MOLECULAR PATHOLOGY OF OVARIAN CARCINOMAS

There is evidence that ovarian cancer may be derived from the progress ive transformation of benign and/or borderline tumours. Mutations invo lving different oncogenes and tumour suppressor genes accumulate durin g the process of malignant transformation, and the alterations of gene s involved in the pathogenesis of familial ovarian cancer are probably early events in ovarian tumorigenesis. BRCA-1 and BRCA-2 act as class ical tumour suppressor genes in hereditary tumours, but their role in sporadic tumours remains controversial; however, a high frequency of a llele losses in BRCA-1 (17q) and BRCA-2 (13q) loci has been observed i n both familial and sporadic tumours. The possible role of mismatch re pair genes and microsatellite instability is also controversial, but a role for them has been proposed in borderline tumours. Mutations in K -ms are specific for mucinous tumours and may be related to mucinous d ifferentiation. Finally, a role in tumour progression has been propose d fdr both c-erb B-2 and p53, but their practical value in prognosis r emains questionable.