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BCR-ABL1(+) acute myeloid leukemia: clonal selection of a BCR-ABL1(-) subclone as a cause of refractory disease with nilotinib treatment.

Abstract
The presence of a Philadelphia chromosome with a corresponding BCR-ABL1 rearrangement is the hallmark of chronic myeloid leukemia, but is considered a very rare event in de novo acute myeloid leukemia (AML). Here, we report the first case in which a dominant Philadelphia chromosome-positive subclone was detected upon relapse in a formerly Philadelphia chromosome-negative MLL-AF6(+) AML. Due to refractory disease under salvage chemotherapy, the patient was started on nilotinib treatment. As a result, the Philadelphia chromosome-positive subclone was eradicated within 1 month; however, disease progressed and was again dominated by the Philadelphia chromosome-negative founding clone, demonstrating rapid clonal expansion under nilotinib-induced selection pressure.
AuthorsNina Rosa Neuendorff, Michaela Schwarz, Philipp Hemmati, Seval Türkmen, Christiane Bommer, Thomas Burmeister, Bernd Dörken, Philipp le Coutre, Renate Arnold, Jörg Westermann
JournalActa haematologica (Acta Haematol) Vol. 133 Issue 2 Pg. 237-41 ( 2015) ISSN: 1421-9662 [Electronic] Switzerland
PMID25401297 (Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2014 S. Karger AG, Basel.
Chemical References
  • BCR-ABL1 fusion protein, human
  • Pyrimidines
  • Fusion Proteins, bcr-abl
  • nilotinib
Topics
  • Aged
  • Fusion Proteins, bcr-abl (genetics)
  • Humans
  • Leukemia, Myeloid, Acute (drug therapy, genetics, pathology)
  • Male
  • Philadelphia Chromosome
  • Pyrimidines (administration & dosage)
  • Recurrence
  • Salvage Therapy (methods)

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