ABSTRACT
This chapter focuses on the information of coagulation-cancer interaction in situ that provides a basis for formulation of key hypotheses for future testing. The heterogeneity of reactivity revealed by immunohistochemical studies permitted formulation of a classification of human tumor types based on their mechanism of interaction with coagulation- or plasminogen activator-initiated pathways. The procoagulant activity of certain tumor cell lines has been correlated with their metastatic potential and drugs that limit thrombin formation or activity block tumor progression in vivo. The urokinase type plasminogen activator (u-PA) is a major tumor cell-drived initiator of local proteolysis in specific tumor types. U-PA initiates proteolysis at the cell surface through complementary binding of u-PA and plasminogen to cell surface receptors. It is conceivable that tumor cells themselves may synthesize coagulation factors that become activated locally apart from tissue factor or an alternative initiator. Systemic coagulation activation may result from specific procoagulant properties of tumor cells.
