneously staining regions.
PG  - 416-20
AB  - Analysis of chromosome rearrangements in tumors is an important means for 
      revealing genetic pathways underlying tumorigenesis and tumor progression. In 
      five of 17 DMBA-induced rat sarcomas, cytogenetic analysis had disclosed 
      homogeneously staining regions (hsrs), which are generally accepted to be 
      cytogenetic signs of gene amplification. Using comparative genomic hybridization 
      (CGH), regional increases in DNA copy number of the proximal part of rat 
      chromosome (RNO) 4 were detected in four of the tumors harboring hsrs. 
      Amplification of the Hgfr/Met oncogene, located at RNO4q21.2, was detected by 
      fluorescence in situ hybridization (FISH) in five tumors. In four of them, a 
      number of flanking genes located in the close vicinity of Hgfr/Met, including 
      Cav1 (q21.1), Wnt2 (q21.2-q21.3), and Cftr (q21.3), also were amplified, though 
      amplification was seen in a lower fraction of the cells than was Hgfr/Met 
      amplification. In the fifth tumor (BL150T), Hgfr/Met was amplified in all cells 
      and was the sole amplified gene of those tested. In addition, the Hgfr/Met FISH 
      signals in BL150T were tightly clustered and formed compact and intense spots 
      compared with the signals seen in the other four tumors. Application of the free 
      chromatin FISH technique to BL150T showed that the genomic Hgfr/Met probe stained 
      the extended chromatin fibers of up to 1.5 Mb with an almost uninterrupted 
      signal, indicating that the BL150T amplicon was build up solely of Hgfr/Met gene 
      sequences. Our results suggest that the Hgfr/Met oncogene is the primary target 
      for amplification in a subset of rat DMBA sarcomas.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Helou, K
AU  - Helou K
AD  - Department of Cell and Molecular Biology-Genetics, Lundberg Laboratory, Goteborg 
      University, Sweden. Khalil.Helou@gen.gu.se
FAU - Walentinsson, A
AU  - Walentinsson A
FAU - Kost-Alimova, M
AU  - Kost-Alimova M
FAU - Levan, G
AU  - Levan G
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
RN  - 0 (Chromatin)
RN  - 57-97-6 (9,10-Dimethyl-1,2-benzanthracene)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - *9,10-Dimethyl-1,2-benzanthracene
MH  - Animals
MH  - Chromatin/*genetics
MH  - Chromosome Mapping
MH  - Gene Amplification/*genetics
MH  - *In Situ Hybridization, Fluorescence
MH  - Proto-Oncogene Proteins c-met/*genetics
MH  - *Proto-Oncogenes
MH  - Rats
MH  - Rats, Inbred BN
MH  - Rats, Long-Evans
MH  - Sarcoma, Experimental/*chemically induced/chemistry/*genetics
MH  - Staining and Labeling
EDAT- 2001/03/10 10:00
MHDA- 2001/05/22 10:01
CRDT- 2001/03/10 10:00
PHST- 2001/03/10 10:00 [pubmed]
PHST- 2001/05/22 10:01 [medline]
PHST- 2001/03/10 10:00 [entrez]
AID - 10.1002/1098-2264(2001)9999:9999<::AID-GCC1109>3.0.CO;2-6 [pii]
AID - 10.1002/1098-2264(2001)9999:9999<::aid-gcc1109>3.0.co;2-6 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2001 Apr;30(4):416-20. doi: 
      10.1002/1098-2264(2001)9999:9999<::aid-gcc1109>3.0.co;2-6.