Abstract It is common knowledge that blood coagulation and fibrinolysis are activated systemically in patients with malignancy. Studies in specific in vitro and animal models of malignancy have implicated either tumour cell procoagulants or urokinase in promoting malignant disease progression, based on the participation of one or the other of these in mechanisms of tumour cell proliferation, invasion, and metastasis. It has recently been shown that individual human tumour types may manifest either a tumour cell-associated coagulation pathway in the absence urokinase, urokinase expression in the absence of a tumour cell-associated coagulation pathway, or neither of these. Mounting evidence suggests that anticoagulant and urokinase therapy are capable of ameliorating the clinical course of a procoagulant tumour type namely, small cell carcinoma of the lung. Clinical trials of agents capable of inhibiting urokinase-initiated proteolysis are required to clarify cause/effect relationships in urokinase-expressing tumours.