The Correlation Between Circulatory Tumor Cells and Venous Thrombosis

Research indicates a strong correlation between cancer and thrombosis, with approximately 20% of blood clots in the U.S. being cancer-related, according to CDC data. Cancer patients face a 4-7 times higher risk of thrombosis compared to non-cancer individuals. Certain cancer treatments, such as chemotherapy and targeted therapy, elevate the likelihood of venous thromboembolism (VTE). Cancer patients with VTE exhibit a significantly higher hazard ratio (H.R.) of 3.4 compared to those without VTE.

The mechanisms underlying cancer-related thrombosis are intricate. Cancer cells can directly activate coagulation and platelets through various factors, including tissue factor (T.F.), particularly prevalent in specific cancers like pancreatic and ovarian, correlating with a heightened VTE risk and poorer prognosis. Additionally, factors such as podoplanin (PDPN), plasminogen activation inhibitor-1 (PAI-1), and cancer procoagulant (C.P.) further promote coagulation. Inflammatory cytokines originating from tumor cells and cancer-derived factors stimulate neutrophil extracellular traps, contributing to thrombosis.

Metastatic tumors facilitate cancer cell dissemination and entry into blood vessels, leading to thrombosis in certain instances. Analyzing circulating tumor cells (CTCs) from biopsies aids in comprehending cancer metastasis and identifying treatment targets. However, isolating these rare CTCs from blood presents a challenge. Endovascular therapy has made strides in thrombosis treatment, with endovascular thrombectomy showing promise in severe thrombosis cases. It is proposed that aspirating thrombi during this procedure could yield CTCs for further examination regarding the impact of cancer cells on thrombogenesis.

This study aims to explore three main topics: (1) Comparing the differences and similarities of leukocyte populations between cancer-associated thrombosis (CAT) and venous thromboembolism (VTE). (2) Characterizing the factors contributing to increased incidence of cancer-associated thrombosis (CAT), with the hypothesis that circulating tumor microemboli (CTM) may express more thrombosis-related proteins than CTCs. (3) Understanding the effects of aspirin or NOACs on cancer-associated thrombosis and CTM formation.