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Coagulation and metastasis: what does the experimental literature tell us?

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TLDR
This work revisits the literature on coagulation in the light of recent studies in which treatment of clinical cohorts with anticoagulant drugs led to diminished metastasis.
Abstract
Inhibition of coagulation greatly limits cancer metastasis in many experimental models. Cancer cells trigger coagulation, through expression of tissue factor or P-selectin ligands that have correlated with worse prognosis in human clinical studies. Cancer cells also affect coagulation through expression of thrombin and release of microparticles that augment coagulation. In the cancer-bearing host, coagulation facilitates tumour progression through release of platelet granule contents, inhibition of Natural Killer cells and recruitment of macrophages. We are revisiting this literature in the light of recent studies in which treatment of clinical cohorts with anticoagulant drugs led to diminished metastasis.

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Crossing the endothelial barrier during metastasis

TL;DR: How cancer cells cross the endothelial barrier during extravasation is described and how different receptors, signalling pathways and circulating cells such as leukocytes and platelets contribute to this process are described.
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Exosome-Mediated Metastasis: Communication from a Distance.

TL;DR: Work on the contribution of exosome cargo to cancer progression, the role ofExosomes in PMN establishment, and the function of exOSomes in organotropic metastasis are reviewed.
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Intravascular Survival and Extravasation of Tumor Cells.

TL;DR: The current understanding of the cellular and molecular mechanisms that allow tumor cells to survive in the intravascular environment and that mediate and promote tumor cell extravasation are reviewed.
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The immune system in cancer metastasis: friend or foe?

TL;DR: Classic and new observations are reviewed, describing the links between the immune system and metastasis that inform the development of cancer therapies.
References
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Journal ArticleDOI

Macrophage Diversity Enhances Tumor Progression and Metastasis

TL;DR: There is persuasive clinical and experimental evidence that macrophages promote cancer initiation and malignant progression, and specialized subpopulations of macrophage may represent important new therapeutic targets.
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CCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis

TL;DR: The mechanistic link between CCL2 expression and macrophage infiltration are correlated with poor prognosis and metastatic disease in human breast cancer and the origin of these macrophages is defined by showing that Gr1-positive inflammatory monocytes are preferentially recruited to pulmonary metastases but not to primary mammary tumours in mice.
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Mechanisms of Thrombus Formation

TL;DR: This review is an account of recent advances in the understanding of the mechanisms of thrombus formation, with emphasis on two independent pathways: one involving primarily platelets and the other initiated by tissue factor.
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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

Contribution of platelets to tumour metastasis.

TL;DR: Contributions of platelets to tumour cell survival and spread suggest platelets as a new avenue for therapy.
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