Bcr-Abl inhibition as a modality of CML therapeutics

Biochim Biophys Acta. 2001 Aug 31;1551(1):M11-8. doi: 10.1016/s0304-419x(01)00022-1.
No abstract available

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / therapeutic use*
  • Benzamides
  • Binding Sites
  • Cell Division / drug effects
  • Clinical Trials as Topic
  • Combined Modality Therapy
  • Drug Resistance
  • Enzyme Inhibitors / therapeutic use*
  • Fusion Proteins, bcr-abl / metabolism
  • Hematopoietic Stem Cell Transplantation
  • Humans
  • Hydroxyurea / therapeutic use
  • Imatinib Mesylate
  • Interferon-alpha / therapeutic use
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy*
  • Middle Aged
  • Models, Molecular
  • Piperazines / chemical synthesis
  • Piperazines / pharmacology
  • Piperazines / therapeutic use*
  • Protein Kinase Inhibitors
  • Pyrimidines / chemical synthesis
  • Pyrimidines / pharmacology
  • Pyrimidines / therapeutic use*
  • Structure-Activity Relationship
  • Tumor Cells, Cultured / drug effects

Substances

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