Clonal cytogenetic abnormalities after tyrosine kinase inhibitor therapy in Ph+ ALL resolution after decitabine therapy

Pediatr Blood Cancer. 2012 Sep;59(3):573-5. doi: 10.1002/pbc.23318. Epub 2011 Sep 9.

Abstract

Mixed chimerism and presence of minimal residual disease after stem cell transplantation (SCT) usually predict leukemia recurrence. In Philadelphia chromosome positive (Ph+) leukemia tyrosine kinase inhibitors can restore remission. These agents can induce clonal cytogenetic abnormalities in the Philadelphia negative cell population (CCA/Ph-), which may rarely progress to acute myeloid leukemia. A child with Ph+ acute lymphoblastic leukemia showed mixed donor chimerism and persistent bcr-abl transcripts after a matched sibling SCT. There was no response to tyrosine kinase inhibitor (TKI) therapy, but she has remained hematologically normal for more than 5 years. CCA/Ph- was detected but resolved with hypomethylating therapy.

Publication types

  • Case Reports

MeSH terms

  • Azacitidine / analogs & derivatives*
  • Azacitidine / therapeutic use
  • Benzamides
  • Child, Preschool
  • Chromosome Aberrations*
  • Decitabine
  • Female
  • Humans
  • Imatinib Mesylate
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • Neoplasm, Residual
  • Philadelphia Chromosome
  • Piperazines / therapeutic use
  • Protein Kinase Inhibitors / therapeutic use*
  • Pyrimidines / therapeutic use
  • Stem Cell Transplantation*

Substances

  • Benzamides
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • Decitabine
  • Imatinib Mesylate
  • Azacitidine