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Blood:CDK6是携带NUP98融合蛋白的急性髓系白血病的一个新的潜在治疗靶点

2020-05-03 QQY MedSci原创

在AML中,NUP98融合蛋白直接调控白血病相关基因表达。 CDK6表达受NUP融合的直接转录调控,NUP98融合变异型AML对CDK6抑制特别敏感。

与核孔蛋白98 (NUP98)相关的融合蛋白在急性髓系白血病(AML)中反复出现,且与预后不良相关。迄今为止,对NUP98-融合依赖性致瘤转化机制的认识不足,阻碍了AML靶向治疗的发展。

研究人员推测不同的NUP98融合蛋白可解除一组常见的转录靶点的调控,这些靶点或可用于靶向治疗。为了破译由不同NUP98-融合蛋白调控的转录程序,研究人员建立了NUP98/NSD1、NUP98/JARID1A和NUP98/DDX10表达可调控的小鼠模型。

通过将NUP98融合蛋白的染色质占位谱与体内急性融合蛋白失活后的转录组谱进行整合分析,研究人员定义了NUP98融合蛋白的直接转录靶点的核心集。其中,CDK6在小鼠和人AML样本中高表达。CDK6缺失可减缓NUP98融合驱动的白血病发生;此外,NUP98融合AML对药物抑制CDK6敏感,无论是在体内还是体外。

综上所述,本研究表明CDK6是NUP98融合蛋白的一个保守的、至关重要的直接靶点,提示CDK4/CDK6抑制剂可作为携带NUP98融合变异的AML患者的一个新的合理的治疗选择。

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    2020-05-05 zhouqu_8
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    2020-05-05 licz0427
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    2020-05-05 shizhenshan

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