New Swedish/German/US study [1] below.
The full text isn't free ($35.95), & the Abstract has limited value in terms of how we can use the info - but the intro has shock value & might cause some to consider D-dimer /fibrinogen blood tests & nattokinase as a supplement (see my earlier post.)
"Cancer is an established risk factor for venous thromboembolism (VTE) and VTE is the second leading cause of death in patients with cancer. The incidence of cancer-related thrombosis is rising and is associated with worse outcomes."
"Despite our growing understanding on tumor-driven procoagulant mechanisms including cancer-released procoagulant proteases, expression of tissue factor on cancer cells and derived microvesicles, as well as alterations in the extracellular matrix of the cancer cell milieu, anticoagulation therapy in cancer patients has remained challenging."
Doctors have no tools, so they keep quiet about the problem.
The published statistics on PCa underestimate PCa deaths. PCa-related clotting events, etc. are not included. If we are not careful, we might avoid a "PCa death" without extending survival.
-Patrick
[1] ncbi.nlm.nih.gov/pubmed/272...
US National Library of Medicine National Institutes of Health
The polyphosphate/factor XII pathway in cancer-associated thrombosis: novel perspectives for safe anticoagulation in patients with malignancies.
Nickel KF1, Labberton L2, Long AT3, Langer F4, Fuchs TA3, Stavrou EX5, Butler LM1, Renné T6.
Author information
1Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Clinical Chemistry, Department of Molecular Medicine and Surgery, Karolinska Institutet and University Hospital, Stockholm, Sweden.
2Clinical Chemistry, Department of Molecular Medicine and Surgery, Karolinska Institutet and University Hospital, Stockholm, Sweden.
3Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
4Clinical Department of Hematology and Oncology, Center for Oncology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
5Divisions of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, OH, USA; Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, OH, USA.
6Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Clinical Chemistry, Department of Molecular Medicine and Surgery, Karolinska Institutet and University Hospital, Stockholm, Sweden. Electronic address: thomas@renne.net.
Abstract
Cancer is an established risk factor for venous thromboembolism (VTE) and VTE is the second leading cause of death in patients with cancer. The incidence of cancer-related thrombosis is rising and is associated with worse outcomes. Despite our growing understanding on tumor-driven procoagulant mechanisms including cancer-released procoagulant proteases, expression of tissue factor on cancer cells and derived microvesicles, as well as alterations in the extracellular matrix of the cancer cell milieu, anticoagulation therapy in cancer patients has remained challenging. This review comments on a newly discovered cancer-associated procoagulant pathway. Experimental VTE models in mice and studies on patient cancer material revealed that prostate cancer cells and associated exosomes display the inorganic polymer polyphosphate on their plasma membrane. Polyphosphate activates blood coagulation factor XII and initiates thrombus formation via the intrinsic pathway of coagulation. Pharmacologic inhibition of factor XII activity protects mice from VTE and reduces thrombin coagulant activity in plasma of prostate cancer patients. Factor XII inhibitors provide thrombo-protection without impairing hemostatic mechanisms and thus, unlike currently used anticoagulants, do not increase bleeding risk. Interference with the polyphosphate/factor XII pathway may provide the novel opportunity for safe anticoagulation therapy in patients with malignancies.
Copyright © 2016 Elsevier Ltd. All rights reserved.
KEYWORDS:
anticoagulation; cancer; contact system; factor XII; polyphosphate; pulmonary embolism
PMID:
27207422
[PubMed - as supplied by publisher]
