There are various forms of endometrial hyperplasia which, in terms of prognosis and therapy, can be subdivided into those having cytological atypia and those lacking this feature. The former may progress into invasive endometrial malignancy through a transitional non-invasive stage. This is a continuous process and, as a result, the distinction between an atypical hyperplasia and an intraepithelial adenocarcinoma (IEA) or an adenocarcinoma with stromal invasion is not histologically reproducible. The concept of endometrioid neoplasia, which includes the entire spectrum of the aforementioned proliferating endometrial lesions, was introduced. Adenocarcinomas arising from an atypical hyperplasia are invariably of the endometrioid cell type, whereas those developing from an atrophic endometrium may be either of the endometrioid or of the. non-endometrioid cell type. Endometrioid adenocarcinomas arising through the hyperplasia-neoplasia sequence are oestrogen induced and tend to be well differentiated and less invasive of the myometrium, lack lymphatic and metastatic involvement and have an excellent prognosis. Oestrogen-induced adenocarcinomas are also endometrioid, arising from an atrophic or a rather weakly proliferating endometrium, but these neoplasms are frequently of higher histological grade and have a somewhat less favourable prognosis. Finally, endometrial carcinomas of the nonendometrioid cell type, mainly serous papillary and clear cell carcinomas, are non-oestrogen induced, non-hyperplasia associated and show adverse aggressive histological features and an extremely poor prognosis. The antigenic characteristics and the molecular events associated with the development of these forms of endometrial malignancy are distinct and allow the description of, at least, two pathogenetic types of endometrial carcinoma.
