Results of recent molecular genetic studies have suggested that low-grade and high-grade serous ovarian cancers are distinct—high-grade cases are characterised by TP53 mutations, whereas low-grade cases typically have KRAS or BRAF mutations.18, 40 Likewise, increasing evidence lends support to the hypothesis that a significant proportion of low-grade serous tumours can develop from borderline precursors, whereas this is not the case for high-grade serous tumours.40 This evidence concerns the gene TP53 and ovarian serous adenocarcinoma.