BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.

@article{Zabriskie2014BCRABL1CM,
  title={BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.},
  author={Matthew S. Zabriskie and Christopher A. Eide and Srinivas Kiran Tantravahi and Nadeem A. Vellore and Johanna C Estrada and Franck Emmanuel Nicolini and Hanna J Khoury and Richard A Larson and Marina Y Konopleva and Jorge E. Cortes and Hagop M Kantarjian and Elias J Jabbour and Steven M. Kornblau and Jeffrey Howard Lipton and Delphine Rea and Leif Stenke and Gisela Barbany and Thoralf Lange and Juan-Carlos Hern{\'a}ndez-Boluda and Gert Jan Ossenkoppele and Richard D Press and Charles T. H. Chuah and Stuart L Goldberg and Meir Wetzler and F X Mahon and Gabriel Etienne and Michele Baccarani and Simona Soverini and Gianantonio Rosti and Philippe Rousselot and Ran Friedman and Marie Deininger and Kimberly R. Reynolds and William L. Heaton and Anna M. Eiring and Anthony D. Pomicter and Jamshid S Khorashad and Todd W Kelley and Riccardo Baron and Brian J. Druker and Michael Werner Nikolaus Deininger and Thomas O'Hare},
  journal={Cancer cell},
  year={2014},
  volume={26 3},
  pages={428-442}
}
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… CONTINUE READING
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