Some genetic alterations are involved in ovarian carcinogenesis. Since some benign and borderline tumors may represent early steps in ovarian carcinogenesis, analysis of precursor lesions could provide evidence that an accumulation of genetic events is required in order for normal ovarian epithelium to generate benign, borderline, malignant tumors. Few pre-invasive ovarian tumors have been studied so far.

60 cases of ovarian epithelial tumors, including benign, borderline, and malignant tumors, were analyzed for microsatellite instability (MSI) by gel analysis of paired germ line and tumor DNA. PCR amplification was performed using the panel of 5 microsatellite markers recommended by the NCI (BAT25, BAT26, D2S123, D5S346, D17S250) and 6 additional markers (D1S160, D1S162, D7S522, D11S860, D17S855, D17S932).

In this study, D2S123 and D5S346 were the most frequently altered markers in malignant ovarian tumors and D11S860 locus showed MSI in 4 adenomas, 4 boderline tomors, and 10 malignant tumors. Other markers displayed instability with only one or two tumors showing MSI. On the basis of NCI criteria, most benign tumors demonstrat microsatellite stable (MSS). In the borderline tumors, 10 tumors revealed MSS, 8 tumors had low-frequency MSI (MSI-L), and two tumors had high frequency MSI (MSI-H). In the malignant tumors, 6 tumors revealed MSS, 2 tumors had MSI-L, and 12 tumors had high MSI-H.

According to the results, MSL-H is more frequently seen in the malignant tumors. D2S123 and D5S346 were the most frequently altered markers in the malignant tumors, and D11S860 locus may be involved in early step of carcinogenesis.