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PNAS:选择性清除急性骨髓性白血病干细胞的潜在新药

2013-03-26 何嫱 生物通

来自上海交通大学、中科院等处的研究人员在新研究中发现了一种可选择性清除急性骨髓性白血病干细胞的潜在药物,从而为改善急性髓细胞白血病患者的治疗预后指出了一条有前景的治疗途径。相关论文发表在3月19日的《美国科学院》(PNAS)上。 来自上海交通大学医学院的陈竺(Zhu Chen)院士、王侃侃(Kan-Kan Wang)研究员和张济(Ji Zhang)研究员是这篇文章的共同通讯作者。陈竺院士3月份刚

来自上海交通大学、中科院等处的研究人员在新研究中发现了一种可选择性清除急性骨髓性白血病干细胞的潜在药物,从而为改善急性髓细胞白血病患者的治疗预后指出了一条有前景的治疗途径。相关论文发表在3月19日的《美国科学院》(PNAS)上。

来自上海交通大学医学院的陈竺(Zhu Chen)院士、王侃侃(Kan-Kan Wang)研究员和张济(Ji Zhang)研究员是这篇文章的共同通讯作者。陈竺院士3月份刚刚卸任卫生部长,以新任中国农工民主党主席身份当选为全国人大常委会副委员长,从而步入国家领导人行列。这篇文章是2013年头3个月里陈院士实验室参与发表的第三篇PNAS文章。

急性骨髓性白血病(Acute myeloid leukemia,AML),是一种骨髓性白细胞(而非淋巴性白细胞)异常增殖的血癌。其特点是骨髓内异常细胞的快速增殖而影响了正常血细胞的产生。急性骨髓性白血病是成年人最常见的急性白血病,我国AML的年发病率是1.62/100000,近年来有增加的趋势,且有越来越多的患者死于该病。

近年来大量的研究表明,白血病患者体内存在一群极微量的细胞群,约占所有白血病细胞的0.1%-1%,这些细胞在白血病的发病及进展中扮演着重要的角色,且由于这些细胞通常对化疗药物不敏感,也是导致白血病复发的罪魁祸首。科学家们将这群白血病细胞称之为白血病干细胞(Leukemia stem cells ,LSCs),认为其可能是治疗干预的一个重要的靶点。然而目前能够靶向LSCs,减慢急性髓细胞性白血病(AML)进程的药物相对较少。

基于体内外研究数据,研究人员在这篇新文章中报告称,一种耐受良好的维生素A衍生物:芬维A铵能够以生理上可实现的浓度清除LSCs,而不影响造血祖/干细胞。芬维A铵能够对于原发AML CD34+细胞,尤其是富含LSC的CD34+CD38-细胞亚群产生一种选择性毒性效应,而对于正常的细胞则没有明显的影响。

通过甲基纤维素克隆形成分析,研究人员进一步证明芬维A铵显着抑制了AML CD34+细胞源性的克隆形成,而不影响正常CD34+细胞。此外,在一个非肥胖性糖尿病/严重联合性免疫缺陷病(SCID)小鼠异种移植模型中,研究人员证实芬维A铵能够显着减少AML干细胞的移植而不影响正常造血干细胞。在进一步的机制研究中,研究人员揭示芬维A铵诱导的细胞死亡与一系列特征性的事件相关,包括活性氧簇快速形成,诱导与应激反应和凋亡相关的基因,以及抑制与NF-κB和Wnt信号相关的基因。进一步的生物信息学分析表明,芬维A胺下调基因与AML患者不良预后显着相关。

基于这些研究结果,研究人员提出芬维A胺是一种选择性靶向LSCs的有效药物,由此为AML治疗提供了一种有潜力的治疗策略。 

急性骨髓性白血病相关的拓展阅读:

doi:10.1002/smll.201202503

Preferential eradication of acute myelogenous leukemia stem cells by fenretinide

Zhang H, Mi JQ, Fang H, Wang Z, Wang C, Wu L, Zhang B, Minden M, Yang WT, Wang HW, Li JM, Xi XD, Chen SJ, Zhang J, Chen Z, Wang KK.

Leukemia stem cells (LSCs) play important roles in leukemia initiation, progression, and relapse, and thus represent a critical target for therapeutic intervention. However, relatively few agents have been shown to target LSCs, slowing progress in the treatment of acute myelogenous leukemia (AML). Based on in vitro and in vivo evidence, we report here that fenretinide, a well-tolerated vitamin A derivative, is capable of eradicating LSCs but not normal hematopoietic progenitor/stem cells at physiologically achievable concentrations. Fenretinide exerted a selective cytotoxic effect on primary AML CD34+ cells, especially the LSC-enriched CD34+CD38- subpopulation, whereas no significant effect was observed on normal counterparts. Methylcellulose colony formation assays further showed that fenretinide significantly suppressed the formation of colonies derived from AML CD34+ cells but not those from normal CD34+ cells. Moreover, fenretinide significantly reduced the in vivo engraftment of AML stem cells but not normal hematopoietic stem cells in a nonobese diabetic/SCID mouse xenotransplantation model. Mechanistic studies revealed that fenretinide-induced cell death was linked to a series of characteristic events, including the rapid generation of reactive oxygen species, induction of genes associated with stress responses and apoptosis, and repression of genes involved in NF-κB and Wnt signaling. Further bioinformatic analysis revealed that the fenretinide-down-regulated genes were significantly correlated with the existing poor-prognosis signatures in AML patients. Based on these findings, we propose that fenretinide is a potent agent that selectively targets LSCs, and may be of value in the treatment of AML.

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    2013-10-26 drwjr
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    2013-03-28 zhouqu_8

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