# Immunohistochemical Evaluation of Phosphatase and Tensin Homolog (PTEN) Expression in Endometrial Lesions: A Cross-Sectional Study in a Tertiary Care Center in South India

## TL;DR

This study examines PTEN protein expression in endometrial lesions to understand its role in cancer development and progression.

## Contribution

The study provides new insights into PTEN's diagnostic and prognostic potential in endometrial carcinogenesis using immunohistochemistry.

## Key findings

- PTEN expression is preserved in benign lesions but decreases in atypical hyperplasia and endometrioid carcinomas.
- Complete PTEN loss correlates with higher tumor grade and myometrial invasion in endometrioid carcinomas.
- All papillary serous carcinomas showed complete PTEN loss, indicating a distinct molecular profile.

## Abstract

Background: Endometrial carcinoma is a common gynecological malignancy, with type I endometrioid carcinoma often arising from precursor lesions like endometrial hyperplasia. The tumor suppressor gene PTEN (phosphatase and tensin homolog) regulates cell proliferation and apoptosis via inhibition of the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway. Its loss is considered an early molecular event in endometrial carcinogenesis. This study aimed to evaluate the immunohistochemical expression of PTEN across various endometrial lesions and correlate its expression with histopathological subtypes and tumor grade.

Methodology: This cross-sectional study was conducted in the Department of Pathology, Sree Balaji Medical College and Hospital, from July 2023 to June 2025. Fifty cases were included: disordered proliferative endometrium (n = 3), endometrial hyperplasia without atypia (n = 23), with atypia (n = 6), endometrial carcinoma (n = 17), and papillary serous carcinoma (n = 3). Tissue sections were stained with hematoxylin and eosin and subsequently subjected to immunohistochemical staining using a rabbit monoclonal PTEN antibody (clone QR042, IVD class, rabbit IgG isotype). PTEN expression was scored based on staining intensity (0-3) and percentage of positive cells (0-4). Statistical analysis was performed using SPSS version 26 (IBM Corp., Armonk, NY).

Results: PTEN expression was preserved in most benign lesions, with moderate to strong staining in disordered proliferative endometrium and hyperplasia without atypia. Reduced staining was seen in hyperplasia with atypia. Among endometrioid carcinomas, 10/15 (66.7%) showed complete loss of PTEN, and loss correlated with higher histological grade and deeper myometrial invasion. All papillary serous carcinomas showed complete loss of PTEN. The association between PTEN expression and histopathological diagnosis was statistically significant (χ² = 52.38; P < 0.001).

Conclusions: Progressive loss of PTEN expression from benign to malignant lesions highlights its potential as an early diagnostic and prognostic marker in endometrial carcinogenesis.