Contribution of platelets to tumour metastasis.
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.read more
Citations
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Platelets as messengers of early-stage cancer
TL;DR: In this paper, the authors reviewed the human studies in which platelet characteristics (e.g., count, volume, protein, and mRNA content) are investigated in early-stage cancer.
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Fucoidan-functionalized activated platelet-hitchhiking micelles simultaneously track tumor cells and remodel the immunosuppressive microenvironment for efficient metastatic cancer treatment
TL;DR: In this paper , a fucoidan-functionalized micelle (FD/DOX) was constructed, which could efficiently adhere to activated platelets through P-selectin, and exhibited excellent anti-tumor and anti-metastasis efficacy on 4T1 spontaneous metastasis model.
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Cross-talk between platelet and tumor microenvironment: Role of multiligand/RAGE axis in platelet activation
TL;DR: In the tumor microenvironment, upon activation, activated platelets interact with tumor cells through paracrine signaling and direct contact, thereby promoting tumor cell growth and thrombosis, and RAGE expression and its ligands could be a useful serological biomarker for diagnosis and treatment of cancer.
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The mechanisms how heparin affects the tumor cell induced VEGF and chemokine release from platelets to attenuate the early metastatic niche formation.
Jan Moritz Ponert,Svenja Schwarz,Reza Haschemi,Jens Müller,Bernd Pötzsch,Gerd Bendas,Martin Schlesinger +6 more
TL;DR: Heparin is able to reduce the mediator release induced by different tumor cells both in a contact and coagulation dependent manner and indicates that different chemokines and growth factors in diverse platelet granules are released in tightly regulated processes by various trigger mechanisms.
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ICAM1 depletion reduces spinal metastasis formation in vivo and improves neurological outcome
Thomas Broggini,Marcus Czabanka,Andras Piffko,Christoph Harms,Christian Hoffmann,Ralf Mrowka,Frank Wenke,Urban Deutsch,Carsten Grötzinger,Peter Vajkoczy +9 more
TL;DR: Applying a reliable animal model for spinal metastases, ICAM1 depletion reduces spinal metastasis formation due to an organ-unspecific reduction of metastasis development.
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