多國研究人員發(fā)現(xiàn),，抑制一種基因發(fā)揮作用可以激活慢性骨髓性白血病患者體內(nèi)生成癌細(xì)胞的干細(xì)胞，使其變得容易受藥物攻擊,。這一成果為白血病以及其他癌癥的治療提供了新思路,。
白血病俗稱血癌，是一種造血系統(tǒng)惡性腫瘤,。慢性骨髓性白血病患者體內(nèi)生成癌細(xì)胞的干細(xì)胞通常處于潛伏期,，幾乎不發(fā)生增殖，因此藥物很難對其奏效,。
日本,、美國和意大利研究人員在１９日出版的《自然》雜志上發(fā)表報(bào)告說，他們從日本和美國８０余名慢性骨髓性白血病患者的骨髓中提取樣本進(jìn)行分析后發(fā)現(xiàn),，凡是一種名為ＰＭＬ的基因表達(dá)活躍的患者,，其體內(nèi)生成癌細(xì)胞的干細(xì)胞基本上都處于休眠狀態(tài)，抗癌藥物難以對它們發(fā)揮作用,。
研究還顯示,，患病實(shí)驗(yàn)鼠被人為去除ＰＭＬ基因后，其體內(nèi)生成癌細(xì)胞的干細(xì)胞變得活躍,。研究人員由此認(rèn)為,，ＰＭＬ基因可抑制生成癌細(xì)胞的干細(xì)胞的活動。
研究人員進(jìn)一步給患白血病的實(shí)驗(yàn)鼠服用抑制ＰＭＬ基因的三氧化二砷,，再用抗癌藥物對實(shí)驗(yàn)鼠進(jìn)行治療,。結(jié)果發(fā)現(xiàn)，實(shí)驗(yàn)鼠體內(nèi)生成癌細(xì)胞的干細(xì)胞以及其他白血病細(xì)胞全部消失,，而且白血病沒有復(fù)發(fā),。
研究人員認(rèn)為，除白血病外,，其他癌癥患者體內(nèi)生成癌細(xì)胞的干細(xì)胞可能也具有休眠的性質(zhì),。他們下一步準(zhǔn)備對其他癌癥患者進(jìn)行相關(guān)的臨床試驗(yàn)。（生物谷援引新華網(wǎng)）
生物谷推薦原始出處：
Nature. 2008 Jun 19;453(7198):1072-8. Epub 2008 May 11
PML targeting eradicates quiescent leukaemia-initiating cells
Ito K, Bernardi R, Morotti A, Matsuoka S, Saglio G, Ikeda Y, Rosenblatt J, Avigan DE, Teruya-Feldstein J, Pandolfi PP.
Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Department of Medicine, Harvard Medical School, New Research Building, 330 Brookline Avenue, Boston, Massachusetts 02215, USA.
The existence of a small population of 'cancer-initiating cells' responsible for tumour maintenance has been firmly demonstrated in leukaemia. This concept is currently being tested in solid tumours. Leukaemia-initiating cells, particularly those that are in a quiescent state, are thought to be resistant to chemotherapy and targeted therapies, resulting in disease relapse. Chronic myeloid leukaemia is a paradigmatic haematopoietic stem cell disease in which the leukaemia-initiating-cell pool is not eradicated by current therapy, leading to disease relapse on drug discontinuation. Here we define the critical role of the promyelocytic leukaemia protein (PML) tumour suppressor in haematopoietic stem cell maintenance, and present a new therapeutic approach for targeting quiescent leukaemia-initiating cells and possibly cancer-initiating cells by pharmacological inhibition of PML.
PMID: 18469801 [PubMed - in process]
