In a series of 128 karyotyped ovarian carcinomas, 42% of cases with ch
romosome 1 clonal structural abnormalities had breaks at band 1p36 (us
ually involving translocations of unknown material). Fluorescent in si
tu hybridization (FISH) studies using combinations of 1 centromere and
1p36.3-specific probes (16 cases) or I centromeric and 17 whole-chrom
osome paint probes (11 cases with 1p+) revealed a trend toward deletio
n of 1pter relative to 1 centromere (63%); intratumor heterogeneity; a
nd the origin of 1p+ in 3/11 cases (27%) from chromosome 17 [t(1;17)(p
36;?)]. The frequency of this specific breakpoint and its involvement
in recurrent translocations suggest that these regions are loci for ge
nes important in the pathogenesis of a subset of sporadic ovarian carc
inomas. (C) Elsevier Science Inc., 1997.