Analysis of leukemia stem cell regulation by leukemia oncogene Evi-1

白血病癌基因Evi-1对白血病干细胞的调控分析

• 批准号: 21890055
• 负责人: SATO Tomohiko
• 金额: $ 1.66万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Research Activity Start-up
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-21890055/
• 关键词: 癌; 白血病; 幹細胞

We have recently generated Evi-1-GFP knock-in mice, which can trace Evi1 mRNA level in vivo, and we revealed that Evi-1 is highly expressed at both fetal and adult hematopoietic stem cells (HSCs). In addition, we also clarified that Evi-1 positive murine HSC (KSL) function as long-term HSC by bone marrow transplantation assay, and that Evi-1 can mark long-term HSC which is the most immature hematopoietic cells. (These data are now on submission) Next, for the analysis of leukemia stem cell regulation by Evi-1, we made chronic myeloid leukemia (CML) mouse of Evi-1-GFP knockin origin by using BCR-ABL oncogene. We revealed that Evi-1 positive KSL cells had highest Evi-1 expression in these model mice which implied that Evi-1 could regulate CML stem cells. Our original analysis of leukemia stem cell is still ongoing for the purpose of establishing specific therapy of CML stem cells.

我们最近建立了Evi-1-GFP敲入小鼠，可以在体内追踪Evi1的mRNA水平，我们发现Evi-1在胎儿和成人的造血干细胞(HSCs)中都有高表达。此外，我们还通过骨髓移植实验明确了Evi-1阳性的小鼠HSC(KSL)具有长期HSC的功能，并且Evi-1可以标记长期HSC作为最不成熟的造血细胞。接下来，为了分析EVI-1对白血病干细胞的调控，我们利用bcr-abl癌基因构建了EVI-1-GFP敲击源的慢性粒细胞白血病(CML)小鼠。我们发现，在这些模型小鼠中，Evi-1阳性的KSL细胞表达最高，提示Evi-1对CML干细胞具有调节作用。我们最初对白血病干细胞的分析仍在进行中，目的是为了建立CML干细胞的特异性治疗。

项目成果

Evi1 expression marks long-term repopulating hematopoietic stem cells.

Evi1 表达标志着造血干细胞的长期再生。

• 发表时间: 2010
• 作者: Keisuke Kataoka;Tomohiko Sato;Akihide Yoshimi;Susumu Goyama;Shunya Arai;Yoichi Imai;Katsuyoshi Kumagai;Naoto Kubota;Takashi Kadowaki;Mineo Kurokawa
• 通讯作者: Mineo Kurokawa

Evi1 Is a Stem Cell-Specific Regulator of Self-Renewal Capacity In the Definitive Hematopoietic System

Evi1 是决定性造血系统中自我更新能力的干细胞特异性调节因子

• 发表时间: 2010
• 作者: Keisuke Kataoka;Tomohiko Sato;Akihide Yoshimi;Susumu Goyama;Takako Tsuruta;Shunya Arai;Yoichi Imai;Katsuyoshi Kumagai;Naoto Kubota;Takashi Kadowaki;Mineo Kurokawa
• 通讯作者: Mineo Kurokawa

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