Development of AML with t(8;21)(q22;q22) and RUNX1-RUNX1T1 fusion following Philadelphia-negative clonal evolution during treatment of CML with Imatinib

Cancer Genet Cytogenet. 2009 Feb;189(1):63-7. doi: 10.1016/j.cancergencyto.2008.09.016.
No abstract available

Publication types

  • Case Reports
  • Letter

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Benzamides
  • Chromosomes, Human, Pair 21 / genetics
  • Chromosomes, Human, Pair 8 / genetics
  • Core Binding Factor Alpha 2 Subunit / genetics*
  • Female
  • Humans
  • Imatinib Mesylate
  • Karyotyping
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics*
  • Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / pathology
  • Middle Aged
  • Oncogene Proteins, Fusion / genetics*
  • Piperazines / therapeutic use*
  • Pyrimidines / therapeutic use*
  • RUNX1 Translocation Partner 1 Protein
  • Translocation, Genetic / genetics*

Substances

  • AML1-ETO fusion protein, human
  • Antineoplastic Agents
  • Benzamides
  • Core Binding Factor Alpha 2 Subunit
  • Oncogene Proteins, Fusion
  • Piperazines
  • Pyrimidines
  • RUNX1 Translocation Partner 1 Protein
  • Imatinib Mesylate