Purpose: Cancer associated intravascular coagulopathy is the primary mechanism of cancer-related stroke, particularly in those without conventional stroke etiologies. Randomized clinical trials have investigated efficacy of vitamin K-dependent oral anticoagulant (warfarin), low-molecular-weight heparin (LMWH) and non-vitamin K-dependent oral anticoagulant (NOAC) for the prevention of systematic venous thromboembolism. However, relatively little is known about the biological changes underlying intravascular coagulopathy and mechanisms of anticoagulation therapy in patients with cancer-related stroke. The aim of this study is to evaluate to determine the biological markers for intravascular coagulopathy causing stroke and for monitoring the effects of anticoagulation therapy, in patients with active cancer and stroke.