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Inhibition of v-fms-induced Tumor Growth in Nude Mice by Castanospermine¹

Pacific Northwest Research Foundation, Seattle, Washington 98104 [G. K. O., N. K. S.]; Department of Pathology, University of Washington, Seattle, Washington 98195 [G. K. O., L. R. R.]; and Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104 [L. R. R.]

Castanospermine, an indolizidine alkaloid isolated from the seeds of the chestnut tree Castanospermum australe, has been shown to prevent the normal glycosylational processing of the v-fms-transforming glycoprotein. v-fms-transformed cells grown in vitro in the presence of castanospermine accumulate immature forms of the glycoprotein that do not reach the cell surface. These treated cells revert to the normal phenotype. We have now extended those studies to an in vivo tumorigenicity model in the nude mouse using v-fms-transformed rat cells (SM-FRE) and dietary administration of castanospermine. Following tumor induction with s.c. injection of 10⁶ SM-FRE cells, mice whose diet had been supplemented with 2.4 mg castanospermine/g food consumed approximately 0.84 mg castanospermine/g mouse/day. Furthermore, these mice had slower growing tumors that were 2.6 times smaller than tumors in control groups at the termination of the experiment 24 days postinjection. These results indicate that castanospermine is effective in slowing the growth of v-fms-transformed cells in vivo, suggesting that this drug may offer an effective therapy against certain tumors, including some arising from activated protooncogenes that encode glycoproteins such as growth factor receptors.

¹ This investigation was supported by USPHS Research Grant CA 40987.

² Supported by Postdoctoral Environmental Pathology Training Grant ES-07032 from the NIH.

³ Recipient of Grant CA 28151 from the National Cancer Institute, Department of Health and Human Services. To whom requests for reprints should be addressed.

Received 7/ 7/87. Revised 10/23/87. Accepted 12/ 2/87.

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