西亚试剂：Ultraviolet-radiation-induced inflammation promotes angiotr

Tobias Bald, Thomas Quast, Jennifer Landsberg, Meri Rogava, Nicole Glodde, Dorys Lopez-Ramos, Judith Kohlmeyer, Stefanie Riesenberg, Debby van den Boorn-Konijnenberg, Cornelia Hömig-Hölzel, Raphael Reuten, Benjamin Schadow, Heike Weighardt, Daniela Wenzel, Iris Helfrich, Dirk Schadendorf, Wilhelm Bloch, Marco E. Bianchi, Claire Lugassy, Raymond L. Barnhill, Manuel Koch, Bernd K. Fleischmann,Irmgard Förster, Wolfgang Kastenmüller, Waldemar Kolanus et al.

Intermittent intense ultraviolet (UV) exposure represents an imp0rtant aetiological factor in the development of malignant melanoma. The ability of UV radiation to cause tumour-initiating mutations in melanocytes is now firmly established, but how the microenvironmental effects of UV radiation influence melanoma pathogenesis is not fully understood. Here we report that repetitive UV exposure of primary cutaneous melanomas in a genetically engineered mouse model promotes me-tastatic progression, independent of its tumour-initiating effects. UV irradiation enhanced the expansion of tumour cells along abluminal blood vessel surfaces and increased the number of lung me-tastases. This effect depended on the recruitment and activation of neutrophils, initiated by the release of high mobility group box 1 (HMGB1) from UV-damaged epidermal keratinocytes and driven by Toll-like receptor 4 (TLR4). The UV-induced neutrophilic

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