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Blood:糖皮质激素可增强FLT3抑制剂的抗FLT3突变型AML活性

2020-08-10 MedSci原创 MedSci原创

用 FLT3抑制剂治疗FLT3-ITD AML可导致持续耐药患者(DTPs)的炎症通路上调; 抗炎糖皮质激素联合FLT3抑制剂可通过上调BIM和下调MCL-1来减少DTPs。

FLT3是一种频发突变的基因,与急性髓系白血病(AML)的预后不良密切相关。虽然大多数AML患者最初对FLT3抑制剂治疗有反应,但最终会因耐药而复发。目前,FLT3抑制剂的耐药性产生机制以及对促进细胞存活的药物初步反应尚不清楚。

近期研究表明,短暂维持的药物敏感细胞亚群,即所谓的耐药持续者(DTP),可以在即使缺乏耐药性突变的情况下从细胞毒性药物暴露中存活下来。通过RNA测序和药物筛选,Gebru等发现,用选择性FLT3抑制剂奎扎替尼(quizartinib)处理FLT3-ITD AML细胞,上调了DTPs的炎症基因,从而增强了其对抗炎糖皮质激素的敏感性。

在机制上,FLT3抑制剂和糖皮质激素的联合使用通过糖皮质激素依赖性受体上调促凋亡蛋白BIM和抗凋亡蛋白MCL-1的蛋白酶体降解,从而增强FLT3突变细胞的细胞死亡,且不影响野生型细胞的存活。此外,研究人员还在原发性AML患者样本和异种移植小鼠模型中证实了奎扎替尼和地塞米松联合应用时的抗白血病活性有所增强。

总而言之,本研究表明,FLT3抑制剂和糖皮质激素联合使用有可能消除DTPs,从而防止FLT3突变型AML的微小残留病灶、突变耐药和复发。

原始出处:

Gebru Melat T,Atkinson Jennifer M,Young Megan et al. Glucocorticoids enhance the anti-leukemic activity of FLT3 inhibitors in FLT3 mutant acute myeloid leukemia. Blood, 2020.

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    2021-06-12 jklm09
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    2020-08-12 fengyi816
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