IntroductionHigh‐grade serous carcinoma (HGSC) accounts for ~70% of epithelial ovarian cancers, with the ovarian surface epithelium (OSE) traditionally being the favoured cell of origin. It was postulated that OSE entrapped in ovarian cortical inclusion cysts (CICs) after ovulation underwent metaplastic transformation to Müllerian‐type epithelium (Müllerian‐CICs). However, it is now believed that a high proportion of HGSCs arise from Müllerian fallopian tube fimbriae, based on a study reporting that this was the most common site of occult lesions in BRCA1/2 mutation carriers undergoing risk‐reducing salpingo‐oophorectomy (RRSO); a subsequent study identified occult tubal cancers in ~70% of ovarian HGSCs. The site of origin of those cases without tubal involvement is controversial, but evidence suggests that a significant proportion arises within the ovary itself from Müllerian‐CICs, through metaplasia of entrapped OSE or from tubal cells entrapped within the ovary postovulation.The OSE is derived embryologically from coelomic epithelium, which is contiguous with the mesothelial lining of the peritoneal cavity and differs from the Müllerian‐CICs thought to give rise to HGSCs. By immunohistochemistry (IHC), OSE is generally positive for calretinin and negative for paired box gene 8 (PAX8); the secretory cells of the fimbria are negative for calretinin and positive for PAX8; the ciliated
Histopathology – Wiley
Published: Jan 1, 2018
Keywords: ; ; ;
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