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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
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