Cancer associated thrombosis (CAT) including venous and arterial thromboembolism (VTE and ATE respectively), as well as subclinical hypercoagulable states pose a risk of serious morbidity and mortality and poor outcomes in cancer patients. It is increasingly clear that rather than being unspecific aftermaths of tumour growth, CAT is causally linked to the molecular phenotype of cancer cells and its genetic and epigenetic oncogenic drivers. Emerging data suggest that mutational events and factors modifying chromatin architecture in cancer cells influence the repertoire of genes (coagulome) the products of which may interact with the hemostatic system either directly or through modification of inflammatory system or release of cancer-related prothrombotic extracellular vesicles (EVs). Single cell transcriptomic analysis of brain tumours reveals the coexistence of multiple coagulant mechanisms associated with different cancer cell subpopulations and sites. These observations may suggest that a multipronged, biologically based approach may be needed to effectively predict and manage CAT.
Keywords: Cancer; Coagulome; Epigenome; Oncogenes; Podoplanin; Thrombosis; Tissue factor.
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