The relationship between oestradiol and epidermal growth factor (EGF) in the control of endometrial proliferation and differentiation in cultures of human endometrial stromal cells was investigated. Oestradiol at a concentration of 10 nmol l-1 increased the incorporation of both [3H]thymidine and [3H]leucine but the differences were significantly different from control only for [3H]leucine incorporation. Concentrations of 0.16, 1.6 and 16 nmol EGF l-1 significantly increased both [3H]thymidine (P < 0.01) and [3H]leucine incorporation (P < 0.01). The pure steroidal antioestrogen, ICI 182,780, inhibited any increase in [3H]thymidine and [3H]leucine incorporation stimulated by oestradiol in endometrial stroma. The monoclonal antibody, ICR 16, directed against the EGF receptor did not inhibit the oestradiol action in stromal cells, indicating that, in this model system, oestradiol does not act by inducing synthesis or release of EGF. However, ICI 182,780 potently inhibited the incorporation of [3H]thymidine stimulated by EGF in endometrial stromal cells, suggesting interdependence between oestradiol and EGF in the control of endometrial stromal proliferation. Oestrogen-free conditioned medium from endometrial stromal cultures did not stimulate either [3H]thymidine or [3H]leucine incorporation, suggesting that oestradiol did not stimulate the secretion of a trophic factor from endometrial stromal cells.