Cancer-associated thrombosis

Furie, Bruce; Furie, Barbara C.

doi:10.1016/j.bcmd.2005.12.018

Cited by 61 publications

(54 citation statements)

References 41 publications

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“…78−80 Nanovesicles that are pinched off from cells interact with other cells 81,82 and thereby mediate interactions between platelets, endothelial cells, and tumor cells which can be expressed by thromboembolism in cancer. 83,84 Further, nanovesicles were shown to stimulate proliferation of cancer cells, mRNA expression for angiogenic factors, as well as adhesion to fibrinogen and endothelial cells 85 and downregulation of antitumoral immune responses in the host. 86 Clinical studies have shown that the concentration of nanovesicles isolated from blood in patients with a range of diseases is changed with respect to healthy subjects.…”

Section: Clinical Relevance Of Cell Nanovesiclesmentioning

confidence: 99%

Stability of membranous nanostructures: a possible key mechanism in cancer progression

Kralj‐Iglič¹

2012

IJN

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Abstract:Membranous nanostructures, such as nanovesicles and nanotubules, are an important pool of biological membranes. Recent results indicate that they constitute cell-cell communication systems and that cancer development is influenced by these systems. Nanovesicles that are pinched off from cancer cells can move within the circulation and interact with distant cells. It has been suggested and indicated by experimental evidence that nanovesicles can induce metastases from the primary tumor in this way. Therefore, it is of importance to understand better the mechanisms of membrane budding and vesiculation. Here, a theoretical description is presented concerning consistently related lateral membrane composition, orientational ordering of membrane constituents, and a stable shape of nanovesicles and nanotubules. It is shown that the character of stable nanostructures reflects the composition of the membrane and the intrinsic shape of its constituents. An extension of the fluid mosaic model of biological membranes is suggested by taking into account curvature-mediated orientational ordering of the membrane constituents on strongly anisotropically curved regions. Based on experimental data for artificial membranes, a possible antimetastatic effect of plasma constituents via mediation of attractive interaction between membranous structures is suggested. This mediated attractive interaction hypothetically suppresses nanovesiculation by causing adhesion of buds to the mother membrane and preventing them from being pinched off from the membrane.

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Section: Clinical Relevance Of Cell Nanovesiclesmentioning

confidence: 99%

Stability of membranous nanostructures: a possible key mechanism in cancer progression

Kralj‐Iglič¹

2012

IJN

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“…These include the release of cancer procoagulant [32,79] , downregulation of tissue factor pathway inhibitor (TFPI) [80][81][82][83] , upregulation of plasminogen activator inhibitor 1 (PAI-1), or cyclooxygenase 2 (COX-2) [84] , deregulation of the protein C system [85] and through a number of other scenarios [32] . At least in part, these procoagulant tendencies in cancer patients could be attributed to the prothrombotic conversion of cancer cells [32,86] , notably their increased levels of TF expression, as well as the elevation of TF found in circulating blood [31,32,45,75,77] . While cancer cells are known to shed TF-containing microparticles into the culture medium (in vitro) and into the bloodstream (in vivo) [32,57,87,88] , other sources of the circulating TF in cancer patients should also be considered, including platelets, monocytes and stromal cells [46,52,53,57,[89][90][91] .…”

Section: Cancer Coagulopathymentioning

confidence: 99%

Tissue Factor and Cancer

Milsom

Rak

2007

Pathophysiol Haemos Thromb

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Tissue factor (TF), the key regulator of haemostasis and angiogenesis, is also involved in the pathology of several diseases, including cardiovascular, inflammatory and neoplastic conditions. In the latter, TF is upregulated by cancer cells, as well as by certain host cells, and it is the interactions between these distinct pools of TF-expressing cells that likely influence tumour progression in several ways. Furthermore, the release of TF microparticles into the circulation is thought to contribute to the systemic coagulopathies commonly observed in cancer patients. The direct regulation of TF by oncogenic events has provided a plausible explanation for the relatively common overexpression of TF in various cancers and its involvement in tumour growth, angiogenesis, metastasis and coagulopathy. However, this constitutive influence is modified by the tumour microenvironment, cellular interactions and host factors rendering TF expression patterns complex and heterogeneous. It appears that in many biological contexts TF plays a central role in disease progression and thereby potentially constitutes an attractive therapeutic target, especially in scenarios where the risk of bleeding can be avoided by selecting appropriate medications, refined dosing or by targeting the signalling component of TF activity. The efficacy and safety of such approaches still awaits clinical verification.

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“…The MP are thought to reflect a balance between cell stimulation, proliferation and death which may be important in cancer related thrombosis. Cancer increases the risk of VTE by four fold and addition of chemotherapy further increases the risk by six to eight fold (Furie and Furie 2006). It is possible that circulating MP shed from cancer cells represent an indication for tumours to metastasize in the absence of any other clinical evidence for metastasis.…”

Section: Microparticles Vte and Cancermentioning

confidence: 99%