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Verfasst von:Bauer, Alexander [VerfasserIn]   i
 Desch, Anna [VerfasserIn]   i
 Wagner, Andreas H. [VerfasserIn]   i
 Hecker, Markus [VerfasserIn]   i
 Utikal, Jochen [VerfasserIn]   i
 Gorzelanny, Christian [VerfasserIn]   i
 Umansky, Viktor [VerfasserIn]   i
Titel:Von Willebrand factor fibers promote cancer-associated platelet aggregation in malignant melanoma of mice and humans
Verf.angabe:Alexander T. Bauer, Jan Suckau, Kathrin Frank, Anna Desch, Lukas Goertz, Andreas H. Wagner, Markus Hecker, Tobias Goerge, Ludmila Umansky, Philipp Beckhove, Jochen Utikal, Christian Gorzelanny, Nancy Diaz-Valdes, Viktor Umansky, and Stefan W. Schneider
E-Jahr:2015
Jahr:14 May 2015
Umfang:11 S.
Fussnoten:Gesehen am 31.01.2018
Titel Quelle:Enthalten in: Blood
Ort Quelle:Washington, DC : American Society of Hematology, 1946
Jahr Quelle:2015
Band/Heft Quelle:125(2015), 20, Seite 3153-3163
ISSN Quelle:1528-0020
Abstract:Tumor-mediated procoagulatory activity leads to venous thromboembolism and supports metastasis in cancer patients. A prerequisite for metastasis formation is the interaction of cancer cells with endothelial cells (ECs) followed by their extravasation. Although it is known that activation of ECs and the release of the procoagulatory protein von Willebrand factor (VWF) is essential for malignancy, the underlying mechanisms remain poorly understood. We hypothesized that VWF fibers in tumor vessels promote tumor-associated thromboembolism and metastasis. Using in vitro settings, mouse models, and human tumor samples, we showed that melanoma cells activate ECs followed by the luminal release of VWF fibers and platelet aggregation in tumor microvessels. Analysis of human blood samples and tumor tissue revealed that a promoted VWF release combined with a local inhibition of proteolytic activity and protein expression of ADAMTS13 (a disintegrin-like and metalloproteinase with thrombospondin type I repeats 13) accounts for this procoagulatory milieu. Blocking endothelial cell activation by the low-molecular-weight heparin tinzaparin was accompanied by a lack of VWF networks and inhibited tumor progression in a transgenic mouse model. Our findings implicate a mechanism wherein tumor-derived vascular endothelial growth factor-A (VEGF-A) promotes tumor progression and angiogenesis. Thus, targeting EC activation envisions new therapeutic strategies attenuating tumor-related angiogenesis and coagulation.
DOI:doi:10.1182/blood-2014-08-595686
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Volltext: http://dx.doi.org/10.1182/blood-2014-08-595686
 kostenfrei: Volltext: http://www.bloodjournal.org/content/125/20/3153
 DOI: https://doi.org/10.1182/blood-2014-08-595686
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:156793868X
Verknüpfungen:→ Zeitschrift

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