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Ponatinib overcomes FGF2-mediated resistance in CML patients without kinase domain mutations by Elie Traer, Nathalie Javidi-Sharifi, Anupriya Agarwal, Jennifer Dunlap, Isabel English, Jacqueline Martinez, Jeffrey W. Tyner, Melissa Wong, and Brian J. Druker Blood Volume 123(10):1516-1524 March 6, 2014 ©2014 by American Society of Hematology Microenvironmental screen identifies FGF2 as a protective molecule for K562 cells in the presence of IM; FGF2 promotes long-term K562 outgrowth and IM resistance. Elie Traer et al. Blood 2014;123:1516-1524 ©2014 by American Society of Hematology FGF2 protection of K562 cells is mediated by FGFR3. Elie Traer et al. Blood 2014;123:1516-1524 ©2014 by American Society of Hematology Long-term IM resistance occurs via FGF2-dependent or -independent mechanisms, and FGF2dependent resistance can be overcome by FGFR inhibition. Elie Traer et al. Blood 2014;123:1516-1524 ©2014 by American Society of Hematology FGF2-dependent resistance is mediated by activation of FGFR-RAS-RAF-MEK-ERK pathway, whereas FGF2-independent resistance is mediated by reactivation of BCR-ABL. Elie Traer et al. Blood 2014;123:1516-1524 ©2014 by American Society of Hematology FGF2 is increased in the bone marrow of patients without KD mutations and decreases with ponatinib treatment. Elie Traer et al. Blood 2014;123:1516-1524 ©2014 by American Society of Hematology