EVIDENCE FOR DIVERGENCE OF DNA COPY NUMBER CHANGES IN SEROUS, MUCINOUS AND ENDOMETRIOID OVARIAN CARCINOMAS

Comparative genomic hybridization was applied to detect and map change s in DNA copy number in 24 well or moderately differentiated epithelia l ovarian carcinomas (eight serous, eight mucinous and eight endometri oid carcinomas). Twenty-three of the 24 tumours showed changes in DNA copy number in one or several regions [median 4, range 1-17). Gains we re more frequent than losses (ratio 1.6:1.0). The most frequent gains occurred in chromosomes lq (38%), 2p (29%), 7q (25%), 8q(38%) and 17q (38%), and the most common losses were located in chromosomes 8p (21%) , 9p (25%) and 13q (21%). High-level amplifications were detected in s even tumours at 1q22-32, 2p15-22, 3qcen-23, 6p21-22 and 89. In the thr ee histological subtypes the copy number karyotypes showed substantial differences. Gains at Iq were observed in endometrioid (five cases) a nd serous tumours (four cases). Increased copy number at 10q was seen in endometrioid tumours only [four cases), whereas gains at 11q occurr ed mostly in serous tumours (four cases). In mucinous tumours, the mos t common copy number change was a gain at 17q (six cases). The results show that, in epithelial ovarian carcinoma, changes in DNA copy numbe r are a rule rather than an exception, chromosomes 1, 2, 7, 8, 9, 13 a nd 17 being the most frequently affected. The diverging pattern of gen etic changes seen in epithelia[ ovarian carcinomas with different hist ological phenotypes suggests that various pathways may lead to tumorig enesis and/or progression in these subgroups.