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Parallel Overexpression of Survivin and Ki-67 mRNA in High-Grade Papillary Urothelial Carcinoma of the Bladder
Michael J. Schwartz, Yao-Tseng Chen, Yingbei Chen, Naoki Kitabayashi, Daniel A. Barocas, Douglas S. Scherr, New York, NY
Department of Urology, New York Presbyterian Hospital. Weill Medical College of Cornell University, New York, New York
Introduction and objective: Ki-67 is a nuclear antigen expressed during the cell cycle. Survivin is an inhibitor of apoptosis. Each has individually been shown to have prognostic value in various tumor types, but little is known about their coexpression in bladder cancer and its significance. We correlated urinary and tissue expression levels of Ki-67 and survivin mRNA with pathology from transurethral resection of bladder tumors (TURBT).
Methods: Urine and bladder tissue was collected from 13 consecutive patients undergoing TURBT. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to quantify Ki-67 and survivin mRNA in urine and tissue, and results were correlated with pathology diagnosis.
Results:Pathology results included 3 high-grade (HG) invasive lesions (T1), 5 HG non-invasive lesions (Ta), 2 carcinoma in situ, 2 non-tumors, and 1 prostate cancer. Survivin mRNA expression paralleled Ki-67 expression, both in biopsy and urine specimens. Tissue expression of survivin mRNA weakly correlated with expression in urine, and the same held true for Ki-67 (Table 1). Invasive lesions required fewer qRT-PCR cycles to reach threshold than non-invasive lesions for survivin and Ki-67, although neither reached statistical significance. Survivin and Ki-67 overexpression in invasive tumor vs. non-tumor was significant (Table 2). All samples with low survivin and Ki-67 mRNA expression showed significant inflammation or necrosis, indicating likely contamination by RNA from non-neoplastic cells or suboptimal RNA quality.
Conclusions: Survivin and Ki-67 show parallel mRNA overexpression in high-grade papillary urothelial carcinoma, particularly in invasive lesions. High survivin and Ki-67 expression in urine may also be indicative of invasive lesions. Tissue samples with carcinoma in situ are inevitably contaminated with non-neoplastic cells and these samples, as well as any tissue sample with a significant non-neoplastic component, cannot be effectively evaluated with this methodology. Our results identify survivin and Ki-67, particularly when evaluated simultaneously, as potential markers in tissue samples and possibly in urine. A larger scale analysis to validate these results is warranted.
