Hemostasis at the edge between physiology and cancer

Area of Science:

• Oncology
• Hematology
• Molecular Biology

Background:

• Hemostasis, the process of blood clotting, plays a dual role in physiology and cancer.
• Tumor cells exploit the coagulation cascade for proliferation, invasion, and immune evasion.
• The tumor microenvironment (TME) actively participates in cancer-associated hypercoagulability.

Purpose of the Study:

• To elucidate the bidirectional interplay between hemostasis and cancer.
• To understand how coagulation promotes tumor growth, angiogenesis, and immune suppression.
• To identify therapeutic targets within the hemostasis-cancer axis.

Main Methods:

• Analysis of molecular mechanisms linking coagulation factors (e.g., tissue factor, thrombin, FXa) to cancer signaling pathways (e.g., MAPK/PI3K).
• Investigation of cytokine and signaling pathway involvement (VEGF, IL-1β, NF-κB, HIF-1α) in TME-mediated coagulation.
• Examination of platelet activation and fibrin matrix roles in tumor progression and immune evasion.

Main Results:

• Tumor cells overexpress tissue factor and activate PAR1/PAR2, driving proliferation and invasion.
• Coagulation factors generated in the TME promote angiogenesis and suppress anti-tumor immunity.
• Platelets and fibrin matrices shield tumors, facilitate metastasis, and recruit immunosuppressive cells.
• Cancer-associated hypercoagulability correlates with venous thromboembolism and poor prognosis (e.g., D-dimer).

Conclusions:

• The hemostasis-cancer axis creates a protumoral niche supporting tumor growth and metastasis.
• Targeting tissue factor, anticoagulation, or antiplatelet therapy shows therapeutic promise.
• Disrupting this axis could inhibit tumor proliferation, immune escape, and metastatic dissemination.