World Journal of Medical Sciences 13 (2): 118-125, 2016 ISSN 1817-3055 © IDOSI Publications, 2016 DOI: 10.5829/idosi.wjms.2016.13.2.1158 Corresponding Author: Dina F. Elyasergy, Department of Pathology, Faculty of Medicine, Cairo University, Egypt. E-mail: dandoon3000@hotmail.com. 118 Expression of PTEN in Endometrioid Carcinoma, Histopathological and Immunohistochemical Study Dalal A. Elwy, Ahmed M. Abd Al-Aziz, Samar A. El Sheikh, Mohammed F. Darweesh and Dina F. Elyasergy Department of Pathology, Faculty of Medicine, Cairo University, Egypt Abstract: Endometrial endometrioid carcinoma (EECA) has a variety of molecular alterations. Currently the most frequently altered is loss of the PTEN (phosphate and tensin homolog) protein, a tumor suppressor gene. The aim of this study was to evaluate the expression pattern of PTEN gene in normal proliferative endometrium and EECA. This work included sixty paraffin-embedded endometrial tissue samples obtained from surgical pathology files of Pathology Department, Faculty of medicine, Cairo University, Kasr El Aini Hospital and other private laboratories; diagnosed as: 30 within normal proliferative (as a control group) and 30 EECA. Immunoreactivity was graded arbitrarily and semi quantitatively by considering the percentage and intensity of staining. The results indicated that PTEN immunoreactivity was noted in all cases of normal proliferative endometrium. In EECA, 46.7% were PTEN negative, 16.7% showed positive immunoreactivity of 10-50% and 36.7% showed positive immunoreactivity of >50%. The difference in immunoreactivity was highly significant (P<0.001). PTEN intensity was significantly higher in normal proliferative endometrium than in EECA (P<0.001). It can be concluded that PTEN expression was significantly higher in cyclical endometrium than in endometrioid carcinoma. Key words: PTEN Endometrial cancer Endometrioid carcinoma Neoplastic endometrium INTRODUCTION value in patient management. Unfortunately several Endometrial carcinoma is the most common predominant criterion for diagnosis of premalignant gynecologic malignancy in developed countries and the lesions (atypical endometrial hyperplasia), have poor second most common in developing countries [1]. There reproducibility [4, 6]. Recent molecular diagnostic are two major classes of endometrial carcinoma. These are methods have provided new ancillary tools for commonly described as Type I (the majority) and Type II premalignant lesion diagnosis. EECA has a variety of cancers, which respectively correspond to endometrioid genetic alternations, including microsatellite instability and non-endometrioid histologic types [2]. Type I (MI) and mutations of PTEN, k-ras and -catenin genes endometrial cancers are primarily associated with [7, 8]. Also, these molecular genetic alternations have unopposed estrogen exposure and develop in a been described in atypical endometrial hyperplasia [8]. background of endometrial hyperplasia [3]. Endometrioid Currently, PTEN is the most frequently altered gene in endometrial carcinoma (EECA) is the prototypical EECA which is located on chromosome 10 [9]. The PTEN endometrial adenocarcinoma. It is thought to develop gene has both lipid and protein phosphate activity and following a continuum of premalignant lesions ranging the combination of the losses of PTEN lipid and protein from endometrial hyperplasia without atypia, to phosphate activity can cause an aberrant cell growth and hyperplasia with atypia and finally to well differentiated an escape from apoptosis, as well as abnormal cell carcinoma [4, 5]. Accurate diagnosis of premalignant spreading and migration [10]. PTEN-null glands (i.e., loss lesions in routine endometrial biopsies has a great clinical of PTEN expression) are shown in a diffuse pattern in studies have shown that cytological atypia which is