ABSTRACT
ABSTRACT Endometrial carcinoma (EC) is the most commonly diagnosed gynecological malignancy among western countries and fourth most common cancer in women. Most ECs are diagnosed and cured at an early stage. However, about 15%–20% of endometrial tumors exhibit an aggressive phenotype. Based on pathological and molecular characteristics, EC has been classied into two groups: type I estrogen-dependent adenocarcinoma, which has a good prognosis and an endometrioid histology, showing microsatellite instability (MSI) and mutations in PTEN, PIK3CA, K-RAS, CTNNB1 (beta-catenin) gene, etc., and type II or non-estrogen-dependent EC associated with poor prognosis and non-endometrioid histology, exhibiting p53 mutations, STK12 HER2/neu amplication, p16 overexpression, and chromosomal instability. EC develops as a result of a stepwise accumulation of alterations specic of each histological type. However, more knowledge is needed to better understand the differences in the molecular biology and the clinical outcome of EC to produce new molecular targets and better therapeutic
CONTENTS
14.1 Fundamentals of Endometrial Cancer ............................................................................386 14.2 Molecular Genetics Associated with Endometrial Carcinoma ...................................386
