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慢性骨髓性白血病干细胞池受到PPARγ激动剂的侵蚀

Stéphane Prost¹, Francis Relouzat¹, Marc Spentchian²

¹CEA, Institute of Emerging Diseases and Innovative Therapies (iMETI), F-92265 Fontenay-aux-Roses, France.

|September 3, 2015

概括

抗糖尿病药物glitazones可帮助消除慢性骨髓性白血病 (CML) 的休眠癌症干细胞,如果与氨酸激酶抑制剂结合使用. 在CML患者中,这种方法可能会导致持续的完整分子反应.

科学领域:

血液学
癌症生物学
药理学

背景情况:

癌症干细胞假设表明由于无法根除这些细胞而复发.
慢性髓性白血病 (CML) 的特征是BCR-ABL瘤蛋白.
氨酸激酶抑制剂 (TKIs) 提高了生存率,但很少达到完整的分子反应 (CMR).

研究的目的:

调查glitazones是否可以消除静止的CML白血病干细胞 (LSC).
确定glitazones是否可以增强TKI治疗以实现CMR.

主要方法:

使用glitazones激活过氧体增殖器激活受体马 (PPARγ).
评估PPARγ激活对CMLLSC中的STAT5,HIF2α和CITED2表达的影响.
临床试验涉及使用伊马替尼和皮奥格利塔治疗的慢性残留病患者.

主要成果:

PPARγ的glitazone激活降低了STAT5,HIF2α和CITED2的表达,这是LSC静止的关键.
三名接受临时pioglitazone和imatinib治疗的CML患者获得了持续的CMR.
在停止使用皮奥格利塔后,持续的CMR持续长达4. 7年.

结论:

格利塔松可以逐渐清除剩余的CMLLSC池.
用TKIs和glitazones进行组合治疗可以通过向LSC来消除癌症.
这一策略为实现CML完整分子反应提供了潜在的途径.

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