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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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Journal ArticleDOI

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.
Journal ArticleDOI

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

Critical Role for TrkB Kinase Function in Anoikis Suppression, Tumorigenesis, and Metastasis

TL;DR: It is reported that TrkB kinase activity is required and, unexpectedly, also sufficient for anoikis suppression, tumor formation, and experimental metastasis, and suggested that targeting the enzymatic activity of TrkB might be beneficial in cancer therapy.
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The dual role of CD44 as a functional P-selectin ligand and fibrin receptor in colon carcinoma cell adhesion

TL;DR: The data offer a novel perspective on the apparent metastatic potential associated with CD44 overexpression on colon carcinoma cells and the critical roles of P-selectin and fibrin(ogen) in metastatic spread and provide a rational basis for the design of new therapeutic strategies to impede metastasis.
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Increased soluble P-selectin in patients with haematological and breast cancer: a comparison with fibrinogen, plasminogen activator inhibitor and von Willebrand factor.

TL;DR: It is concluded that the platelet marker soluble P-selectin is raised in both haematological and breast cancer, and is higher in the former, but is unrelated to the type or stage of breast cancer.
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Inflammation and melanoma growth and metastasis: The role of platelet-activating factor (PAF) and its receptor

TL;DR: The group has recently demonstrated that PAF receptor antagonists can effectively inhibit the metastatic potential of human melanoma cells in nude mice and it is proposed that these cells are better equipped to respond to PAF within the tumor microenvironment when compared to their non-metastatic counterparts.
Journal ArticleDOI

Platelet glycoprotein VI facilitates experimental lung metastasis in syngenic mouse models

TL;DR: The results demonstrate that the presence of platelet GPVI facilitates experimental tumor metastasis but does not contribute to the growth of primary tumors.
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