Non-tissue factor procoagulants in cancer cells

Gordon, Stuart G.; Chelladurai, Mohanathasan

doi:10.1007/bf01307182

Cited by 14 publications

(5 citation statements)

References 125 publications

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“…A variety of protease molecules such as thrombin are produced directly by tumor cells and stimulate PARs that initiate TCIPA [448-450] (Figs. 3b, 5, and 6).…”

Section: Tumor Proteasesmentioning

confidence: 99%

Platelets and cancer: a casual or causal relationship: revisited

Menter

Tucker

Kopetz

et al. 2014

Cancer Metastasis Rev

277

256

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Human platelets arise as subcellular fragments of megakaryocytes in bone marrow. The physiologic demand, presence of disease such as cancer, or drug effects can regulate the production circulating platelets. Platelet biology is essential to hemostasis, vascular integrity, angiogenesis, inflammation, innate immunity, wound healing, and cancer biology. The most critical biological platelet response is serving as “First Responders” during the wounding process. The exposure of extracellular matrix proteins and intracellular components occurs after wounding. Numerous platelet receptors recognize matrix proteins that trigger platelet activation, adhesion, aggregation, and stabilization. Once activated, platelets change shape and degranulate to release growth factors and bioactive lipids into the blood stream. This cyclic process recruits and aggregates platelets along with thrombogenesis. This process facilitates wound closure or can recognize circulating pathologic bodies. Cancer cell entry into the blood stream triggers platelet-mediated recognition and is amplified by cell surface receptors, cellular products, extracellular factors, and immune cells. In some cases, these interactions suppress immune recognition and elimination of cancer cells or promote arrest at the endothelium, or entrapment in the microvasculature, and survival. This supports survival and spread of cancer cells and the establishment of secondary lesions to serve as important targets for prevention and therapy.

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“…A variety of protease molecules such as thrombin are produced directly by tumor cells and stimulate PARs that initiate TCIPA [448-450] (Figs. 3b, 5, and 6).…”

Section: Tumor Proteasesmentioning

confidence: 99%

Platelets and cancer: a casual or causal relationship: revisited

Menter

Tucker

Kopetz

et al. 2014

Cancer Metastasis Rev

277

256

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“…Procoagulants produced by cancer cells may be divided into two general groups: tissue factors4 and nontissue factors 11. Of the latter, CP has been investigated extensively.…”

Section: Discussionmentioning

confidence: 99%

“…Increased coagulation induced by cancer cells is believed to be related to the metastatic ability of cancers and systemic abnormal coagulation. Previously reported tumor procoagulants produced by cancer cells include tissue factor 2‐9 and cancer procoagulant (CP) 10‐15. Tissue factor binds to factor VII in the presence of Ca 2+ , and increases blood coagulation by indirectly activating factor IX and factor X6.…”

mentioning

confidence: 99%

Generation of a monoclonal antibody that inhibits the procoagulant activity of various cancer cell lines

Inufusa

Adachi

Suzuki

et al. 1998

Cancer

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“…Venous thrombosis may be the first indication of malignancy in an otherwise healthy person [2-7}. This article primarily addresses the issue of TF as a tumor procoagulant; non-TF tumor procoagulants are reviewed by Gordon and Chelladurai in a separate chapter [12]. Several procoagulant activities have been identi-fled in tumor cell extracts that act at different steps in the intrinsic and extrinsic pathways of blood coagulation, including tissue factor (TF) (see below), a factor X activating enzyme [8,9], and expression of a surface that supports the assembly of the prothrombinase complex [10,11].…”

mentioning

confidence: 99%

Tissue factor as a tumor procoagulant

Rao

1992

Cancer Metast Rev

136

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Tissue factor is a cell surface glycoprotein responsible for initiating the extrinsic pathway of coagulation. Many tumor cell homogenates and intact tumor cells have been shown to contain tissue factor activity. Immunohistochemical studies show that many tumors associated with Trousseau's syndrome express tissue factor on their cell surfaces. Tumor cells shed membrane fragments which carry tissue factor that can account for the activation of the clotting system. Tumor cells also produce soluble substances that can induce tissue factor expression on host cells, such as endothelium and monocytes, at sites distant from the tumor. Although, all the functional TF molecules are localized on the outer cell membrane in many tumor cells, the procoagulant activity on the intact cell surface is largely dormant and can be greatly enhanced upon cell injury or damage. Tissue factor procoagulant activity on the cell surface can be modulated by alterations in the plasma membrane without loss of cell viability. Tissue factor activity on cell surfaces is largely regulated by a plasma inhibitor, tissue factor pathway inhibitor. This inhibitor binds to both functional and non-functional tissue factor/VIIa complexes on the cell surface and prevents non-functional tissue factor/VIIa complexes from becoming functional after cell injury or lysis. Heparin, but not warfarin, therapy is effective in preventing the occurrence of devastating thrombotic events in patients with Trousseau's syndrome and the reason(s) for this are still unknown.

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Non-tissue factor procoagulants in cancer cells

Cited by 14 publications

References 125 publications

Platelets and cancer: a casual or causal relationship: revisited

Platelets and cancer: a casual or causal relationship: revisited

Generation of a monoclonal antibody that inhibits the procoagulant activity of various cancer cell lines

Tissue factor as a tumor procoagulant

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