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Imatinib (STI571, Gleevec/Glivec) is a potent selective tyrosine kinase
inhibitor and is used successfully in the treatment of chronic myeloid leukemia
(CML). While karyotype alterations, in addition to the Philadelphia chromosome,
are a common phenomenon of progressing CML, the observation of BCR-ABL-negative
leukemic clones with distinct aberrant karyotypes under an imatinib regimen is
not yet understood. Here we test the hypothesis that such tumor clones may be
induced de novo from normal cells by imatinib.
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