Pilot studies have shown that administration of the peptide Pepstatin reduces or prevents ascites fluid accumulation in mice carrying a mastocytoma tumor. The basis for this action is believed to be Pepstatin's ability to prevent leukokinin formation in ascites fluid. The proposed investigation would broaden investigations with Pepstatin to include an evaluation of its ability to increase survival time of tumor-bearing animals as well as continue to evaluate its negative effects on ascites fluid accumulation in these animals. In addition, leukokinin formation will be investigated in ascites fluids of humans, and the properties of the components of this system compared to those previously found in mice ascites fluid and human plasma. The ability of Pepstatin to reduce leukokinin formation in human ascites fluid will be investigated by "in vitro" techniques. The role of chemical mediators other than leukokinins which may be involved in ascites fluid accumulation will be studied. The formation or presence of these mediators in pathological fluids of neoplastic disease will be determined by bioassay and isolation when possible from such fluids.