**5.3 Pathology/molecular abnormality**

The growth pattern of HGSOC is diverse, encompassing glandular, solid, large papillae with high mitotic rate and frequent necrosis [21]. HGSOC is characterized by recurrent mutations in *RB1, CDK12, BRCA1, BRCA2, NF1 and TP53*, and also frequent DNA losses and gains. This makes it chromosomally unstable with the potential of developing acquired chemoresistance [22, 23]. Thus, the homozygous and heterozygous loss is an important mechanism in tumour suppressor genes inactivation [1]. Also, studies have shown that homologous recombination is defective in almost half of HGSOC, and this deficiency is a key determinant of platinum sensitivity and treatment with Poly ADP-ribose polymerase inhibitors (PARPi) [22, 24]. HGSOC can be molecularly stratified into four different prognostic subtypes namely: mesenchymal-C1, immune-C2, differentiated-C4, and proliferative-C5, and into seven copy-number signatures [22, 25–27].
