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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.
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

Activated integrin αvβ3 cooperates with metalloproteinase MMP-9 in regulating migration of metastatic breast cancer cells

TL;DR: The results indicate a causal relationship between the expression of activated integrin αvβ3 and production of enzymatically active MMP-9 in metastatic breast cancer cells, and these molecules cooperate to enhance breast cancer cell migration toward specific matrix proteins.
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Platelet–cancer interactions: mechanisms and pharmacology of tumour cell-induced platelet aggregation

TL;DR: During haematogenous metastasis, cancer cells migrate to the vasculature and interact with platelets resulting in tumour cell‐induced platelet aggregation (TCIPA) and this work reviews the literature on this phenomenon.
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Platelets actively sequester angiogenesis regulators

TL;DR: It is shown that accumulation of angiogenesis regulators in platelets of animals bearing malignant tumors exceeds significantly their concentration in plasma or serum, as well as their levels in Platelets from non-tumor-bearing animals.
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Deadly allies: the fatal interplay between platelets and metastasizing cancer cells

TL;DR: This review gives a comprehensive overview on the most important platelet receptors and their putative involvement in hematogenous metastasis of malignant tumors and suggests that targeted inhibition of certain platelet surface receptors may result in enhanced experimental tumor metastasis.
Journal ArticleDOI

Historical review: megakaryopoiesis and thrombopoiesis

TL;DR: The study of thrombopoiesis has evolved greatly since an era when platelets were termed "the dust of the blood," only about 100 years ago, and the physiologic mechanisms that drive proplatelet formation can be recapitulated in cell-free systems and their biochemistry evaluated.
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