Comparative gene expression profiling analysis of urothelial carcinoma of the renal pelvis and bladder
1 Laboratory of Cancer Genetics, Van Andel Research Institute, 333 Bostwick Avenue NE, Grand Rapids, MI 49503, USA
2 Laboratory of Computational Biology, Van Andel Research Institute, 333 Bostwick Avenue NE, Grand Rapids, MI 49503, USA
3 Department of Pathology, Northwestern University, Feinberg School of Medicine, 251 E. Huron, Chicago, Illinois 60611, USA
4 NCCS-VARI Translational Research Laboratory, National Cancer Centre, 11 Hospital Drive, Singapore 169610
5 Pathology and Laboratory Medicine Institute, Glickman Urological and Kidney Institute, Genomic Medicine Institute and Taussig Cancer Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA
6 Center for Systems and Computational Biology, The Wistar Institute, Philadelphia, PA 19104, USA
BMC Medical Genomics 2010, 3:58 doi:10.1186/1755-8794-3-58Published: 15 December 2010
Urothelial carcinoma (UC) can arise at any location along the urothelial tract, including the urethra, bladder, ureter, or renal pelvis. Although tumors arising in these various locations have similar morphology, it is unclear whether the gene expression profiles are similar between the upper-tract (ureter and renal pelvis) and lower-tract (bladder and urethra) carcinomas. Because differences may facilitate different screening and treatment modalities, we sought to examine the relationship between urothelial carcinoma of the renal pelvis (rUC) and urothelial carcinoma of the bladder (bUC).
Fresh tumor tissue was collected from patients with bUC (n = 10) and benign mucosa from the bladder of individuals undergoing resection for non-UC conditions (n = 7). Gene expression profiles from these samples were determined using high-throughput Affymetrix gene expression microarray chips. Bioinformatic approaches were used to compare the gene expression profiles of these samples with those of rUC samples and normal kidney samples that had been described previously.
Using unsupervised analytic approaches, rUC and bUC were indistinguishable. Yet when a supervised analytic approach was used, a small number of differentially expressed genes were identified; these differences were most likely limited to a single pathway--the chloride ion binding activity pathway--which was more frequently activated in rUC than in bUC.
We found that the gene expression profiles of UCs from the upper and lower tract were extremely similar, suggesting that similar pathogenic mechanisms likely function in the development of these tumors. The differential expression of genes in the identified pathway may represent a new avenue for detection of upper-tract tumors.