Current CML therapy: progress and dilemma

Leukemia. 2003 Jun;17(6):1010-2. doi: 10.1038/sj.leu.2402951.

Abstract

Rarely has progress in treatment of leukemia been as dramatic and convincing as with the BCR-ABL tyrosine kinase inhibitor imatinib.(1) Imatinib induces remissions of CML as fast as hydroxyurea, achieves rates of cytogenetic remissions that by far exceed those induced by interferon alpha and has a toxicity profile as favourable as that of hydroxyurea and much superior to that of interferon alpha.(2) In addition, the causal approach of this new drug, which may well serve as a model for new treatment modalities in other neoplasias is reassuring.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Benzamides
  • Clinical Trials as Topic
  • Enzyme Inhibitors / therapeutic use
  • Fusion Proteins, bcr-abl
  • Humans
  • Hydroxyurea / therapeutic use
  • Imatinib Mesylate
  • Interferon-alpha / therapeutic use
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
  • Piperazines / therapeutic use
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Protein-Tyrosine Kinases / metabolism
  • Pyrimidines / therapeutic use
  • Stem Cell Transplantation

Substances

  • Antineoplastic Agents
  • Benzamides
  • Enzyme Inhibitors
  • Interferon-alpha
  • Piperazines
  • Pyrimidines
  • Imatinib Mesylate
  • Protein-Tyrosine Kinases
  • Fusion Proteins, bcr-abl
  • Hydroxyurea