Nature Communications (Jan 2019)

Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms

  • Haijiao Zhang,
  • Samantha Savage,
  • Anna Reister Schultz,
  • Daniel Bottomly,
  • Libbey White,
  • Erik Segerdell,
  • Beth Wilmot,
  • Shannon K. McWeeney,
  • Christopher A. Eide,
  • Tamilla Nechiporuk,
  • Amy Carlos,
  • Rachel Henson,
  • Chenwei Lin,
  • Robert Searles,
  • Hoang Ho,
  • Yee Ling Lam,
  • Richard Sweat,
  • Courtney Follit,
  • Vinay Jain,
  • Evan Lind,
  • Gautam Borthakur,
  • Guillermo Garcia-Manero,
  • Farhad Ravandi,
  • Hagop M. Kantarjian,
  • Jorge Cortes,
  • Robert Collins,
  • Daelynn R. Buelow,
  • Sharyn D. Baker,
  • Brian J. Druker,
  • Jeffrey W. Tyner

DOI
https://doi.org/10.1038/s41467-018-08263-x
Journal volume & issue
Vol. 10, no. 1
pp. 1 – 13

Abstract

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FLT3 is commonly mutated in acute myeloid leukaemia and treatment with FLT3 inhibitors often ends with relapse. Here, the authors perform exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, to show that resistance occurs due to diverse molecular mechanisms, not primarily due to secondary FLT3 mutations.