Figure 1: Fallopian tube hypothesis on the origin of high-grade serous carcinoma (HGSC). Fallopian tube epithelium (FTE) cells of the fimbriated ends undergo initial neoplastic transformation, becoming serous tubal intraepithelial carcinoma (STIC). STIC cells possess resistance to anoikis that favors settlement and invasion of the ovarian surface. The ovarian microenvironment, rich in hormonal and inflammatory factors, drives the full neoplastic transformation to invasive HGSC (A). Alternatively, the normal FTE cells are entrapped in the ovary favored by their anatomical proximity and physiological ovulation process. Entrapped FTE cells undergo progressive neoplastic transformation inside the ovary through the accumulation of molecular alterations (B).