Introduction

Endometrial adenocarcinoma is a heterogenous group of tumors with variable pathological, clinical, epidemiological, and genetic properties. Although, each of these perspectives contribute an aspect of understanding to the biology of this most common of all gynecological malignancies, they must be combined to achieve maximum benefit in patient care. This chapter is oriented along the simplified lines of a dichotomous model of sporadic disease in which the clinicopathological groups of endometrioid (type I) and nonendometrioid (type II) endometrial carcinomas are a launching point to consider their most commonly encountered characteristics. The former are subject to endocrine modulation and transit a PTEN tumor suppressor inactivated precursor stage of endometrial intraepithelial neoplasia (EIN), whereas the latter are characterized by p53 inactivation and a brief, if any, premalignant phase. A potential mechanism of unopposed estrogen promotion of endometrial carcinogenesis is its positive selection for PTEN-mutant epithelial cells, enabling clonal expansion and subsequent accumulation

From: Current Clinical Oncology: Molecular Pathology of Gynecologic Cancer Edited by: A. Giordano, A. Bovicelli, and R. Kurman © Humana Press Inc., Totowa, NJ

Norma glands

PTEN Mutation

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