Related Experiment Video
Updated: Jun 13, 2026

Rapid Point-of-Care Assay of Enoxaparin Anticoagulant Efficacy in Whole Blood
Published on: October 12, 2012
Enoxaparin, Tinzaparin, and Apixaban Modulate Cancer Cell Procoagulant Activity and Viability: Comparison with
Mohammed A Baghdadi1,2, Pedro Henrique Fernandes do Carmo Las Casas1, Elisabeth Mbemba1
1Research Group "Cancer-Angiogenesis-Thrombosis and Hemostasis", Research Team "Cancer, Vessels, Biology and Therapeutics" (CaVITE), Saint-Antoine Research Center (CRSA), INSERM UMR_S_938, Saint-Antoine University Hospital, University Institute of Cancerology (UIC), Assistance Publique-Hôpitaux de Paris (AP-HP), Sorbonne University, 75012 Paris, France.
This study investigated how anticoagulants and quercetin affect cancer cells and thrombosis. Tinzaparin and quercetin reduced cancer cell viability, impacting hypercoagulability and potentially tumor progression.
Area of Science:
- Oncology
- Hematology
- Pharmacology
Background:
- Cancer cells and their extracellular vesicles drive hypercoagulability and vascular issues.
- Standard anticoagulants' effects on cancer cells and endothelial responses are not fully understood.
Purpose of the Study:
- Compare low-molecular-weight heparins (LMWHs), apixaban, and quercetin on cancer cell viability, thrombin generation, and endothelial injury.
- Investigate potential dual effects on thrombosis and tumor progression.
Main Methods:
- Analyzed pancreatic (BXPC3) and breast (MCF7) cancer cells and vesicles for tissue factor (TF) expression and thrombin generation.
- Assessed cancer cell viability, thrombin generation, and endothelial cell (HUVEC) responses to agents and cancer cell-derived extracellular vesicles (CaCe-dEVs).
Main Results:
- Tinzaparin and quercetin reduced cancer cell viability; enoxaparin and apixaban did not.
- All agents inhibited TF-mediated thrombin generation, with tinzaparin most effective against BXPC3 cells.
- Quercetin offered limited endothelial protection; LMWHs and apixaban did not prevent CaCe-dEVs-induced endothelial damage.
Conclusions:
- LMWHs, apixaban, and quercetin modulate cancer-associated hypercoagulability beyond anticoagulation.
- Quercetin and tinzaparin exhibit cytotoxic potential, suggesting dual roles in reducing thrombosis risk and impacting tumor progression.
- Further research is warranted to explore these dual effects.
Related Concept Videos
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Venous Thrombosis III: Interprofessional Care
Cancer Therapies
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Combination Therapies and Personalized Medicine
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

