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Open AccessJournal ArticleDOI

Contribution of platelets to tumour metastasis.

Brunhilde Felding-Habermann
- 01 Feb 2011 - 
- Vol. 11, Iss: 2, pp 123-134
TLDR
Contributions of platelets to tumour cell survival and spread suggest platelets as a new avenue for therapy.
Abstract
Experimental evidence suggests that platelets contribute to metastasis through adhesive and haemostatic functions that promote cancer cell survival, immune evasion and interactions with vascular cells to assist organ colonization from the bloodstream. Extensive experimental evidence shows that platelets support tumour metastasis. The activation of platelets and the coagulation system have a crucial role in the progression of cancer. Within the circulatory system, platelets guard tumour cells from immune elimination and promote their arrest at the endothelium, supporting the establishment of secondary lesions. These contributions of platelets to tumour cell survival and spread suggest platelets as a new avenue for therapy.

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Citations
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Microenvironmental regulation of tumor progression and metastasis.

TL;DR: The paradoxical roles of the tumor microenvironment during specific stages of cancer progression and metastasis are discussed, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.
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Emerging Biological Principles of Metastasis

TL;DR: The cellular and molecular mechanisms involved in metastasis are summarized, with a focus on carcinomas where the most is known, and the general principles of metastasis that have begun to emerge are highlighted.
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Direct Signaling between Platelets and Cancer Cells Induces an Epithelial-Mesenchymal-Like Transition and Promotes Metastasis

TL;DR: It is shown that platelet-tumor cell interactions are sufficient to prime tumor cells for subsequent metastasis and inhibit NF-κB signaling in cancer cells, resulting in their transition to an invasive mesenchymal-like phenotype and enhanced metastasis in vivo.
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The physics of cancer: the role of physical interactions and mechanical forces in metastasis

TL;DR: The metastatic process is reconstructed and the importance of key physical and mechanical processes at each step of the cascade is described, which may help to solve some long-standing questions in disease progression and lead to new approaches to developing cancer diagnostics and therapies.
References
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Journal ArticleDOI

Role of von Willebrand factor in tumor metastasis.

TL;DR: The results suggest that VWF plays a role in tumor metastasis, independently of its role in hemostasis, as well as suggesting a potential implication in various pathologies where this process is involved.
Journal ArticleDOI

The role of tissue factor pathway inhibitor in tumor growth and metastasis.

TL;DR: The evidence supporting the dual inhibitory functions on TF-driven coagulation and signaling strengthen the rationale for considering TFPI as a potential anticancer agent.
Journal Article

Immobilized platelets support human colon carcinoma cell tethering, rolling and firm adhesion under dynamic flow conditions

TL;DR: Analysis of the ability of 3 human colon carcinoma cell lines to bind to surface-anchored platelets under flow and to identify the receptors involved in these processes suggests that platelets primarily recruit LS174T cells through a 2-step, sequential process of adhesive interactions that is distinct from that elaborated for neutrophils.
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Neutrophil Recruitment under Shear Flow: It's All about Endothelial Cell Rings and Gaps

TL;DR: The role of adhesion molecule signaling in endothelial cells and their downstream targets during the process of transendothelial migration at cell‐cell borders (paracellular transmigration) is focused on.
Journal ArticleDOI

Therapeutic expression of the platelet-specific integrin, αIIbβ3, in a murine model for Glanzmann thrombasthenia

TL;DR: Bone marrow from β3-deficient (β3–/–) mice was transduced with the ITGβ3-cassette to investigate whether the platelet progeny could establish hemostasis in vivo, and human β3 formed a stable complex with murine αIIb, effectively restoring platelet function.
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