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Presence of atypical thrombopoietin receptor (MPL) mutations in triple-negative essential thrombocythemia patients by Xénia Cabagnols, Fabrizia Favale, Florence Pasquier, Kahia Messaoudi, Jean Philippe Defour, Jean Christophe Ianotto, Christophe Marzac, Jean Pierre Le Couédic, Nathalie Droin, Ilyas Chachoua, Remi Favier, Mâboyba Khadija Diop, Valérie Ugo, Nicole Casadevall, Najet Debili, Hana Raslova, Christine BellannéChantelot, Stefan N. Constantinescu, Olivier Bluteau, Isabelle Plo, and William Vainchenker Blood Volume 127(3):333-342 January 21, 2016 ©2016 by American Society of Hematology Genomic analysis. Xénia Cabagnols et al. Blood 2016;127:333-342 ©2016 by American Society of Hematology MPLS204P does not exhibit cellular trafficking defects. Xénia Cabagnols et al. Blood 2016;127:333-342 ©2016 by American Society of Hematology MPLS204P does not present proliferative advantage in bulky cultures. Xénia Cabagnols et al. Blood 2016;127:333-342 ©2016 by American Society of Hematology MPLS204P is a weak gain-of-function mutant. Xénia Cabagnols et al. Blood 2016;127:333-342 ©2016 by American Society of Hematology UT7 MPL S204P cells are less cytokine-dependent than UT7 MPL WT. (A) Growth of UT7 MPLS204P and UT7 MPLWT at limiting dilution without cytokines. Xénia Cabagnols et al. Blood 2016;127:333-342 ©2016 by American Society of Hematology Analysis of the MPLY591N mutant. Xénia Cabagnols et al. Blood 2016;127:333-342 ©2016 by American Society of Hematology
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