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.
