Affiliation:
1. Department of Gynaecological Oncology, Dharamshila Narayana Superspeciality Hospital, Delhi, India,
2. Department of Anatomic Pathology, Dharamshila Narayana Superspeciality Hospital, Delhi, India,
Abstract
Objectives:
The aim of the study was to determine the mismatch repair (MMR) proteins and p53 expression by immunohistochemistry in operable endometrial carcinoma (EC) patients. The study aimed to analyze and correlate clinicopathological factors and survival with MMR and p53 immunohistochemistry markers.
Material and Methods:
A retrospective cohort study of 115 cases of carcinoma endometrium who underwent primary surgery in our hospital from July 1, 2013, to December 31, 2020, with a minimum follow-up of 1 year. Available tissue blocks were stained for IHC expression of MMR and p53 proteins. Patients were stratified into Type I and Type II on basis of histopathology. Clinicopathological factors, overall survival (OS), and disease-free survival (DFS) were then compared on the basis of MMR deficiency and p53 status.
Results:
The mean age of study population was 58.9 years with a mean body mass index of 31.61 kg/m2. The mean follow-up was 41.29 months. Ninety-seven patients underwent IHC staining for MMR and p53 proteins. Among these 97 patients, 79 patients belonged to Type I histopathology and 18 patients belonged to Type II histopathology. The 79 patients of Type I histopathology were further divided into MSS or microsatellite stable group and MSI or microsatellite instable group. MMR deficit status was seen in 17 (21.5%) patients and 62 (78.5%) patients were MSS. For the 18 cases of Type II ECs, 5 (27.8%) patients were p53 positive whereas 13 (72.2%) patients were p53 negative. For patients with Type I histopathology; the clinicopathological factors such as stage, age, grade of the tumor, lymph-vascular space involvement, lymph node status, and myometrial invasion were compared between the MSI and MSS groups. Patients with microsatellite instability were more likely to present with a higher grade, a positive lymph node status, and with lymph-vascular space invasion. The OS and DFS are not significantly affected in patients with loss of MMR proteins. Due to a smaller number of cases in p53 group, clinicopathological features and survival could not be compared.
Conclusion:
Analyzing of immunohistochemistry status for evaluating the microsatellite instability in patients with Type I endometrioid adenocarcinomas is an alternative and efficient tool in predicting the prognosis for these patients. Further studies with more sample size can help us in studying the impact of MSI and p53 on OS and DFS and for guiding in the management of the same.