Local inhibition of ADAMTS13 promotes VWF fiber formation in microvessels obtained from human melanoma patients. Cryosections of human malignant melanoma tissue, healthy control skin, and basal cell carcinoma were analyzed by immunofluorescence stainings for VWF and CD31 (A-C) or thrombospondin (TSP) (D-E). Nuclei were stained with DAPI. Analysis of healthy skin (A) and human basal cell carcinoma (B) as control demonstrate storage of VWF in the vessel wall (arrowheads). ULVWF fibers are detected in the lumen of the microvessels, correlating to reduced VWF within the vessel wall indicative of EC activation (C, arrows). These ULVWF fibers bind platelets (D, arrows) and are associated with microthrombi formation in distinct microvessels (E, asterisk; n = 5 to 6; scale bars = 20 µm). Quantification showed significantly increased numbers of vessels with luminal VWF fibers in tumor vasculature compared with healthy skin (F). Systemic VWF level in blood samples of malignant melanoma patients was increased compared with healthy control (G). By contrast, only a slight reduction of ADAMTS13 activity was observed (H). Tumor-derived cytokines and growth factors were measured in healthy control skin and tumor of human malignant melanoma by bio-plex. Cytokine levels of IFN-γ (I), TNF-α (J), and IL-6 (K) were increased in tumor samples compared with control skin. The concentration of VEGF-A was significantly increased within melanoma compared with control (L). Results of 9 different melanoma patients are shown (*P < .05, **P < .005, ***P < .001). Bars indicate the mean ± SD.