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Analysis of Aprotinin-induced Enhancement of Metastasis of Lewis Lung Tumors in Mice¹

Department of Experimental Pathology, Roswell Park Memorial Institute, Buffalo, New York 14263

The antiproteinase, aprotinin, has been reported by some workers to inhibit the growth and development of a number of different types of primary cancers in animals; however, its effects on metastasis particularly need clarification. As proteolytic enzymes are thought to be involved in some steps of metastasis, we have investigated 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. The results suggest that the metastasis-enhancing effect of aprotinin is 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, we conclude that antiproteinases may do more harm than good if used in cancer therapy.

¹ This work was partially supported by Grants CA-17609 from the National Cancer Institute and CO21 from the American Cancer Society.

² Recipient of American Cancer Society Institutional Research Grant IN-54S-25. Partial support also provided by Bayer U. K., Ltd. Permanent address: University Department of Clinical Biochemistry and Metabolic Medicine, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, United Kingdom.

³ To whom requests for reprints should be addressed.

Received 1/ 8/81. Accepted 3/19/81.