Figure 1.

Virchow’s triad showing the main parameters of thrombosis. Regarding hypercoagulation, note the effects of the secreted platelet agonist tissue factor, ADP, thrombin and thromboxane A₂ on the pathways inducing platelet activation and fibrin formation. Tumour cells are able to secrete these platelet agonists, which, following induction of platelet activation, cause the release of microparticles and a host of factors that can facilitate tumour progression and thrombotic complications. The direct and indirect interactions between platelet receptors/ligands and cognate ligands/receptors on tumour cells are shown. The inhibition of PAR1 and PAR4 receptors, the P2Y12 and P2Y1 receptors, and the production of thromboxane A₂ (TXA₂) are indicated as mechanisms that prevent platelet activation and downstream effects.