Smooth muscle neoplasms of the uterus.

Recent investigations, using DNA technology, of the molecular biology of smooth muscle tumours of the uterus have confirmed their monoclonality and have strengthened the view that oestrogen and oestrogen receptors play a major role in the pathogenesis of fibromyomata. In addition, increasing evidence suggests that progesterone, insulin-like growth factors, epidermal growth factors and other proteins are also involved. The mechanisms whereby gonadotrophin-releasing hormone agonists cause shrinkage of fibromyomata remain controversial but both vascular changes and cellular atrophy appear to play a role. A shift of emphasis in the study of fibromyomata has resulted from the demonstration that the myometrium adjacent to fibromyomata is not normal and shows some similarities to the tumours themselves.