The structure of the 17p amplicon from 9 human sarcoma specimens evaluated
by comparative genomic hybridization (CGH) has been studied by analyzing 28
microsatellite markers by FCR. Eleven sarcoma specimens showing no DNA cop
y number increases at 17p by CGH were analyzed as control samples. Five spe
cimens were analyzed by Southern blotting using probes that have previously
shown amplification at the 17p12 region in astrocytoma and high-grade oste
osarcoma samples. Microsatellite marker analyses revealed that all samples
but I showing copy number increases at 17p by CGH displayed allelic imbalan
ce that confirmed the CGH findings. Seven of these 9 cases displayed gain i
n copy number by microsatellite marker analysis. Four cases displaying gain
in copy number were associated with loss of heterozygosity at other loci.
Southern blot analysis showed amplification in 3 cases, all of them had sho
wn copy number increases by CGH and microsatellite marker analysis, except
one case, which was not included in the microsatellite marker analysis. Our
results reveal the complexity of the 17p amplicon in sarcomas, suggesting
that multiple target genes are involved in tumorigenesis. Int. J. Cancer 82
:329-333, 1999. (C) 1999 Wiley-Liss, Inc.