TP53 and ovarian serous adenocarcinoma: Subsequent analysis also showed that the presence of a tandem duplicator phenotype besides the well known homologous recombination deficiency as mechanisms that drive mutagenesis in a significant proportion of patients [37], suggesting that except TP53 other known actionable driver mutations are still elusive [38, 43, 44], contrary to the distinct entity of low grade serous ovarian cancer where cases with somatic mutations generally show stability across samples and time [48].