复旦高材生Cancer Cell文章

【字体: www.ebiotrade.com 时间:2009年06月12日 来源:生物通

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  生物通报道,密歇根大学医学院内科学系分子医学与遗传学分部,细胞与发育生物学系,病理系的研究人员在最新一期的Cancer Cell发表p53与脑瘤研究进展,Expression of Mutant p53 Proteins Implicates a Lineage Relationship between Neural Stem Cells and Malignant Astrocytic Glioma in a Murine Model。

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生物通报道,密歇根大学医学院内科学系分子医学与遗传学分部,细胞与发育生物学系,病理系的研究人员在最新一期的Cancer Cell发表p53与脑瘤研究进展,Expression of Mutant p53 Proteins Implicates a Lineage Relationship between Neural Stem Cells and Malignant Astrocytic Glioma in a Murine Model

 

文章通讯作者朱源(Yuan Zhu,生物通译),早年毕业于复旦大学,毕业当年获复旦大学优秀毕业生奖,后赴美深造,现任密歇根大学医学院内科学和细胞发育生物学系助理教授。

 

近期,人类成胶质细胞瘤的发病机制研究获得进展,鉴定出了一系列发病基因和核心发病路径。然而,这些基因是个别的发生突变还是系列的发生突变导致肿瘤的发生,这一机制一直了解很少。研究者对成胶质细胞瘤的癌细胞的起源也十分感兴趣。

 

P53基因被喻为是人类癌症的卫士,很多癌症的发生与p53有关联。朱源等人尝试在模式动物小鼠身上突变p53基因,结果发现p53缺乏并不影响成体脑细胞的生长发育,但是在胶质细胞瘤发生过程中会诱导多种致癌突变事件蓄积,加速肿瘤的发生。研究发现,缺乏p53首先导致脑室下区(subventricular zone,SVZ)致癌事件蓄积,接下来促进Olig2+ transit-amplifying 祖细胞样细胞增殖,导致SVZ区内发生启动胶质细胞肿瘤发生过程。

(生物通 小茜)

 

生物通推荐原文摘要:Expression of Mutant p53 Proteins Implicates a Lineage Relationship between Neural Stem Cells and Malignant Astrocytic Glioma in a Murine Model

 

Yuan Wang1,2,6,Jiong Yang1,2,6,Huarui Zheng1,2,Gerald J. Tomasek1,2,Peng Zhang1,2,Paul E. McKeever3,Eva Y.-H.P. Lee4,5andYuan Zhu1,2,,

1 Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA

2 Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA

3 Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA

4 Department of Developmental and Cell Biology, University of California, Irvine, Irvine, CA 92697, USA

5 Department of Biological Chemistry, University of California, Irvine, Irvine, CA 92697, USA

6 These authors contributed equally to this work

Summary

Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood. Further, the cell of origin of glioblastoma is largely elusive. By targeting a p53 in-frame deletion mutation to the brain, we show that p53 deficiency provides no significant growth advantage to adult brain cells, but appears to induce pleiotropic accumulation of cooperative oncogenic alterations driving gliomagenesis. Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2+ transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.

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