Chronic myelogenous leukaemia - New therapeutic principles

Michael E. O'Dwyer, Brian Druker

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

The deregulated tyrosine kinase activity of the BCR-ABL fusion protein is the cause of malignant transformation in almost all cases of chronic myelogenous leukaemia (CML), making BCR-ABL an ideal target for pharmacological inhibition. Signal transduction inhibitor (STI571) (formerly 2CGP57 148B), is an ABL specific, tyrosine kinase inhibitor. In preclinical studies, it has been shown to selectively kill BCR-ABL expressing cells, both in-vitro and in vivo. The results of clinical studies to date are highly encouraging and STI571 promises to be an important addition to the therapy of CML.

Original languageEnglish (US)
Pages (from-to)3-9
Number of pages7
JournalJournal of Internal Medicine
Volume250
Issue number1
DOIs
StatePublished - 2001

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Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Protein-Tyrosine Kinases
Signal Transduction
Pharmacology
Therapeutics
Proteins
Imatinib Mesylate
Clinical Studies
In Vitro Techniques

Keywords

  • BCR-ABL
  • Chronic myelogenous leukaemia
  • Signal transduction
  • STI571
  • Therapy
  • Tyrosine kinase inhibitor

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Chronic myelogenous leukaemia - New therapeutic principles. / O'Dwyer, Michael E.; Druker, Brian.

In: Journal of Internal Medicine, Vol. 250, No. 1, 2001, p. 3-9.

Research output: Contribution to journalArticle

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