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文献和实验Detection of BCR-ABL Mutations and Resistance to Imatinib Mesylate
The major mechanism of imatinib resistance for patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with mutations in the Bcr-Abl fusion tyrosine kinase that reduce the capacity of imatinib to inhibit kinase
-4 and C-5 centers ( 3 ). After formatron of the mesylate, from the recycled material the amine function is introduced through azrde displacement of the mesylate, followed by reduction ( 4 ) and protectron with the t -BOC group. Finally, the lactone
Inhibitors of Cellular Signaling Targets: Designs and Limitations
. Because of their central role in cellular signaling, as well as their primary role in disease progression, protein kinases are attractive therapeutic targets (2 ,3 ). Seven molecules targeting protein kinases, imatinib mesylate (Gleevec) and trastuzumab (Herceptin
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