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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

Contrasting Actions of Selective Inhibitors of Angiopoietin-1 and Angiopoietin-2 on the Normalization of Tumor Blood Vessels

TL;DR: Findings are consistent with a model whereby inhibition of Ang2 leads to normalization of tumor blood vessels by permitting the unopposed action of Ang1, but decreases tumor vascularity primarily by blocking Ang2 actions.
Journal ArticleDOI

Cancer cells in transit: the vascular interactions of tumor cells.

TL;DR: This review presents the current mechanistic knowledge on vascular interactions of tumor cells, and it discusses biochemical and cell and molecular biology techniques used for the identification of novel receptor-ligand pairs mediating these interactions.
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Extrinsic-pathway activation in cancer with high factor VIIa and tissue factor.

TL;DR: In this paper, the activation of coagulation in 106 patients with solid tumours and 72 healthy volunteers was studied by measuring plasma levels of tissue factor, factor VIIa, factor XIIa, thrombin-antithrombin complex, and prothrombin fragments 1 + 2.

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Mechanisms and Consequences of Neutrophil Interaction with the Endothelium

TL;DR: In this paper, the authors focused on the signaling events during the interaction of neutrophils with the endothelium and focused on different inflammatory signals that can activate several pathways, such as neutrophil extravasation, superoxide production and degranulation.
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