Elsevier

Neoplasia

Volume 10, Issue 10, October 2008, Pages 1049-1056, IN1-IN2
Neoplasia

Decoy Receptor 3 Is a Prognostic Factor in Renal Cell Cancer1,2

https://doi.org/10.1593/neo.08626Get rights and content
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open access

Abstract

BACKGROUND: Decoy receptor 3 (DcR3) is a soluble protein that binds to and inactivates the death ligand CD95L. Here, we studied a possible association between DcR3 expression and prognosis in patients with renal cell carcinomas (RCCs). METHODS: A tissue microarray containing RCC tumor tissue samples and corresponding normal tissue samples was generated. Decoy receptor 3 expression in tumors of 560 patients was examined by immunohistochemistry. The effect of DcR3 expression on disease-specific survival and progression-free survival was assessed using univariate analysis and multivariate Cox regression analysis. Decoy receptor 3 serum levels were determined by ELISA. FINDINGS: High DcR3 expression was associated with high-grade (P = .005) and high-stage (P = .048) RCCs. The incidence of distant metastasis (P = .03) and lymph node metastasis (P = .002) was significantly higher in the group with high DcR3 expression. Decoy receptor 3 expression correlated negatively with disease-specific survival (P < .001) and progression-free survival (P < .001) in univariate analyses. A multivariate Cox regression analysis retained DcR3 expression as an independent prognostic factor that outperformed the Karnofsky performance status. In patients with high-stage RCCs expressing DcR3, the 2-year survival probability was 25%, whereas in patients with DcR3-negative tumors, the survival probability was 65% (P < .001). Moreover, DcR3 serum levels were significantly higher in patients with high-stage localized disease (P = .007) and metastatic disease (P = .001). INTERPRETATION: DcR3 expression is an independent prognostic factor of RCC progression and mortality. Therefore, the assessment of DcR3 expression levels offers valuable prognostic information that could be used to select patients for adjuvant therapy studies.

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1

This work was supported by a grant from the Deutsche Krebshilfe to W.R. (German Cancer Aid, Max Eder Program), a Gerok scholarship (German Cancer Research Center) to N.W., the Tissue Bank of the National Center for Tumor Diseases Heidelberg, and National Institutes of Health grants GM079070 and DK076430 to S.K.

2

This article refers to supplementary materials, which are designated by Tables W1 to W4 and Figures W1 to W3 and are available online at www.neoplasia.com.