Previous investigations demonstrated that mouse tumors cause platelet aggregation (PA) and increase platelet turnover. Depletion of platelets by neuraminidase and inhibition of PA by aspirin reduced the munber of metastases (Gasic et al., Int. J. Cancer 11, 704, 1973). The purpose of this investigation was to study further interaction of cells from various mouse and human tumors with platelets. Cells of 7 mouse tumors (1 mammary adenocarcinomas, 5 sarcomas, I melanoma) and 14 human tumors (8 breast, 3 colonic adenocarcinomas, 1 cancer of the ureter, 1 Wilms tumor, and 1 neuroblastoma) aggregated homologous platelets suspended in heparinized plasma. Three mouse tumors (2 mammary and 1 sarcoma) and 5 human tumors (2 breast, 1 sarcoma, 1 Wilms, and 1 neuroblastoma) did not. PA was accompanied by the release of radio-activity from 14C-serotonin labeled platelets (range 15–90%). PA activity was not correlated with fibrinolytic or procoagulant activity. The contribution of plasminogen activators, thrombin, and tumor immune complexes has been excluded. However, gamma globulin of tumor bearing mice contained a “blocking factor” which delayed PA. Since enzymatic removal of ADP reduced PA it is possible that the ADP release either by tumors or by platelets played a contributory role. The pattern of PA by tumor cells rossembled that induced by collagen. Indeed preliminary evidence suggests that collagen-like material associated with tumor cells might be involved in platelet adherence to these cells and subsequent aggregation.(Supported by NIH Grants CA-15728, HL 14217. HL 15226, and by a Univ. of Penna.’s General Research Support Grant.)
The efficacy of diffusion weighted imaging and apparent diffusion coefficients mapping for liver metastasis of colonic adenocarcinomas
