Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer

被引:877
作者
Wang, SY
Gao, J
Lei, QY
Rozengurt, N
Pritchard, C
Jiao, J
Thomas, GV
Li, G
Roy-Burman, P
Nelson, PS
Liu, X
Wu, H [5 ]
机构
[1] Univ Calif Los Angeles, Sch Med, Dept Mol & Med Pharmacol, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA
[3] Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98109 USA
[4] Univ So Calif, Keck Sch Med, Dept Pathol, Los Angeles, CA 90033 USA
[5] Univ Calif Los Angeles, Sch Med, Howard Hughes Med Inst, Los Angeles, CA 90095 USA
关键词
D O I
10.1016/S1535-6108(03)00215-0
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The murine Pten prostate cancer model described in this study recapitulates the disease progression seen in humans: initiation of prostate cancer with prostatic intraepithelial neoplasia (PIN), followed by progression to invasive adenocarcinoma, and subsequent metastasis with defined kinetics. Furthermore, while Pten null prostate cancers regress after androgen ablation, they are capable of proliferating in the absence of androgen. Global assessment of molecular changes caused by homozygous Pten deletion identified key genes known to be relevant to human prostate cancer, including those "signature" genes associated with human cancer metastasis. This murine prostate cancer model provides a unique tool for both exploring the molecular mechanism underlying prostate cancer and for development of new targeted therapies.
引用
收藏
页码:209 / 221
页数:13
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