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Departments of Pharmacology [Y. Y., S. R.] and Obstetrics and Gynecology [S. R.] and Comprehensive Cancer Center [S. R.], University of Minnesota, Minneapolis, Minnesota 55455; Laboratory of Cell Regulation and Carcinogenesis, Division of Basic Science, National Cancer Institute, Bethesda, Maryland 20892 [J. E. G.]; and Renal Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215 [V. P. S.]
A transgenic mouse model was used to evaluate the effect of endostatin treatment on spontaneous tumorigenesis. In this model system, female mice develop multiple mammary adenocarcinomas and male mice develop prostate cancer. Female mice treated with mouse endostatin during a 12–15-week period showed delayed tumor development by 4–6 weeks and significantly decreased tumor burden. Furthermore, endostatin treatment reduced the number of malignant lesions per mouse. In a separate set of experiments, male mice treated with endostatin showed a survival advantage, and their life spans were prolonged by 10.5 weeks over control animals. These data demonstrate that mouse endostatin is effective in delaying spontaneous tumor development and growth.
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