The clinical link between cancer and thrombosis has been recognized by Armand Trousseau in 1865. It has become clear that activation of coagulation and fibrinolysis plays an important role not only in the pathophysiology of Trousseau's syndrome, but also in the progression of solid malignancies. In particular, tissue factor is critical for both primary tumour growth and haematogenous metastasis. Haemostatic perturbations in cancer patients are, at least in part, controlled by defined genetic events in molecular tumourigenesis, including activating and inactivating mutations of oncogenes and tumour suppressor genes, respectively. While long-term treatment with low-molecular-weight heparin (LMWH) is considered standard therapy for established venous thromboembolism (VTE), pharmacological VTE prophylaxis in ambulatory cancer patients and the management of complex systemic coagulopathies remain a challenge and have to be decided on an individual basis and in a risk-adapted manner. Experimental and preclinical studies further suggest that LMWH may be beneficial in cancer therapy, but this innovative concept has not yet been proven beyond doubt in rigorously designed clinical trials.
