The molecular events that occur during the development of endometrial carcinoma are largely uncharacterized. Carcinomas of the endometrium are associated as extracolonic malignant tumors in patients with hereditary nonpolyposis colorectal cancer syndrome. Endometrium and ovary may develop histologically homologue cancers especially endometrioid and papillary serous carcinomas. Colon and ovarian carcinoma might serve as model systems for the molecular analysis in endometrial carcinoma. We sought to analyze in endometrial carcinoma frequent molecular mechanisms of colon and ovarian carcinoma, including Ki-ras codon 12 mutations, microsatellite instability, p53 and c-erb B-2 immunohistochemical expression and allelic loss on chromosome 17q. Our results indicate that molecular mechanisms in endometrial carcinoma are different than those responsible for colorectal carcinomas and that uterine papillary serous carcinomas shares with its ovarian counterpart several molecular alterations in contrast to the histologically homologue uterine and ovarian endometrioid carcinoma. Furthermore there is a molecular basis to distinguish uterine endometrioid and papillary serous carcinoma.