Dynamic and transient cancer stem cells nurture melanoma.
Dynamic and transient cancer stem cells nurture melanoma.
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DOI：
10.1038/nm0710-758
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发表时间：
2010-07
期刊：
影响因子：
82.9
通讯作者：
Rich J
中科院分区：
文献类型：
--
作者：
Weinberg R;Fisher DE;Rich J
一种流行且有争议的理论是，肿瘤是由一群固定的干细胞样瘤细胞发起和维持的。对人类细胞和老鼠的研究为这一理论增加了一个转折，表明这种干细胞样细胞可能比之前认为的更具可塑性。Alexander Roesch等人。发现一组分裂缓慢的细胞可以维持黑色素瘤的生长和自我更新--这是癌症干细胞的特征。然而，细胞可以通过组蛋白修饰物JARID1B介导的表观遗传变化来转换表型，这表明了一种可塑性过程。他们发现，表达JAR1D1B的人类细胞在移植到小鼠体内时可以启动和维持黑色素瘤的生长，而JARD1B阴性的细胞只能启动肿瘤。然而，JARD1B阴性的细胞可以激活JARD1B来支持肿瘤的生长。癌症干细胞可能是“移动的”靶子吗？那么，这意味着什么呢？
A popular—and controversial—theory is that tumors are initiated and maintained by a fixed population of stem cell–like tumor cells. Research on human cells and mice adds a twist to this theory, suggesting that such stem cell–like cells might be more plastic than previously thought. Alexander Roesch et al. find that a group of cells, which divide slowly, can sustain melanoma growth and self-renew—hallmarks of cancer stem cells. However, the cells can switch phenotype through epigenetic changes mediated by JARID1B, a histone modifier, suggesting a plastic process. They found that human cells expressing JAR1D1B could initiate and sustain melanoma growth when implanted into mice, whereas JARD1B-negative cells could only initiate tumors. JARD1B-negative cells, however, could switch on JARD1B to support tumor growth. Might cancer stem cells be ‘moving’ targets? What, then, are the therapeutic implications?
影响因子：
64.5
作者：
Roesch A;Fukunaga-Kalabis M;Schmidt EC;Zabierowski SE;Brafford PA;Vultur A;Basu D;Gimotty P;Vogt T;Herlyn M
通讯作者：
Herlyn M
影响因子：
64.8
作者：
Quintana, Elsa;Shackleton, Mark;Sabel, Michael S.;Fullen, Douglas R.;Johnson, Timothy M.;Morrison, Sean J.
通讯作者：
Morrison, Sean J.
影响因子：
64.5
作者：
Sharma SV;Lee DY;Li B;Quinlan MP;Takahashi F;Maheswaran S;McDermott U;Azizian N;Zou L;Fischbach MA;Wong KK;Brandstetter K;Wittner B;Ramaswamy S;Classon M;Settleman J
通讯作者：
Settleman J