Abstract
Thrombosis is a major cause of morbidity and mortality in cancer patients. Many clinical
factors contribute to the high thrombotic risk of this condition, including the type
of malignancy, its disease stage, anticancer therapies, and comorbidities. However,
the cancer cell-specific prothrombotic properties together with the host cell inflammatory
response are important players in the pathogenesis of the cancer-associated hypercoagulability.
Tissue factor (TF) is the most important procoagulant protein expressed by cancer
cells, and with other cancer tissue procoagulant properties highly contributes to
the procoagulant phenotype of malignant cells. Recent discoveries indicate that oncogenes
determine the procoagulant protein expression, including TF, in cancer tissues. In
addition, in malignancy, TF is also overexpressed by host normal blood cells triggered
by cancer-derived inflammatory stimuli. As a consequence, a subclinical activation
of blood coagulation is typically present in cancer patients, as demonstrated by abnormalities
of circulating thrombotic biomarkers. The relevance of measuring these biomarkers
to determine the patient thrombotic risk level is under active investigation. The
goal is to identify the high-risk subgroups to establish more accurate and targeted
anticoagulation strategies to prevent thrombosis in cancer patients. Ultimately, the
clarification of specific molecular mechanisms triggering blood coagulation in specific
cancer types may also indicate alternative ways to inhibit clotting activation in
these conditions.
Keywords
thrombosis - cancer - tissue factor - tumor cells - risk factors
