**5.1 Origin and epidemiology of high-grade serous ovarian cancer**

EOC genomic predisposition is now recognized in about 15% of affected women, where Breast cancer susceptibility genes *BRCA1* and *BRCA2* were identified as the main causative agents of hereditary EOC. Different forms of mutations in these genes and other double-strand DNA break repair genes are mainly associated with susceptibility to HGSOC [1].

High-grade serous ovarian cancer (HGSOC) is the most common form of EOC, accounting for about 75% of all EOC (**Figure 1**). It has been found to originate from the fallopian tube epithelium due to its link with IGF-1R/AKT pathway, which is activated by follicular fluid [17]. However, the molecular basis of how it is transferred to the ovaries is yet to be understood. A recent study revealed that follicular fluid plays a vital role in events leading to the development and intraperitoneal metastasis of HGCOS, by supporting migration, proliferation, invasion, anchorage, adhesion and anoikis insensitivity [18].
