Microsatellite instability (MSI) and p16/p53 protein status in different subtypes of endometrial carcinoma: with emphasis on tumor aggressiveness

Objective: We investigated microsatellite instability (MSI) in endometrial cancer (EC) and correlated results with traditional markers (p16, p53, Ki-67) to predict tumor aggressiveness. Materials and Methods: Records of patients admitted with EC between 2010 and 2022 were reviewed, and the widest immunohistochemical (IHC) panel including (1) estrogen or progesterone receptors (ER, PR), (2) mismatch repair (MMR) proteins (MLH1, PMS2, MSH2, MSH6), (3) Ki-67, (4) p16 and (5) p53 proteins were recorded. Chi square test was used for statistical analysis. Results: Total of 44 female patients with pathology reports containing all five IHC panel markers were included. Mean age was 64.1±12.51 years. Type I EC was the most common pathology (72%). ER or PR positivity were very prominent in type I tumors in comparison with non-endometrioid (type II) tumors (84% vs 16%, respectively; p 10% (p<0.05). Conclusion: A wider IHC panel including all of MSI (MLH1, PMS2, MSH2, MSH6), ER, PR, p16, p53 and Ki-67 may help oncologic planning in patients with different subtypes of EC, since first three markers can be used for tumor differentiation and others indicate the necessity of aggressive treatment.