ANALYSIS OF APROTININ-INDUCED ENHANCEMENT OF METASTASIS OF LEWIS LUNG-TUMORS IN MICE

Abstract

The antiproteinase, aprotinin, has been reported to inhibit the growth and development of a number of different types of primary cancers; its effects on metastasis particularly need clarification. As proteolytic enzymes are thought to be involved in some steps of metastasis, the effects of aprotinin on the spontaneous metastasis of Lewis lung (LL) tumors in mice together with its effects on the detachment of cells from primary LL cancers, the development of lung tumors from i.v. injections of LL cells, LL cell adhesion in vitro and LL cell retention in the lungs were investigated. The metastasis-enhancing effect of aprotinin may be due partly to promotion of the retention of circulating cancer cells at the vascular endothelium. As these effects could well occur with cancers in general, antiproteinases may do more harm than good if used in cancer therapy.