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  • 1.
    Zabriskie, Matthew S.
    et al.
    University of Utah, USA.
    Eide, Christopher A.
    Oregon Health & Science University, USA ; Howard Hughes Medical Institute, USA.
    Tantravahi, Srinivas K.
    University of Utah, USA.
    Vellore, Nadeem A.
    University of Utah, USA.
    Estrada, Johanna
    University of Utah, USA.
    Nicolini, Franck E.
    Centre Hospitalier Lyon Sud, France.
    Khoury, Hanna J.
    Emory University, USA.
    Larson, Richard A.
    University of Chicago, USA.
    Konopleva, Marina
    University of Texas, USA.
    Cortes, Jorge E.
    University of Texas, USA.
    Kantarjian, Hagop
    Jabbour, Elias J.
    Kornblau, Steven M.
    Lipton, Jeffrey H.
    Rea, Delphine
    Stenke, Leif
    Barbany, Gisela
    Lange, Thoralf
    Hernandez-Boluda, Juan-Carlos
    Ossenkoppele, Gert J.
    Press, Richard D.
    Chuah, Charles
    Goldberg, Stuart L.
    Wetzler, Meir
    Mahon, Francois-Xavier
    Etienne, Gabriel
    Baccarani, Michele
    Soverini, Simona
    Rosti, Gianantonio
    Rousselot, Philippe
    Friedman, Ran
    Linnaeus University, Faculty of Health and Life Sciences, Department of Chemistry and Biomedical Sciences. Ctr Biomat Chem.
    Deininger, Marie
    Reynolds, Kimberly R.
    Heaton, William L.
    Eiring, Anna M.
    Pomicter, Anthony D.
    Khorashad, Jamshid S.
    Kelley, Todd W.
    Baron, Riccardo
    Druker, Brian J.
    Deininger, Michael W.
    O'Hare, Thomas
    BCR-ABL1 Compound Mutations Combining Key Kinase Domain Positions Confer Clinical Resistance to Ponatinib in Ph Chromosome-Positive Leukemia2014In: Cancer Cell, ISSN 1535-6108, E-ISSN 1878-3686, Vol. 26, no 3, p. 428-442Article in journal (Refereed)
    Abstract [en]

    Ponatinib is the only currently approved tyrosine kinase inhibitor (TKI) that suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph+) leukemia, including the recalcitrant BCR-ABL1(T315I) mutant. However, emergence of compound mutations in a BCR-ABL1 allele may confer ponatinib resistance. We found that clinically reported BCR-ABL1 compound mutants center on 12 key positions and confer varying resistance to imatinib, nilotinib, dasatinib, ponatinib, rebastinib, and bosutinib. T315I-inclusive compound mutants confer high-level resistance to TKIs, including ponatinib. In vitro resistance profiling was predictive of treatment outcomes in Ph+ leukemia patients. Structural explanations for compound mutation-based resistance were obtained through molecular dynamics simulations. Our findings demonstrate that BCR-ABL1 compound mutants confer different levels of TKI resistance, necessitating rational treatment selection to optimize clinical outcome.

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