Pushing the limits of targeted therapy in chronic myeloid leukaemia
Pushing the limits of targeted therapy in chronic myeloid leukaemia
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DOI：
10.1038/nrc3408
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发表时间：
2012-11
影响因子：
78.5
通讯作者：
T. O'hare;M. Zabriskie;A. Eiring;M. Deininger
中科院分区：
文献类型：
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作者：
T. O'hare;M. Zabriskie;A. Eiring;M. Deininger
Tyrosine kinase inhibitor (TKI) therapy targeting the BCR-ABL1 kinase is effective against chronic myeloid leukaemia (CML), but is not curative for most patients. Minimal residual disease (MRD) is thought to reside in TKI-insensitive leukaemia stem cells (LSCs) that are not fully addicted to BCR-ABL1. Recent conceptual advances in both CML biology and therapeutic intervention have increased the potential for the elimination of CML cells, including LSCs, through simultaneous inhibition of BCR-ABL1 and other newly identified, crucial targets.
