INTERPHASE CYTOGENETIC ANALYSIS OF MUCINOUS OVARIAN NEOPLASMS

Extending our previous efforts to characterize ovarian neoplasms by in terphase cytogenetics, we analyzed a series of 32 mucinous tumors by n onisotopic in situ hybridization with seven different centromere-speci fic probes as well as by flow and image DNA cytometry; we then compare d the data with results of p53 and Ki67 immunohistochemistry and MYC D NA-PCR analysis and of the clinical follow-ups. Of the tumors studied, 11 of 14 (78.6%) mucinous carcinomas, 7 of 7 (100%) mucinous tumors o f low malignant potential (LMP), and 7 of 11 (63.6%) mucinous cystaden omas demonstrated chromosomal aberrations. The mean number of chromoso mal aberrations (+/- SD) was slightly higher in DNA cytometrically non diploid cases than in diploid cases (2.0 +/- 1.6 versus 1.6 +/- 1.2, n ot significant) but did not differ significantly among the study group s (carcinomas: 1.7 +/- 1.4, tumors of LMP: 1.9 +/- 0.7; adenomas: 1.4 +/- 1.4). Aberrations affected chromosomes 1 (14 of 27 cases) and 6 (1 2 of 31) most frequently, followed by chromosomes 17 (7 of 28), 7 (6 o f 29), and X (6 of 28). Signal gain for centromere 1, which was the mo st prevalent finding (13 of 27), was observed in 3 of 10 mucinous cyst adenomas, 2 of 4 mucinous tumors of LMP, and 8 of 13 mucinous carcinom as. All six moderately and poorly differentiated carcinomas demonstrat ed this aberration. Signal gain of centromere 6 (3 of 13) and centrome re 7 (4 of 13) were found only in carcinomas (p < 0.05 and p < 0.025, respectively). The interphase cytogenetic results correlated neither w ith proliferative activity, immunohistochemical p53 accumulation, MYC DNA amplification, nor postoperative outcome. Compared with serous ova rian neoplasms (Lab Invest 1996, 75:473-485), mucinous tumors demonstr ated signal gain for chromosome 1 (p < 0.0001) and signal loss for chr omosomes 6 (p < 0.001) and X (p < 0.01) significantly more often. Loss of centromere 17 was more characteristic for serous than for mucinous carcinomas (p < 0.05). Our observations show that chromosomal aberrat ions in mucinous ovarian neoplasms are apparently not random. These re sults support the notion that the molecular genetic changes in mucinou s neoplasms differ from those in serous tumors.