Imatinib mesylate in the treatment of hematologic malignancies

Expert Opin Biol Ther. 2007 Oct;7(10):1597-611. doi: 10.1517/14712598.7.10.1597.

Abstract

The treatment of hematologic malignancies has been based for many years on chemotherapy and possibly, for the more aggressive forms, stem cell transplantation. In 2001, the signal transduction inhibitor 571 (STI571, imatinib mesylate) was reported to have striking effects in chronic myeloid leukaemia patients. Since then, imatinib became the first molecular-targeted agent approved for the treatment of human cancer and was later on demonstrated to be effective in other malignancies, such as Philadelphia positive acute lymphoid leukemia, hypereosinophilic syndromes, gastrointestinal stromal tumours and more recently, systemic mastocytosis and other myeloprolipherative disease-carrying platelet-derived growth factor receptor abnormalities. In this article, the authors review the evidence which led to imatinib approval in the treatment of several of the above mentioned diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / pharmacokinetics
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • Benzamides
  • Drug Interactions
  • Drug Resistance
  • Fusion Proteins, bcr-abl / genetics
  • Fusion Proteins, bcr-abl / metabolism
  • Hematologic Neoplasms / drug therapy*
  • Hematologic Neoplasms / enzymology
  • Hematologic Neoplasms / genetics
  • Hematologic Neoplasms / metabolism
  • Humans
  • Hypereosinophilic Syndrome / drug therapy
  • Imatinib Mesylate
  • Leukemia, Lymphoid / drug therapy
  • Leukemia, Lymphoid / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • Mastocytosis, Systemic / drug therapy
  • Myeloproliferative Disorders / drug therapy
  • Myeloproliferative Disorders / genetics
  • Myeloproliferative Disorders / metabolism
  • Oncogene Proteins, Fusion / genetics
  • Oncogene Proteins, Fusion / metabolism
  • Philadelphia Chromosome
  • Piperazines / adverse effects
  • Piperazines / pharmacokinetics
  • Piperazines / pharmacology
  • Piperazines / therapeutic use*
  • Protein Kinase Inhibitors / adverse effects
  • Protein Kinase Inhibitors / pharmacokinetics
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use*
  • Pyrimidines / adverse effects
  • Pyrimidines / pharmacokinetics
  • Pyrimidines / pharmacology
  • Pyrimidines / therapeutic use*
  • Receptor, Platelet-Derived Growth Factor alpha / genetics
  • Receptor, Platelet-Derived Growth Factor alpha / metabolism
  • Receptors, Platelet-Derived Growth Factor / genetics
  • Receptors, Platelet-Derived Growth Factor / metabolism
  • Signal Transduction / drug effects
  • Treatment Outcome
  • mRNA Cleavage and Polyadenylation Factors / genetics
  • mRNA Cleavage and Polyadenylation Factors / metabolism

Substances

  • Antineoplastic Agents
  • Benzamides
  • Oncogene Proteins, Fusion
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • mRNA Cleavage and Polyadenylation Factors
  • Imatinib Mesylate
  • FIP1L1-PDGFRA fusion protein, human
  • Receptor, Platelet-Derived Growth Factor alpha
  • Receptors, Platelet-Derived Growth Factor
  • Fusion Proteins, bcr-abl