TP53 and neoplasm: Kurman and Shih’s “dualistic” model of epithelial OC pathogenesis divides OC into two main categories, type I (low-grade, relatively indolent and genetically stable tumours that typically arise from recognizable precursor lesions, such as endometriosis (or so-called borderline) and type II (high-grade serous carcinomas, virtually all of which harbour mutant TP53 alleles) [11].