Author/Authors :
Thompson، نويسنده , , Floyd H. and Nelson، نويسنده , , Mark A. and Trent، نويسنده , , Jeffrey M. and Guan، نويسنده , , Xin-Yuan and Liu، نويسنده , , Yun and Yang، نويسنده , , Jin-Ming and Emerson، نويسنده , , Julia and Adair، نويسنده , , Laurence and Wymer، نويسنده , , Julie and Balfour، نويسنده , , Celia and Massey، نويسنده , , Kathy and Weinstein، نويسنده , , Ronald and Alberts، نويسنده , , David S. and Ta، نويسنده ,
Abstract :
In this study of ovarian carcinoma, we extended previous findings by performing FISH using chromosome 19 paint and microFISH probes and patient samples with and without abnormalities of chromosome 19 identified by G-banding. Karyotype interpretations of der(19) were confirmed, while additional 19 translocations were also detected by FISH with 19WCP in some cases. Similar FISH studies of ovarian carcinoma cell lines found chromosome 19 abnormalities even after extensive in vitro culture. MicroFISH probes were generated by chromosome microdissection from two cases with hsr(19) and mapped to 19q13.2 and 19q13.1-.2, respectively. FISH with these microFISH probes alone or in combination with a 19 WCP probe to four patient samples and seven cell lines showed that 65% of chromosome 19 structural abnormalities contained 19q13.1–q13.2 sequences, sometimes as large hsrs. Ovarian cancer cell lines showed amplification and overexpression of the AKT2 putative oncogene, but not the ERCC-2 DNA repair gene in this chromosomal region. In addition to AKT2, amplification and over-expression of other yet-unidentified genes in the 19q13.1–q13.2 region may contribute to ovarian carcinoma pathogenesis or progression.
