Virchow’s triad of venous stasis, vascular damage, and blood hypercoagulability is the hallmark of VTE formation. Despite many studies done in recent times, the exact pathophysiology of cancer and VTE is still unknown. Various Tumor related, treatment-related and patient-related risk factors (RF) have been identified. Tissue-factor (TF), microparticles (MPs), inflammatory cytokines, and cancer procoagulants (CP) are some of the tumor-related risk factors. Tumor cellderived TNFa, IL-1b, and VEGF also contribute to cancer-induced hypercoagulability by other mechanisms, firstly they induce TF expression on monocytes. Several tumorrelated characteristics such as tumor site, type, stage (especially metastasis), histological variance and duration, are considered risk factors for the development of cancer-associated VTE. Surgery is the most important treatment-related risk factor in VTE in cancer patients along with other risk factors like hospital admission, chemotherapy, hormonal therapy, radiation therapy. patient-related factors such as age, gender, race, performance status, comorbidities, prior thrombosis, and prothrombotic mutations, are associated with an increased VTE risk in cancer patients. Several biomarkers have been investigated to quantitate and to predict the risk of VTE in cancer patients most important being D dimer, RF. Elevated levels of Ddimers are predictive of a higher risk of recurrent VTE in patients with cancer. Prechemotherapy platelet count has been shown associated with increased VTE risks in at least one study.
Keywords: Biomarkers of thrombosis in cancer, Cancer procoagulant, Coagulation cascade, D dimer in cancer, Hypercoagulability in cancer, Malignancy, Microparticles (MPs), Oncogene, Pathophysiology of thrombosis in cancer, Prechemotherapy platelet count, Risk factors for cancer thrombosis, Thrombosis in cancer, Tissue factor, Tumor suppressor gene, VEGF in cancer, Virchow’s Triad.