| It was well known that blood coagulation cascade were activated and the concentration of thrombin or fibrin was increased in overt malignant disease. An increased incidence of deep venous thrombosis (DVT) and venous thromboembolism (VTE) in patients with known cancers has been convincingly demonstrated. However, the relationship of hemostasis to cancer is more than a secondary one; it is clear that cells and proteins of hemostatic system are intimately involved in tumor growth and spread. Idopathic DVT in an apparently healthy individual has been a recognized harbinger of subsequently malignancy since the description by Trousseau over 100 years ago of the syndrome bearing his name. Cancer risk within the first 2 years after idiopathic DVT is about 10% and includes many, but not all, tumor types. This risk persists for a quarter of a century or more after the DVT. In another study, cancer was the final diagnosis in 25% of patients with idiopathic DVT, compared with only 4% of those with secondary DVT. An epidemiological cohort study showed that the total mortality of 3052 middle-aged men clinically free of malignancy was higher in those with persistent activation of the hemostatic pathway than in others, owing to a higher mortality from all cancers, due in turn largely to a higher mortality from cancers of the digestive tract. Increased thrombin generation and activity appear to increase the incidence and aggressiveness of malignancy. So, the relation between the imbalance of coagulation pathway and malignancy may be more complexity. Is thrombin at work direct as a tumor initiator or promoter years before clinical cancer?Although the best described function of thrombin concerns its role in the regulation of blood coagulation, it has also been shown to be a powerful agonist that can elicit a variety of cell responses, including mitogenesis through its receptors-...
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