Cancer patients are highly susceptible to thromboembolic complications, which some have
estimated accounts for a significant percentage of the morbidity and mortality of the disease.
Not all of the mechanisms for the production of the hypercoagulable state characteristic of
cancer are entirely understood. Those that are known seem to interdigitate the biology of
cancer with the major regulatory pathways that mediate blood coagulation, platelet–vessel
wall interaction, fibrinolysis and inflammatory cytokine production. In other words, the events …