停用酪氨酸激酶抑制剂（TKI）治疗后BCR-ABL1突变克隆的减少。
Reduction of BCR-ABL1 mutant clones after discontinuation of TKI therapy.
作者信息
Beel Karolien, Janssens Ann, Verhoef Gregor, Vandenberghe Peter
机构信息
Center for Human Genetics, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium.
出版信息
Leuk Res. 2009 Dec;33(12):1703-5. doi: 10.1016/j.leukres.2009.04.021. Epub 2009 May 19.
In this letter we describe two case reports of CML patients with acquired mutations of the BCR-ABL1 kinase domain, in whom the mutant clone regressed and drug sensitivity was restored after temporary interruption of TKI. We believe that temporary interruption of an ATP-competitive tyrosine kinase inhibitor and switching to non-selective therapy can be a valid therapeutic option in CML patients. In addition, we highlight the potential of a flow cytometric CRKL phosphorylation assay to explore TKI sensitivity in CML cells ex vivo, and its correlation with clinical and haematological sensitivity or resistance.
在本信函中，我们描述了两例慢性粒细胞白血病（CML）患者的病例报告，这两名患者的BCR-ABL1激酶结构域发生了获得性突变，在酪氨酸激酶抑制剂（TKI）暂时中断后，突变克隆消退且药物敏感性得以恢复。我们认为，暂时中断ATP竞争性酪氨酸激酶抑制剂并改用非选择性疗法可能是CML患者的一种有效治疗选择。此外，我们强调了流式细胞术CRKL磷酸化检测在体外探索CML细胞对TKI敏感性及其与临床和血液学敏感性或耐药性相关性方面的潜力。
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