Patients with cancer are at high risk of both thromboembolic and haemorrhagic events during the course of their disease. The pathogenesis of haemostatic dysfunction in cancer is complex and involves the interplay of multiple factors. There is growing evidence that interactions between malignancies and the coagulation system are not random but can represent coordinated and clinically-significant adaptations that enhance tumour cell survival, proliferation and metastatic potential. A detailed understanding of the interactions between the haemostatic systems and the pathophysiology of metastasis may not only provide insight into strategies that could potentially reduce the incidence of thrombohaemorrhagic events and complications, but could also help design strategies that are capable of modifying tumour biology, progression and metastatic potential in ways that could enhance anticancer therapies and thereby improve overall survival.