Abstract
Aim: Microsatellite instability (MSI) has recently emerged as one of the most important pathways in endometrial carcinogenesis, especially in endometrioid subtype (type I). However, non-endometrioid subtypes, like serous, papillary or mucinous tumors, have long been known to overexpress p16 and/or p53 genes. In the present study, we investigated the immunohistochemical (IHC) panel in all subtypes of endometrial cancer (EC), and correlated the results with nuclear mitosis index (Ki-67) as a marker of tumoral mitosis rate. Methods: Medical records of patients admitted with EC and underwent surgery between 2010 and 2022 were reviewed. IHC panel results of estrogen and progesterone receptors (ER, PR), mismatch repair (MMR) proteins MLH1, PMS2, MSH2, MSH6, Ki-67 and p16/p53 status were recorded. Chi square test was used for statistical analysis. Results: Total of 44 female patients (with pathology reports including all of IHC panel markers) were included. Mean age was 64.1±12.51 years. Type I EC was the most common pathology (72%). ER and PR positivity were very prominent in type I tumors in comparison with non-endometrioid (type II) tumors (84% vs 16%, respectively; p
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