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发表于 2010-5-27 15:17 |显示全部帖子
下次发的时候请把文章标题以及摘要都贴出来,方便读者筛选信息。谢谢
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Cancer Cell. 2010 May 18;17(5):497-509.) x- F3 |. Q, ~5 J1 {# V
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PLAGL2 regulates Wnt signaling to impede differentiation in neural stem cells and gliomas." N) U: s! {! v, M/ h6 m# ~7 w
Zheng H, Ying H, Wiedemeyer R, Yan H, Quayle SN, Ivanova EV, Paik JH, Zhang H, Xiao Y, Perry SR, Hu J, Vinjamoori A, Gan B, Sahin E, Chheda MG, Brennan C, Wang YA, Hahn WC, Chin L, DePinho RA.
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Belfer Institute for Applied Cancer Science, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
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Cancer Cell. 2010 May 18;17(5):417-8. * h4 m/ F, `- |' o2 P8 A% ?

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A hallmark feature of glioblastoma is its strong self-renewal potential and immature differentiation state, which contributes to its plasticity and therapeutic resistance. Here, integrated genomic and biological analyses identified PLAGL2 as a potent protooncogene targeted for amplification/gain in malignant gliomas. Enhanced PLAGL2 expression strongly suppresses neural stem cell (NSC) and glioma-initiating cell differentiation while promoting their self-renewal capacity upon differentiation induction. Transcriptome analysis revealed that these differentiation-suppressive activities are attributable in part to PLAGL2 modulation of Wnt/beta-catenin signaling. Inhibition of Wnt signaling partially restores PLAGL2-expressing NSC differentiation capacity. The identification of PLAGL2 as a glioma oncogene highlights the importance of a growing class of cancer genes functioning to impart stem cell-like characteristics in malignant cells. (c) 2010 Elsevier Inc. All rights reserved.. A% L# v% f. d1 R$ |6 u0 l! M5 E
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PMID: 20478531 [PubMed - in process]
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