A developmental view of endometrial hyperplasia and carcinoma based on experimental research.
On the basis of experimental research, using rabbit uterine epithelium as a model, it is postulated that human endometrial hyperplasia or carcinoma may be due to derangement of intrinsic growth mechanisms such as cell proliferation, migration, loss and differentiation. Ovarian hormones, estrogen inhibitor or amplifying factors, prostaglandins, stroma-epithelial interactions, proteolytic activity and hormone receptors, all regulate the described intrinsic growth mechanisms, and their excess or lack could result in altered growth patterns. It is also proposed that different types of endometrial carcinoma could result from neoplastic transformation of cells at different stages of differentiation. Since cells at those stages could respond to various hormones in different ways, it would seem of therapeutic value to know the cell of origin in each type of endometrial carcinoma.
D000818:Animals; D002454:Cell Differentiation; D002455:Cell Division; D002471:Cell Transformation, Neoplastic; D004714:Endometrial Hyperplasia / Q000473:pathology*; D004717:Endometrium / Q000187:drug effects; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D011374:Progesterone / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology; D011817:Rabbits; D014594:Uterine Neoplasms / Q000473:pathology*
D004967:Estrogens; D011453:Prostaglandins; D011374:Progesterone