BCR-ABL-negative chronic myeloid leukemia

Curr Hematol Malig Rep. 2007 May;2(2):75-82. doi: 10.1007/s11899-007-0011-5.

Abstract

Constitutive activation of protein tyrosine kinases plays a central role in the pathogenesis of myeloproliferative disorders, including BCR-ABL-negative chronic myeloid leukemia. Current research is focused on elucidating the full spectrum of causative mutations in this rare, heterogeneous disease. Activated tyrosine kinases are excellent targets for signal transduction therapy, and an accurate diagnosis including morphology, karyotyping, and molecular genetics will become increasingly important to direct individualized treatment. In addition, new molecular findings need to be incorporated into disease classification systems.

Publication types

  • Review

MeSH terms

  • Aged
  • Aneuploidy
  • Enzyme Activation
  • Humans
  • Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative* / classification
  • Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative* / diagnosis
  • Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative* / enzymology
  • Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative* / genetics
  • Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative* / pathology
  • Middle Aged
  • Mutation
  • Oncogene Proteins, Fusion / genetics
  • Oncogene Proteins, Fusion / physiology
  • Protein Kinases / genetics
  • Protein Kinases / physiology
  • Risk Factors
  • Signal Transduction / genetics
  • Translocation, Genetic

Substances

  • Oncogene Proteins, Fusion
  • Protein Kinases