Fibrin and Cancer Cell Growth: Problems in the Evaluation of Experimental Models

Studies on the role of fibrin in experimental cancer growth should take into account the following problems: 1) during growth and dissemination of experimental tumours, haemostatic changes may occur which vary depending on the route of inoculation of cancer cells and on the tissue wherethe tumour grows. Thrombocytopenia, haemolytic microangiopathic anaemia and decreased survival of fibrinogen were observed during spontaneous dissemination to the lung of i.m. implanted Lewis Lung Carcinoma cells, not when metastatic growth occurred after surgical removal of the primary tumour or lung nodules developed following i.v. injection of the same cells. 2) Treatment of experimental tumours with drugs active on the haemostatic system may have different effects depending on the stage of growth of the tumour. This observation (which we have made with both warfarin and a defibrinating enzyme in murine metastasizing tumours) could suggest that fibrin may play different roles at different phases of cancer cell growth. 3) The supposed antiturooral activity of drugs active on the haemostatic system may be also influenced by other factors, such as a direct activity on cancer cells or on the host’s immune system or on blood supply to the tumour. As an example, non steroidal antiinflammatory drugs may act not only as antiplatelet agent but also as inhibitors of prostaglandin synthesis by cancer cells and some snake venoms may influence cancer cell growth not only through defibrination, but also with their iinnu-nodepressant properties. (Supported by Italian CNR and NIM. MCI, USA).