THE ANTIBIOTIC, dactinomycin, and the alkaloid, vincristine sulfate, have each produced objective tumor regression in children with a variety of malignant neoplasms.1The best responses to dactinomycin have occurred in cases of Wilms' tumor and rhabdomyosarcoma, although tumor regression has occasionally been observed in children with lymphoma, neuroblastoma, and other neoplasms. The antitumor spectrum of vincristine sulfate has included lymphomas, Wilms' tumor, rhabdomyosarcoma, neuroblastoma, Ewing's sarcoma, retinoblastoma, and liposarcoma. Dactinomycin acts by binding the guanine moiety of deoxyribonucleic acid and thereby preventing the formation of the enzyme, ribonucleic acid polymerase.2As a result, ribonucleic acid and protein synthesis are suppressed and cellular damage occurs. Although the specific mechanism of action of vincristine sulfate is unknown, it prevents cell division by interfering in some way with the formation of organization of the spindle tubules of the mitotic apparatus.3 Since the limiting toxic effect of dactinomycin therapy is most