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Recent studies indicate that a rare population of primitive quiescent
BCR-ABL(+) cells are innately insensitive to imatinib mesylate (IM) and persist
after IM therapy of patients with chronic myeloid leukemia (CML). New approaches
to the eradication of these cells are therefore likely to be crucial to the
development of curative therapies for CML. We have now found that Ara-C,
LY294002 (a PI-3 (phosphatidylinositol-3' kinase) kinase inhibitor), 17AAG (a
heat-shock protein (HSP)-90 antagonist) and lonafarnib (a farnesyltransfease
inhibitor) all enhance the toxicity of IM on K562 cells and on the total CD34(+)
leukemic cell population from chronic phase CML patients.
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