Defining aggressive prostate cancer using a 12-gene model

被引:88
作者
Bismar, Tarek A.
Demichelis, Francesca
Riva, Alberto
Kim, Robert
Varambally, Sooryanarayana
He, Le
Kutok, Jeff
Aster, Jonathan C.
Tang, Jeffery
Kuefer, Rainer
Hofer, Matthias D.
Febbo, Phillip G.
Chinnaiyan, Arul M.
Rubin, Mark A.
机构
[1] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Cambridge, MA 02138 USA
[3] ITC Irst, SRA Div, Trento, Italy
[4] Univ Trent, Dept Informat & Commun Technol, Trento, Italy
[5] Childrens Hosp, Informat Program, Boston, MA 02115 USA
[6] Univ Michigan, Dept Pathol & Urol, Ann Arbor, MI 48109 USA
[7] Univ Hosp, Ulm, Germany
[8] Dana Farber Canc Inst, Boston, MA 02115 USA
来源
NEOPLASIA | 2006年 / 8卷 / 01期
关键词
metastasis; cancer; proteomics; prostate cancer; bioinformatics;
D O I
10.1593/neo.05664
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The critical clinical question in prostate cancer research is: How do we develop means of distinguishing aggressive disease from indolent disease? Using a combination of proteomic and expression array data, we identified a set of 36 genes with concordant dysregulation of protein products that could be evaluated in situ by quantitative immunohistochemistry. Another five prostate cancer biomarkers were included using linear discriminant analysis, we determined that the optimal model used to predict prostate cancer progression consisted of 12 proteins. Using a separate patient population, transcriptional levels of the 12 genes encoding for these proteins predicted prostate-specific antigen failure in 79 men following surgery for clinically localized prostate cancer (P=.0015). This study demonstrates that cross-platform models can lead to predictive models with the possible advantage of being more robust through this selection process.
引用
收藏
页码:59 / 68
页数:10
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