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2004, Volume 4, Issue 1: 99-114. Doi: 10.3934/dcdsb.2004.4.99
This issue Previous Article Macrophage-tumour interactions: In vivo dynamics Next Article The steady state of a maturity structured tumor cord cell population

A mathematical model of BCR-ABL autophosphorylation, signaling through the CRKL pathway, and Gleevec dynamics in chronic myeloid leukemia

  • 1.

    Department of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, California 90095-1569

  • 2.

    Biocybernetics Laboratory, Departments of Computer Science and Medicine, University of California, Los Angeles, Los Angeles, California 90095-1596

Received:  October 31, 2002
Revised:  May 31, 2003
Published:  January 2004
Abstract Related Papers Cited by
    Abstract
  • A mathematical model is presented that describes several signaling events that occur in cells from patients with chronic myeloid leukemia, i.e. autophosphorylation of the Bcr-Abl oncoprotein and subsequent signaling through the Crkl pathway. Dynamical effects of the drug STI-571 (Gleevec) on these events are examined, and a minimal concentration for drug effectiveness is predicted by simulation. Most importantly, the model suggests that, for cells in blast crisis, cellular drug clearance mechanisms such as drug efflux pumps dramatically reduce the effectiveness of Gleevec. This is a new prediction regarding the efficacy of Gleevec. In addition, it is speculated that these resistance mechanisms might be present from the onset of disease.
    Mathematics Subject Classification: 92C45, 92B05.

    Citation:
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