TuHE IMPORTANCE of the coagulation mechanism in the intravascular metastatic spread of tumors has been established by the extensive work of Wood,9 and Cliffton and Agostino.2 Anticoagulation by various agents reduced the incidence of pulmonary embolic tumor growths after intravenous tumor cell injection, while agents inducing a hypercoagulable state increased this incidence. A similar effect of long term anticoagulation with Coumadin on the incidence of spontaneous pulmonary metastases in tumor bearing mice was noted by Orme.6 Though the relationship has been well established, the conditions and parameters of treatment under which it will persist have not been. Anticoagulation has preceded tumor implantation, the level of anticoagulation has infrequently been determined, and anticoagulation has usually been of short duration. To assess the breadth of this effect of anticoagulation, several host-tumor systems were studied with long-term Coumadin therapy instituted, following establishment of the primary tumor and the level of anticoagulation held constant in the usual therapeutic range of two to three times the mean prothrombin time of normal subjects.
Materials and MethodsThe host-tumor systems studied were the anaplastic sarcoma T241 of Lewis under study. For mice in the study the prothrombin time was determined immediately prior to their being killed. For the Lewis T241-C57 system ten mice from each group were killed on days 7, 9, 11, 13, and 163
Long-term oral administration of sodium warfarin significantly reduced the incidence of spontaneous metastases in the lungs from 83 percent in controls to 8 percent in treated C57/BL/6N mice. The size and weight of primary tumors in mice treated with warfarin were less than in control mice. Length of survival was unaffected.
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