Imatinib mesylate (IM) binds to the BCR-ABL protein, inhibiting its kinase activity and effectively controlling diseases driven by this kinase. IM resistance has been associated with kinase mutations or increased BCR-ABL expression. However, disease progression may be mediated by other mechanisms that render tumor cells independent of BCR-ABL. To demonstrate this potential, IM-resistant cells were found in chronic myelogenous leukemia patients with continuous BCR-ABL gene expression but undetectable BCR-ABL protein expression. These cells were unresponsive to IM and acquired BCR-ABL-independent signaling characteristics. IM resistance in some patients may be mediated through loss of kinase target dependence.
Imatinib mesylate ( IM ) binds to the BCR - ABL protein , inhibiting its kinase activity and effectively controlling diseases driven by this kinase . IM resistance has been associated with kinase mutations or increased BCR - ABL expression . However , disease progression may be mediated by other mechanisms that render tumor cells independent of BCR - ABL . To demonstrate this potential , IM - resistant cells were found in chronic myelogenous leukemia patients with continuous BCR - ABL gene expression but undetectable BCR - ABL protein expression . These cells were unresponsive to IM and acquired BCR - ABL - independent signaling characteristics . IM resistance in some patients may be mediated through loss of kinase target dependence .
What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?
What tyrosine kinase , involved in a Philadelphia- chromosome positive chronic myelogenous leukemia , is the target of Imatinib ( Gleevec ) ?
BCR-ABL
BCR-ABL