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Cooper S et al. – In this review, the authors describe agents which overcome the T315I mutation, as well as native BCR–ABL, via several mechanisms, including increased degradation of BCR–ABL, optimization of direct inhibition of the BCR–ABL kinase, inhibition of BCR–ABL–mediated cell growth via interruption of the BCR–ABL–mediated transcription, protein synthesis or post–translational modification, all of which lead to decreased proliferation and malignant cell death.


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