PMID- 9408753
OWN - NLM
STAT- MEDLINE
DCOM- 19980113
LR  - 20191024
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 20
IP  - 4
DP  - 1997 Dec
TI  - Increased copy number at 17q22-q24 by CGH in breast cancer is due to high-level 
      amplification of two separate regions.
PG  - 372-6
AB  - Studies by comparative genomic hybridization (CGH) have defined a chromosomal 
      site at 17q22-q24 that is often overrepresented in breast cancer, neuroblastoma, 
      and several other tumor types. Due to the limited resolution and dynamic range of 
      CGH, it remain unclear whether this gain reflects high-level amplification of 
      small subregion(s) or low-level gain of most of the distal 17q. We used 32 
      physically mapped 17q probes to construct more accurate copy number profiles for 
      14 breast cancer cell lines by interphase fluorescence in situ hybridization 
      (FISH). Six cell lines (43%) showed an increased copy number of the 17q-22q24 
      region by CGH, and seven (50%) by FISH. FISH copy number profiles had a 
      substantially higher dynamic range than did CGH profiles. FISH revealed two 
      independent, highly amplified regions (A and B) at 17q23, separated by about 5 Mb 
      of non-amplified DNA. These regions were distinctly telomeric from the ERBB2 gene 
      locus. However, region A was often co-amplified with ERBB2, whereas B was 
      amplified in cell lines that showed no ERBB2 amplification. We conclude that 
      distal 17q gains recently discovered in breast cancer by CGH are due to 
      high-level amplifications of two different regions at 17q23. This chromosomal 
      region has previously been reported to undergo allelic loss and therefore was 
      thought to harbor a tumor suppressor gene. The present FISH data provide support 
      for the presence, and a starting point for the positional isolation, of 17q23 
      genes whose upregulation by amplification may play a role in the progression of 
      breast cancer and many other tumor types.
FAU - Barlund, M
AU  - Barlund M
AD  - Laboratory of Cancer Genetics, Institute of Medical Technology, University of 
      Tempere, Finland.
FAU - Tirkkonen, M
AU  - Tirkkonen M
FAU - Forozan, F
AU  - Forozan F
FAU - Tanner, M M
AU  - Tanner MM
FAU - Kallioniemi, O
AU  - Kallioniemi O
FAU - Kallioniemi, A
AU  - Kallioniemi A
LA  - eng
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 (DNA Probes)
RN  - 0 (DNA, Neoplasm)
SB  - IM
MH  - Breast Neoplasms/*genetics
MH  - Chromosome Mapping
MH  - Chromosomes, Human, Pair 17/*genetics
MH  - DNA Probes
MH  - DNA, Neoplasm/analysis
MH  - *Gene Amplification
MH  - *Gene Dosage
MH  - Genes, Neoplasm
MH  - Genes, Tumor Suppressor
MH  - Genes, erbB-2/genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Nucleic Acid Hybridization
MH  - Tumor Cells, Cultured
EDAT- 1997/12/31 23:47
MHDA- 2000/06/20 09:00
CRDT- 1997/12/31 23:47
PHST- 1997/12/31 23:47 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/12/31 23:47 [entrez]
AID - 10.1002/(SICI)1098-2264(199712)20:4<372::AID-GCC8>3.0.CO;2-Z [pii]
AID - 10.1002/(sici)1098-2264(199712)20:4<372::aid-gcc8>3.0.co;2-z [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 1997 Dec;20(4):372-6. doi: 
      10.1002/(sici)1098-2264(199712)20:4<372::aid-gcc8>3.0.co;2-z.