The high affinity interaction between the urokinase-type plasminogen activator (uPA) and its
glycolipid-anchored receptor (uPAR) is decisive for cell surface-associated plasminogen
activation. Because plasmin activity controls fibrinolysis in a variety of pathological
conditions, including cancer and wound healing, several intervention studies have focused
on targeting the uPA· uPAR interaction in vivo. Evaluations of such studies in
xenotransplanted tumor models are, however, complicated by the pronounced species …