Tumor interaction with hemostasis: the rationale for the use of platelet inhibitors and anticoagulants in the treatment of cancer.
Clinical and experimental observations have firmly established the concept of a two-way interaction between malignancy and the hemostatic system. On the one hand, certain tumors can activate platelets and the coagulation mechanism in vivo, on the other, a convincing case has been made for the involvement of platelets and fibrin in tumor growth and metastasis. A large number of clinical and experimental studies have been conducted in order to test the efficacy of platelet inhibitors and anticoagulants as adjuvants in the treatment of cancer. Antiplatelet drugs gave variable results, depending on the drug and the tumor system tested. Prostaglandin synthetic pathways by both the host and tumor seem to be an important determinant in the response to platelet function inhibitors. Of the various anticoagulants tested, the coumarin derivatives gave somewhat consistent antitumor effect in certain human and experimental cancer. The antitumor effect of oral anticoagulants does not appear to be a primary drug effect and seems related to their role as vitamin K antagonists. It should be emphasized that although the antitumor potential of antithrombotic agents is a subject of keen interest at the present, their use in treating human cancer is still controversial.
D000925:Anticoagulants / Q000627:therapeutic use; D001779:Blood Coagulation Factors / Q000378:metabolism; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D006133:Growth Substances / Q000378:metabolism; D006487:Hemostasis; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D009362:Neoplasm Metastasis / Q000517:prevention & control; D009369:Neoplasms / Q000503:physiopathology* / Q000628:therapy; D014859:Warfarin / Q000627:therapeutic use
D000925:Anticoagulants; D001779:Blood Coagulation Factors; D006133:Growth Substances; D014859:Warfarin; D006493:Heparin