![]() ![]() ![]() These differences were also reflected in tumor burden, with Braf V600E Map3k1 fl/fl mice presenting more melanomas on average than the Braf V600E mice ( P < 0.0001 Figure 2e). Moreover, whereas 72.7% (40/55) of Braf V600E mice developed melanoma with a median latency of 32 weeks, Braf V600E Map3k1 fl/fl mice developed tumors with 95.7% penetrance (22/23) and a median latency of only 8 weeks ( P < 0.0001 Figure 2d). Notably, the nevi from Braf V600E Map3k1 fl/fl mice were more abundant ( P = 0.011) and larger ( P < 0.0001) than the nevi in Braf V600E mice ( Figure 2b and c). However, when Map3k1 fl/fl mice were crossed to mice carrying a conditional-inducible Braf +/LSL-V600E allele, the topical administration of tamoxifen induced a progressive melanocytic hyperplasia leading to the development of pigmented dermal nevi ( Figure 2a). ![]() 23 AND ME AND SNAPGENE VIEWER SKINBy itself, Map3k1 deletion did not induce any pigmented lesions or skin tumors in the mice ( Figure 2a), indicating that the loss of Map3k1 alone is not sufficient to induce melanocyte proliferation. To investigate the role of Map3k1 in melanomagenesis, we generated Tyr::CreERT2 +/o Map3k1 fl/fl ( Map3k1 fl/fl) mice to allow conditional deletion of Map3k1 in melanocytes following topical application of tamoxifen to the dorsal skin of juvenile mice. Journal of Investigative Dermatology Symposium Proceedings.Resources for Clinical Research in the JID.Montagna Symposium on the Biology of Skin.Methods and Techniques for Skin Research. ![]()
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