Imatinib and chronic myeloid leukemia: validating the promise of molecularly targeted therapy.

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Abstract

The Bcr-Abl tyrosine kinase inhibitor imatinib (Glivec, formerly STI571, Novartis Pharma AG, Basel, Switzerland) produces complete hematologic and cytogenetic responses in a substantial percentage of chronic myeloid leukemia patients. Imatinib is effective in chronic phase, accelerated phase and blast crisis, with lower response rates in patients with more advanced disease. Although responses have been durable in chronic phase patients, relapses have been common in blast crisis. Relapse has been associated with reactivation of Bcr-Abl kinase activity. The clinical development of imatinib illustrates the effectiveness of targeting molecular pathogenetic events. Hopefully, this example can be extended to other malignancies.

Original languageEnglish (US)
JournalEuropean journal of cancer (Oxford, England : 1990)
Volume38 Suppl 5
StatePublished - Sep 2002

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Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Blast Crisis
bcr-abl Fusion Proteins
Therapeutics
Recurrence
Switzerland
Cytogenetics
Phosphotransferases
Imatinib Mesylate
Neoplasms

ASJC Scopus subject areas

  • Cancer Research
  • Hematology
  • Oncology

Cite this

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abstract = "The Bcr-Abl tyrosine kinase inhibitor imatinib (Glivec, formerly STI571, Novartis Pharma AG, Basel, Switzerland) produces complete hematologic and cytogenetic responses in a substantial percentage of chronic myeloid leukemia patients. Imatinib is effective in chronic phase, accelerated phase and blast crisis, with lower response rates in patients with more advanced disease. Although responses have been durable in chronic phase patients, relapses have been common in blast crisis. Relapse has been associated with reactivation of Bcr-Abl kinase activity. The clinical development of imatinib illustrates the effectiveness of targeting molecular pathogenetic events. Hopefully, this example can be extended to other malignancies.",
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