Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis

被引:0
|
作者
Jennifer C King
Jin Xu
John Wongvipat
Haley Hieronymus
Brett S Carver
David H Leung
Barry S Taylor
Chris Sander
Robert D Cardiff
Suzana S Couto
William L Gerald
Charles L Sawyers
机构
[1] Human Oncology and Pathogenesis Program,Department of Physiology and Biophysics
[2] Memorial Sloan-Kettering Cancer Center,Department of Pathology and Laboratory Medicine
[3] Computational and Systems Biology Center,undefined
[4] Memorial Sloan-Kettering Cancer Center,undefined
[5] Weill Medical College of Cornell University,undefined
[6] Center for Comparative Medicine,undefined
[7] University of California,undefined
[8] Laboratory of Comparative Pathology,undefined
[9] Memorial Sloan-Kettering Cancer Center,undefined
[10] Howard Hughes Medical Institute,undefined
[11] Memorial Sloan-Kettering Cancer Center,undefined
来源
Nature Genetics | 2009年 / 41卷
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学科分类号
摘要
Charles Sawyers and colleagues report that mice expressing a TMPRSS2-ERG fusion develop prostatic intraepithelial neoplasia, but only in the context of PI3-kinase pathway activation mediated by either Pten loss or Akt activation. They also find that human TMPRSS2-ERG–positive tumors are enriched for PTEN loss, suggesting that these two events cooperate in human prostate tumorigenesis.
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页码:524 / 526
页数:2
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