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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

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Journal ArticleDOI

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TL;DR: It is shown that P-selectin, which normally binds leukocyte ligands, can promote tumor growth and facilitate the metastatic seeding of a mucin-producing carcinoma.
Journal ArticleDOI

Platelet-derived lysophosphatidic acid supports the progression of osteolytic bone metastases in breast cancer

TL;DR: The data suggest that, at the bone metastatic site, tumor cells stimulate the production of LPA from activated platelets, which enhances both tumor growth and cytokine-mediated bone destruction.
Journal ArticleDOI

Synergistic effects of L- and P-selectin in facilitating tumor metastasis can involve non-mucin ligands and implicate leukocytes as enhancers of metastasis

TL;DR: L-selectin on neutrophils, monocytes, and/or NK cells has a role in facilitating metastasis, acting beyond the early time points wherein P- selectin mediates interactions of platelet with tumor cells.
Journal ArticleDOI

Selectins promote tumor metastasis

TL;DR: There is accumulating evidence for the potential of selectins to contribute to a number of pathophysiological processes, including cancer metastasis, and current evidence for selectins as potential facilitators of metastasis is discussed.
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