ABSTRACT
Many cancer patients reportedly have a hypercoagulable state, with recurrent thrombosis
due to the impact of cancer cells and chemotherapy on the coagulation cascade. Studies
have demonstrated that unfractionated heparin (UFH) or low-molecular-weight heparin
(LMWH) interferes with various processes involved in tumor growth and metastasis.
These processes might include fibrin formation, binding of heparin to angiogenic growth
factors such as basic fibroblast growth factor and vascular endothelial growth factor,
modulation of tissue factor, and other mechanisms. Clinical trials have indicated
a clinically relevant effect of LMWH as compared with UFH on the survival of cancer
patients with deep vein thrombosis. Similarly, the impact of warfarin on the survival
of cancer patients with thromboembolic disorders was demonstrated. Recent studies
from our laboratory defined the role of an LMWH (tinzaparin), warfarin, anti-factor
VIIa, and recombinant tissue factor pathway inhibitor in the modulation of angiogenesis,
tumor growth, and tumor metastasis.
KEYWORD
Heparin - LMWH - warfarin - TF/VIIa - TFPI - FGF2 - VEGF - cancer - coagulation -
platelet - angiogenesis - venous thrombosis