據(jù)日本媒體8月8日報道,，日本研究人員在最新出版的《細胞—干細胞》（Cell Stem Cell）雜志上發(fā)表報告說，他們發(fā)現(xiàn)了導(dǎo)致急性白血病復(fù)發(fā)的一個基因,，如果能找到抑制該基因發(fā)揮作用的方法,，就有可能防止急性白血病的復(fù)發(fā)。
急性白血病患者中有70%到80%的人都會復(fù)發(fā),。其原因是數(shù)量極少的白血病干細胞反復(fù)分裂，使白血病細胞大量增殖,?？拱┧幬镫m然能夠殺滅白血病細胞,，但難以殺滅其中的白血病干細胞，造成急性白血病屢治屢發(fā),。東京大學(xué)教授黑川峰夫等人注意到,，急性白血病復(fù)發(fā)患者體內(nèi)的基因“Evi－1”在造血干細胞中非常活躍,，他們推測這一基因可能同樣作用于白血病干細胞,，使其不斷分裂，導(dǎo)致白血病細胞大量增殖,。
研究小組從患白血病的實驗鼠體內(nèi)取出白血病細胞,，去除了“Evi－1”基因后再移植到10只健康實驗鼠體內(nèi)。研究小組還給另外10只健康實驗鼠完整移植了白血病細胞（含“Evi－1”）,。結(jié)果發(fā)現(xiàn),，前一組實驗鼠比后一組實驗鼠平均晚發(fā)病一個月；而在殺滅兩組實驗鼠體內(nèi)的白血病細胞后,，前一組實驗鼠沒有復(fù)發(fā)急性白血病,，后一組卻再次發(fā)病。 （Bioon.com）
研究人員認為,，對照實驗已經(jīng)說明,，“Evi－1”對急性白血病的發(fā)作和復(fù)發(fā)有推動作用，而這與它作用于白血病干細胞有直接關(guān)系,。（生物谷Bioon.com）
生物谷推薦原始出處：
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
[email protected]
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.
