Hemostasis and Malignancy

Semin Thromb Hemost. 1998;24(2):93-109. doi: 10.1055/s-2007-995829.

Abstract

There is considerable evidence that the hemostatic system is involved in the growth and spread of malignant disease. There is an increased incidence of thromboembolic disease in patients with cancers and hemostatic abnormalities are extremely common in such patients. Antihemostatic agents have been successfully used to treat a variety of experimental tumors, and several clinical trials in humans have been initiated. Although metastasis is undoubtedly multifactorial, intravascular coagulation activation and peritumor fibrin deposition seem to be important. The mechanisms by which hemostatic activation facilitates the malignant process remain to be completely elucidated. Of central importance may be the presence on malignant cells of tissue factor and urokinase receptor. Recent studies have suggested that these proteins, and others, may be involved at several stages of metastasis, including the key event of neovascularization. Tissue factor, the principal initiator of coagulation, may have additional roles, outside of fibrin formation, that are central to the biology of some solid tumors.

Publication types

  • Review

MeSH terms

  • Animals
  • Anticoagulants / therapeutic use
  • Antineoplastic Agents / therapeutic use
  • Biomarkers
  • Blood Coagulation Tests
  • Cell Adhesion
  • Cysteine Endopeptidases / physiology
  • Disseminated Intravascular Coagulation / blood
  • Disseminated Intravascular Coagulation / drug therapy
  • Disseminated Intravascular Coagulation / etiology*
  • Factor Xa / physiology
  • Fibrin / physiology
  • Fibrinolysis / drug effects
  • Hemostasis / drug effects
  • Hemostasis / physiology*
  • Heparin / therapeutic use
  • Humans
  • Monocytes / metabolism
  • Neoplasm Metastasis / physiopathology*
  • Neoplasm Metastasis / prevention & control
  • Neoplasm Proteins / physiology
  • Neoplasms / blood*
  • Neoplasms / complications
  • Neoplasms, Experimental / blood
  • Neoplastic Cells, Circulating
  • Neovascularization, Pathologic / prevention & control
  • Platelet Activation
  • Platelet Aggregation Inhibitors / therapeutic use
  • Receptors, Thrombin / physiology
  • Thrombophilia / blood
  • Thrombophilia / drug therapy
  • Thrombophilia / etiology*
  • Thrombophlebitis / epidemiology
  • Thrombophlebitis / etiology
  • Thromboplastin / physiology
  • Thromboplastin / urine
  • Vitamin K / antagonists & inhibitors

Substances

  • Anticoagulants
  • Antineoplastic Agents
  • Biomarkers
  • Neoplasm Proteins
  • Platelet Aggregation Inhibitors
  • Receptors, Thrombin
  • Vitamin K
  • Fibrin
  • Heparin
  • Thromboplastin
  • Factor Xa
  • Cysteine Endopeptidases
  • cancer procoagulant