New French review paper below .
I'm glad to see it, since it bolsters my view that metastasis largely depends on coagulation factors & microclots. Coagulation & clotting are not specifically mentioned, so I'll recap the clotting process:
i) activation of platelets (this is mentioned)
ii) aggregation of platelets to form a plug. Fibrinogen connects the platelets.
iii) the enzyme thrombin converts fibrinogen to fibrin. Fibrin not only provides the glue for the platelet plug, but also forms the body of the clot that builds around the plug.
According to the paper:
"It is now well recognized that major roles of platelets in the poor outcome of cancer patients occurs during hematogenous dissemination of cancer cells."
"Due to a plethora of factors released upon activation, platelet functions are ... connected to tumor growth ..."
Ideally, a newly diagnosed cancer patient would be placed on an anticoagulation drug as a metastasis inhibitor. However, there are no such protocols. The most common anticoagulant, Warfarin (Coumadin) is too dangerous to be used as a prophylactic. It is one of the top drugs responsible for ER visits.
Nattokinase is an otc enzyme that mimics plasmin & degrades fibrin - i.e. dissolves clots. But it also inhibits platelet aggregation .
I have written elsewhere about the use of nattokinase, & the importance of monitoring/controling coagulation factors.
Blood. 2016 May 6. pii: blood-2016-01-636399. [Epub ahead of print]
Metastasis: new functional implications of platelets and megakaryocytes.
Leblanc R1, Peyruchaud O2.
1INSERM U1068, Institut Paoli-Calmettes and Universite Aix-Marseille, Marseille, France;
2Faculte de Medecine Lyon Est, INSERM, UMR1033, UCB Lyon 1, Lyon, France email@example.com.
Platelets are essential components of hemostasis. Due to a plethora of factors released upon activation, platelet functions are also connected to tumor growth, notably by acting on angiogenesis. It is now well recognized that major roles of platelets in the poor outcome of cancer patients occurs during hematogenous dissemination of cancer cells. In this review we describe recent insights into the molecular mechanisms supporting the pro-metastatic activity of platelets. Platelets have been shown to promote survival of circulating tumor cells (CTCs) in the bloodstream by conferring resistance to the shear stress and attack from natural killer cells. Recently, platelets were found to promote and/or maintain the state of epithelial to mesenchymal transition on CTCs through platelet secretion of transforming growth factor β in response to CTC activation. At a later stage in the metastatic process, platelets promote extravasation and establishment of metastatic cells in distant organs as observed in bone. This particular environment is also the site of hematopoiesis, megakaryocytopoiesis and platelet production. Increasing the number of megakaryocytes (MKs) in the bone marrow results in a high bone mass phenotype and inhibits skeletal metastasis formation of prostate cancer cells. As a result of their specific location in vascular niches in the bone marrow, MK activity might contribute to the "seed and soil" suitability between CTCs and bone. In conclusion, recent findings have made a great advance in our knowledge on how platelets contribute to the metastatic dissemination of cancer cells and which may support the development of new anti-metastasis therapies.
Copyright © 2016 American Society of Hematology.
PMID: 27154188 [PubMed - as supplied by publisher]