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  Indian J Med Microbiol
 

Figure 1: The pathophysiology of cancer-associated hypercoagulability and the pharmacological mechanism of anticoagulants. Cancer cell secretes several molecules, including tissue factors, cancer procoagulants, cytokines, and cancer mucin to accelerate coagulation cascade and platelet activation and then result in thromboembolism. Heparin promotes the activity of antithrombin III and then blocks the function of activated coagulation factors Xa and IIa. Low-molecular-weight-heparin blocks the function of Xa. Direct oral anticoagulants inhibit the function of coagulation factor Xa or IIa. Vitamin K antagonist, warfarin, block the synthesis of coagulation factors II, VII, IX, and X by inhibiting the function of carboxylase in hepatocytes (light gray line, activating; dot line inhibiting)

Figure 1: The pathophysiology of cancer-associated hypercoagulability and the pharmacological mechanism of anticoagulants. Cancer cell secretes several molecules, including tissue factors, cancer procoagulants, cytokines, and cancer mucin to accelerate coagulation cascade and platelet activation and then result in thromboembolism. Heparin promotes the activity of antithrombin III and then blocks the function of activated coagulation factors Xa and IIa. Low-molecular-weight-heparin blocks the function of Xa. Direct oral anticoagulants inhibit the function of coagulation factor Xa or IIa. Vitamin K antagonist, warfarin, block the synthesis of coagulation factors II, VII, IX, and X by inhibiting the function of carboxylase in hepatocytes (light gray line, activating; dot line inhibiting)