Abstract

Introduction Inhibition of coagulation factor XI (FXI) has become a promising new antithrombotic strategy with a presumably low bleeding risk [1]. While it is efficacious and safe in prevention of postoperative venous thromboembolism in orthopedic patients [2] [3] [4] [5], its role in treatment and prophylaxis of cancer-associated thrombosis (CAT) is less clear. Here, we provide mechanistic insights into FXI inhibition in tumor cell-induced coagulation activation.

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