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We hypothesized that comparative genomic studies of serous OVCAs and FTCs should point to gene regions critically involved in their tumorigenesis. Array comparative genomic hybridization (array CGH) analysis indicated that serous OVCAs and serous FTCs displayed common but also more distinctive patterns of recurrent changes. Targeted gene identification using a dedicated multiplex ligation\u2010dependent probe amplification (MLPA) probe set directly identified <jats:italic>EIF2C2<\/jats:italic> on 8q as a potentially important driver gene. Other previously unappreciated gained\/amplified genes included <jats:italic>PSMB4<\/jats:italic> on 1q, <jats:italic>MTSS1<\/jats:italic> on 8q, <jats:italic>TEAD4<\/jats:italic> and <jats:italic>TSPAN9<\/jats:italic> on 12p, and <jats:italic>BCAS4<\/jats:italic> on 20q. <jats:italic>SPINT2<\/jats:italic> and <jats:italic>ACTN4<\/jats:italic> on 19q were predominantly found in FTCs. Gains\/amplifications of <jats:italic>CCNE1<\/jats:italic> and <jats:italic>MYC<\/jats:italic>, often in conjunction with changes in genes of the AKT pathway, <jats:italic>EVI1<\/jats:italic> and <jats:italic>PTK2<\/jats:italic>, seemed to be involved at earlier stages, whereas changes of <jats:italic>ERBB2<\/jats:italic> were associated with advanced stages. The only <jats:italic>BRCA1<\/jats:italic>\u2010mutated FTC shared common denominators with the sporadic tumours. In conclusion, the data suggest that serous OVCAs and FTCs, although related, exhibit differences in genomic profiles. In addition to known pathways, new genes\/pathways are likely to be involved, with changes in an miRNA\u2010associated gene, <jats:italic>EIF2C2<\/jats:italic>, as one important new feature. Dedicated MLPA sets constitute potentially important tools for differential diagnosis and may provide footholds for tailored therapy. Copyright \u00a9 2007 Pathological Society of Great Britain and Ireland. 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