1Post Graduate, Department of Pathology, Sree Balaji Medical College and Hospital, Bharath Institute of Higher Education and Research, Chennai
2Associate Professor, Department of Pathology, Sree Balaji Medical College and Hospital, Bharath Institute of Higher Education and Research, Chennai
3 Professor and Head, Department of Pathology, Sree Balaji Medical College and Hospital, Bharath Institute of Higher Education and Research, Chennai
*Corresponding Author: Dr. Hemalatha Ganapathy Professor and Head, Department of Pathology, Sree Balaji Medical College and Hospital, Bharath Institute of Higher Education and Research, Chennai-73. E Mail- hemalathagnpthy@yahoo.com, M No- 9444108134
Online published on 27 March, 2020.
An excess of estrogen relative to progestin, if sufficiently prolonged or marked, can induce exaggerated endometrial proliferation (hyperplasia), which is an important precursor of endometrial carcinoma.1 The importance of unopposed estrogen stimulation for the development of endometrial hyperplasia and subsequently adenocarcinoma is well documented. However, the histogenetic mechanisms for the development of different endometrial lesions such as hyperplasia, polyps, and adenocarcinoma have not been fully characterized to date. This study is aimed at determining the expression of the proliferation marker-Ki-67 in endometrial hyperplasia.
Endometrial carcinoma, proliferation marker-Ki-67
