eight patients who had a stable or partial response, suggesting that, in addition to causing sclerosis of bone, APD may have an antitumour effect. Factors released from tumours stimulate osteoblastic activity3 and osteolysis mediated by osteoclasts.4 APD is a potent inhibitor of osteoclast function, and such inhibition combined with the osteoblastic factors produced by tumour cells may explain the bony sclerosis seen in this study.APD reduces morbidity from lytic metastases when used in conjunction with standard chemotherapy,' and this study shows that it may be active when used alone.We are grateful to the staff of the day ward, Christie Hospital; the departments of chemical pathology at Christie Hospital and Withington Hospital; Mrs H Morten and Mr J Turnbull for performing the radioimmunoassays; and Ciba-Geigy Ltd for supplies of
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