The pathogenesis of venous thromboembolism in cancer: emerging links with tumour biology.

Paul Winter

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

Venous thromboembolism (VTE) is a frequent complication in individuals with cancer and is considered to be a cause of substantial mortality. Epidemiological studies identify malignancy as an independent VTE risk factor and show that cancer patients are at increased risk of both initial and recurrent VTE events. The risk due to cancer is compounded by the effects of chemotherapy and other treatments. The pathogenesis of cancer-associated VTE is complex involving multiple interactions between tumours and various components of haemostasis. The development of a systemic hypercoagulable state is considered a key pathogenetic feature and is attributed to tumour expression of tissue factor and other procoagulants, activation of vascular cells by tumour-derived cytokines and adhesive interactions between tumour cells and host cells. An increasing body of evidence indicates that the activation of haemostasis in malignant disease contributes to tumour growth and progression by stimulation of intracellular signalling pathways. The interaction of tissue factor, thrombin and other coagulation factors with protease activated receptor (PAR) proteins expressed by tumour cells and host vascular cells leads to the induction of genes related to the processes of angiogenesis, cell survival and cell adhesion and migration.
Original languageEnglish
Pages (from-to)126-133
Number of pages8
JournalHematological Oncology
Volume24(3)
Issue number3
DOIs
Publication statusPublished - Sep 2006

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Venous Thromboembolism
Neoplasms
Thromboplastin
Hemostasis
Blood Vessels
Proteinase-Activated Receptors
Blood Coagulation Factors
Cell Adhesion
Thrombin
Adhesives
Cell Movement
Epidemiologic Studies
Cell Survival
Cytokines
Drug Therapy

Cite this

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abstract = "Venous thromboembolism (VTE) is a frequent complication in individuals with cancer and is considered to be a cause of substantial mortality. Epidemiological studies identify malignancy as an independent VTE risk factor and show that cancer patients are at increased risk of both initial and recurrent VTE events. The risk due to cancer is compounded by the effects of chemotherapy and other treatments. The pathogenesis of cancer-associated VTE is complex involving multiple interactions between tumours and various components of haemostasis. The development of a systemic hypercoagulable state is considered a key pathogenetic feature and is attributed to tumour expression of tissue factor and other procoagulants, activation of vascular cells by tumour-derived cytokines and adhesive interactions between tumour cells and host cells. An increasing body of evidence indicates that the activation of haemostasis in malignant disease contributes to tumour growth and progression by stimulation of intracellular signalling pathways. The interaction of tissue factor, thrombin and other coagulation factors with protease activated receptor (PAR) proteins expressed by tumour cells and host vascular cells leads to the induction of genes related to the processes of angiogenesis, cell survival and cell adhesion and migration.",
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The pathogenesis of venous thromboembolism in cancer: emerging links with tumour biology. / Winter, Paul.

In: Hematological Oncology, Vol. 24(3), No. 3, 09.2006, p. 126-133.

Research output: Contribution to journalArticle

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