据日本媒体8月8日报道，日本研究人员在最新出版的《细胞—干细胞》（Cell Stem Cell）杂志上发表报告说，他们发现了导致急性白血病复发的一个基因，如果能找到抑制该基因发挥作用的方法，就有可能防止急性白血病的复发。
急性白血病患者中有70%到80%的人都会复发。其原因是数量极少的白血病干细胞反复分裂，使白血病细胞大量增殖。抗癌药物虽然能够杀灭白血病细胞，但难以杀灭其中的白血病干细胞，造成急性白血病屡治屡发。东京大学教授黑川峰夫等人注意到，急性白血病复发患者体内的基因“Evi－1”在造血干细胞中非常活跃，他们推测这一基因可能同样作用于白血病干细胞，使其不断分裂，导致白血病细胞大量增殖。
研究小组从患白血病的实验鼠体内取出白血病细胞，去除了“Evi－1”基因后再移植到10只健康实验鼠体内。研究小组还给另外10只健康实验鼠完整移植了白血病细胞（含“Evi－1”）。结果发现，前一组实验鼠比后一组实验鼠平均晚发病一个月；而在杀灭两组实验鼠体内的白血病细胞后，前一组实验鼠没有复发急性白血病，后一组却再次发病。 （Bioon.com）
研究人员认为，对照实验已经说明，“Evi－1”对急性白血病的发作和复发有推动作用，而这与它作用于白血病干细胞有直接关系。（生物谷Bioon.com）
生物谷推荐原始出处：
Cell Stem Cell，Vol 3, 207-220, 07 August 2008，usumu Goyama, Mineo Kurokawa
Evi-1 Is a Critical Regulator for Hematopoietic Stem Cells and Transformed Leukemic Cells
Susumu Goyama,1 Go Yamamoto,1 Munetake Shimabe,1 Tomohiko Sato,1 Motoshi Ichikawa,1 Seishi Ogawa,1,2,3 Shigeru Chiba,1,2 and Mineo Kurokawa1,
1 Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
2 Department of Cell Therapy and Transplantation Medicine, Graduate School of Medicine, University of Tokyo, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
3 Department of Regeneration Medicine for Hematopoiesis, Graduate School of Medicine, University of Tokyo, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
Corresponding author
Mineo Kurokawa
kurokawa-tky@umin.ac.jp
Summary
Evi-1 has been recognized as one of the dominant oncogenes associated with murine and human myeloid leukemia. Here, we show that hematopoietic stem cells (HSCs) in Evi-1-deficient embryos are severely reduced in number with defective proliferative and repopulating capacity. Selective ablation of Evi-1 in Tie2+ cells mimics Evi-1 deficiency, suggesting that Evi-1 function is required in Tie2+ hematopoietic stem/progenitors. Conditional deletion of Evi-1 in the adult hematopoietic system revealed that Evi-1-deficient bone marrow HSCs cannot maintain hematopoiesis and lose their repopulating ability. In contrast, Evi-1 is dispensable for blood cell lineage commitment. Evi-1+/− mice exhibit the intermediate phenotype for HSC activity, suggesting a gene dosage requirement for Evi-1. We further demonstrate that disruption of Evi-1 in transformed leukemic cells leads to significant loss of their proliferative activity both in vitro and in vivo. Thus, Evi-1 is a common and critical regulator essential for proliferation of embryonic/adult HSCs and transformed leukemic cells.
