慢性髓系白血病中伊马替尼耐药与D363G BCR::ABL1激酶结构域突变相关

IF 0.7 Q4 HEMATOLOGY
Stephen E Langabeer, Stuart Macleod, Úna Bhreathnach, Kamal Fadalla
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引用次数: 0

摘要

获得性对酪氨酸激酶抑制剂(TKIs)的耐药性仍然是慢性髓性白血病(CML)治疗中的一个挑战。研究最多的TKI耐药原因是在BCR::ABL1酪氨酸激酶结构域(KDM)内获得突变,其中大多数发生在该区域的7个密码子上。本文描述了一例CML,其中存在罕见的D363G BCR::ABL1 KDM导致一线伊马替尼的次优反应。切换到达沙替尼导致实现持续的主要分子反应,在随后由于副作用切换到博舒替尼后保持。报告此类病例对于任何具有这种罕见突变的CML患者的未来管理都很重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G <i>BCR::ABL1</i> Kinase Domain Mutation.

Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation.

Acquired resistance to tyrosine kinase inhibitors (TKIs) remains a therapeutic challenge in the treatment of chronic myeloid leukemia (CML). The most studied reason for TKI resistance is the acquisition of mutations within the BCR::ABL1 tyrosine kinase domain (KDM) and of which the majority of which occur at seven codons within this region. A case of CML is described in which presence of a rare D363G BCR::ABL1 KDM resulted in a suboptimal response to frontline imatinib. Switching to dasatinib resulted in achieving a sustained major molecular response that was maintained after a subsequent switch to bosutinib due to the side effects. Reporting of such cases is important for the future management of any CML patients with this rare mutation.

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