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Advances in Urology
Volume 2014, Article ID 184602, 6 pages
http://dx.doi.org/10.1155/2014/184602
Research Article

IL1RN and KRT13 Expression in Bladder Cancer: Association with Pathologic Characteristics and Smoking Status

1Department of Urology, Mannheim Medical Center, University of Heidelberg, Theodor-Kutzer-Ufer 1–3, 68167 Mannheim, Germany
2Department for Statistical Analysis, Mannheim Medical Center, University of Heidelberg, Mannheim, Germany

Received 27 February 2014; Revised 23 June 2014; Accepted 26 June 2014; Published 8 July 2014

Academic Editor: Matthew Nielsen

Copyright © 2014 Thomas S. Worst et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Purpose. To validate microarray data on cytokeratin 13 (KRT13) and interleukin-1 receptor antagonist (IL1RN) expression in urothelial carcinoma of the urinary bladder (UCB) and to correlate our findings with pathologic characteristics and tobacco smoking. Methods. UCB tissue samples ( ) and control samples ( ) were obtained from transurethral resection and radical cystectomy specimens. Immunohistochemical staining of KRT13 and IL1RN was performed and semiquantitative expression scores were assessed. Smoking status was evaluated using a standardized questionnaire. Expression scores were correlated with pathologic characteristics (tumor stage and grade) and with smoking status. Results. Loss of KRT13 and IL1RN expression was observed in UCB tissue samples when compared to controls ( , ) in which KRT13 and IL1RN expression were high. IL1RN expression was significantly reduced in muscle-invasive tumors ( ). In tissue samples of current smokers, a significant downregulation of IL1RN was found when compared to never smokers ( ). Conclusion. Decreased expressions of KRT13 and IL1RN are common features of UCB and are associated with aggressive disease. Tobacco smoking may enhance the loss of IL1RN, indicating an overweight of proinflammatory mediators involved in UCB progression. Further validation of the influence of smoking on IL1RN expression is warranted.