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寻找可防止白血病复发的干细胞

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发表于 2012-4-6 22:55 |显示全部帖子
   科学日报(2012.4.5) --研究者们在<Cell>出版的一个期刊四月份的<Cell Stem Cell>上报道说已经发现一种能够阻断白血病干细胞的路径的方法。老鼠实验进一步表明联合治疗的路径可能会使慢性粒细胞白血病突然好转。
: t7 k0 m1 V, U* a1 ?/ f6 t' v/ C   和大部分的服用了一些药物,比如像而今的伊马替尼(亦称做格到),慢性粒细胞白血病的病人不同,那些人们的病情经常是刚要缓解一下,不料却发现他们的癌症又复发了。那些留下的白血病干细胞顽强的抵御着现有的治疗方式,才导致癌症又得以重现。
! ~! M' A1 q/ ]" S; g+ k+ i   “伊马替尼能抑制癌蛋白(它能够导致慢性粒细胞白血病),它缓解病情的效果简直令人难以置信,”  哈佛大学医学院的斯科特.阿姆斯特朗说,“但是有一个越来越明显的迹象就是它并不对付绝大多数的未成熟的癌细胞。问题就是:我们如何来根除那些细胞?”/ |! p8 o7 Z6 U, V
这篇《Cell Stem Cell 》的研究集中在的血液干细胞发展中的一个广为人知的重要时期上,但不是成年期。这些在老鼠身上的新发现表明白血病干细胞依靠它们早期发展的路径可以得以恢复。; Q( ?% i- G7 y# ~: k
    这就使得对所谓的靶向针对β-连环蛋白路径的治疗容易攻击到白血病干细胞,在某种程度上正常血干细胞则不能做到。这个现象表明伊马替尼加上亏损的β-连环蛋白能够帮助防止疾病再次发生。给予老鼠的β-连环蛋白抑制剂也帮助清除掉白血病干细胞,就像是已经应用了缓解疼痛的药物一样能间接的降低β-连环蛋白的水平。7 _, o1 M7 Q) [
    阿姆斯特朗说为了确定β-连环蛋白的阻断剂在人体内能够像在老鼠体内一样的工作还有更多的工作需要做。如果是这样,很可能慢性粒细胞白血病的患者就不是仅有的甚至不是第一批从这种新的治疗方法中获益的。
. Z6 j* o5 s) C5 A) A   “这个很需要时间,因为慢性粒细胞白血病的人们已经做的足够好了,”他说到。但是β-连环蛋白抑制剂可能只是医生们对付一些其他的更难以治愈的白血病种类时才会用到,或者是结肠癌,或者是用在那些变得严重的慢性粒细胞白血病的人们。' x: _1 r# L9 E+ C# Y
    “需要说明的是这种方法对白血病而言是很重要的,但是并不适用于正常细胞。”阿姆斯特朗说,“它给了我们一种治愈的希望”一种作用于β-连环蛋白的药物可能一次就正好能够就把白血病连同它的干细胞除掉,而不会伤害到正常的血液干细胞# X" _. f) v7 T6 I% a: |( l
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2 f- U+ V( p; k7 u, u3 M7 X( V附原文:
, O8 d6 u- C# @- x  R) {To Prevent Leukemia's Dreaded Return, Go for the Stem Cells
! v! B& b8 h) S2 k/ I5 P9 q& F  pScienceDaily (Apr. 5, 2012) — Researchers reporting in the April Cell Stem Cell, a Cell Press publication, have found a way to stop leukemia stem cells in their tracks. The advance in mice suggests that a combination approach to therapy might stamp out chronic myeloid leukemia (CML) for good.# q8 j$ C* v" ]$ C0 w+ {8 l  R2 a

" y* r% |+ w$ I) I+ o, SThat's in contrast to the vast majority of CML patients taking drugs like imatinib (aka Gleevec) today, who often go into remission only to see their cancer return again. It is those lingering leukemia stem cells, which stubbornly resist existing therapies, that fuel the cancer's comeback.
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! l/ V7 o7 Y% `& w1 U- ~% Y"Imatinib inhibits the oncoprotein [that drives CML] and it is incredibly effective at putting patients into remission," said Scott Armstrong of Harvard Medical School. "But there is growing evidence that this doesn't rid the body of the most immature cancer cells. The question is: How can we eradicate those cells?"
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# q7 R' N$ v' u6 U1 @The Cell Stem Cell study focused on a pathway known to be important in blood stem cells during development but not in adulthood. The new findings in mice suggest that leukemia stem cells revert back to their dependence on that early developmental pathway.- X. v7 q2 ^9 m; i- v7 i

( r" e! l' ^6 z: L6 |6 jThat leaves leukemia stem cells vulnerable to treatments aimed at the so-called β-catenin pathway in a way that normal blood stem cells aren't. The evidence shows that imatinib plus the loss of β-catenin can help to prevent recurrence of the disease. β-catenin inhibitors given to mice also helped to eliminate leukemia stem cells, as did a pain-relieving drug already in use that lowers β-catenin levels, if indirectly.  e4 ^- e- ~7 d
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Armstrong says there is more work to do to ensure that β-catenin blockers would work in the same way in humans that they do in the mice. If so, it's likely CML patients won't be the only or even the first to gain from the new treatment strategy.8 j" R& s8 X9 z9 P. B# H

- V7 e* _# z! D( P"It will take time because people with CML already do pretty well," he says. But β-catenin inhibitors might be just what the doctor ordered in the case of some other, harder-to-treat forms of leukemia, in colon cancer, or perhaps in patients who have entered an acute stage of CML.
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7 G* ~" n$ |6 B8 L0 I. K"The appeal is that this pathway is important for the leukemia, but not for normal cells," Armstrong says. "It gives us an angle for therapy." A drug targeted at β-catenin might just get rid of leukemia and its stem cells once and for all, while leaving healthy blood stem cells unscathed.
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5 i$ p( x$ D& Phttp://www.sciencedaily.com/releases/2012/04/120405131417.htm
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