Author/Authors :
Thompson، نويسنده , , Floyd H and Taetle، نويسنده , , Raymond and Trent، نويسنده , , Jeffrey C.S. and Liu، نويسنده , , Yun and Massey-Brown، نويسنده , , Kathy A. Scott، نويسنده , , Katherine M and Weinstein، نويسنده , , Ronald S and Emerson، نويسنده , , Julia C and Alberts، نويسنده , , David L and Nelson، نويسنده , , Mark A، نويسنده ,
Abstract :
In a series of 128 karyotyped ovarian carcinomas, 42% of cases with chromosome 1 clonal structural abnormalities had breaks at band 1p36 (usually involving translocations of unknown material). Fluorescent in situ hybridization (FISH) studies using combinations of 1 centromere and 1p36.3–specific probes (16 cases) or 1 centromeric and 17 whole-chromosome paint probes (11 cases with 1p+) revealed a trend toward deletion of 1pter relative to 1 centromere (63%); intratumor heterogeneity; and the origin of 1p+ in 3/11 cases (27%) from chromosome 17 [t(1;17)(p36;?)]. The frequency of this specific breakpoint and its involvement in recurrent translocations suggest that these regions are loci for genes important in the pathogenesis of a subset of sporadic ovarian carcinomas.
