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Alterations in Transcription Clusters Underlie Development of Bladder Cancer Along Papillary and Nonpapillary Pathways
0022-5347/05/1744-1497/0 THE JOURNAL OF UROLOGY® Copyright © 2005 by AMERICAN UROLOGICAL ASSOCIATION
Vol. 174, 1497–1499, October 2005 Printed in U.S.A.
DOI: 10.1097/01.ju.0000175573.97783.e8
Urological Survey URO-SCIENCE Alterations in Transcription Clusters Underlie Development of Bladder Cancer Along Papillary and Nonpapillary Pathways J. H. KIM, T. TUZIAK, L. HU, Z. WANG, J. BONDARUK, M. KIM, G. FULLER, C. DINNEY, H. B. GROSSMAN, K. BAGGERLY, W. ZHANG AND B. CZERNIAK, Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, Texas Lab Invest, 85: 532–549, 2005 Bladder cancer develops in the urothelial lining from intraurothelial preneoplasia via two pathways, papillary and nonpapillary, which correspond to nonaggressive and aggressive forms of the disease. Because these two forms of cancer may develop via distinct molecular events, we examined the gene expression patterns in the development of bladder cancer from preneoplasia along papillary and nonpapillary pathways. The expression profiles of 19 pairs of RNA samples from adjacent urothelium and tumors were analyzed using cDNA microarrays. For selected genes their expressions were verified on a cohort of 251 bladder cancer patients using tissue microarray and immunohistochemistry and were related to clinicopathological parameters including follow-up data. We identified alterations in seven gene clusters controlling proliferation, differentiation, and programmed cell death that were common for papillary and nonpapillary cancer. In contrast, genes controlling cellular and stromal interactions were altered in the nonpapillary cancer. The expression levels of only two genes from this group could be used to define an aggressive form of the disease. Tumors characterized by the low expression of e-cadherin and the high expression of DNA alpha-topoisomerase II had a high propensity for distant metastasis and were associated with poor survival. Editorial Comment: The authors show differences in gene alterations between papillary and nonpapillary pathways, and also identify candidate aggressive behavior genes in bladder cancer. Timothy L. Ratliff, Ph.D.
Recent Advances in Understanding the Biology of Diabetes-Associated Bladder Complications and Novel Therapy N. YOSHIMURA, M. B. CHANCELLOR, K. E. ANDERSSON AND G. J. CHRIST, Department of Urology and Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania BJU Int, 95: 733–738, 2005 No Abstract
Molecular Prognostic Factors in Bladder Cancer M. BUSCARINI, M. L. QUEK, P. GILL, G. XIA, D. I. QUINN AND J. P. STEIN, Department of Urology, Kenneth Norris, Jr. Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, California BJU Int, 95: 739 –742, 2005 No Abstract
Cell Responses to FGFR3 Signaling: Growth, Differentiation and Apoptosis C. G. L’HOTE AND M. A. KNOWLES, Cancer Research UK Clinical Centre, St. James’s University Hospital, Leeds, United Kingdom Exp Cell Res, 304: 417– 431, 2005 FGFR3 is a receptor tyrosine kinase (RTK) of the FGF receptor family, known to have a negative regulatory effect on long bone growth. Fgfr3 knockout mice display longer bones and, accordingly, most 1497
Vol. 174, 1497–1499, October 2005 Printed in U.S.A.
DOI: 10.1097/01.ju.0000175573.97783.e8
Urological Survey URO-SCIENCE Alterations in Transcription Clusters Underlie Development of Bladder Cancer Along Papillary and Nonpapillary Pathways J. H. KIM, T. TUZIAK, L. HU, Z. WANG, J. BONDARUK, M. KIM, G. FULLER, C. DINNEY, H. B. GROSSMAN, K. BAGGERLY, W. ZHANG AND B. CZERNIAK, Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, Texas Lab Invest, 85: 532–549, 2005 Bladder cancer develops in the urothelial lining from intraurothelial preneoplasia via two pathways, papillary and nonpapillary, which correspond to nonaggressive and aggressive forms of the disease. Because these two forms of cancer may develop via distinct molecular events, we examined the gene expression patterns in the development of bladder cancer from preneoplasia along papillary and nonpapillary pathways. The expression profiles of 19 pairs of RNA samples from adjacent urothelium and tumors were analyzed using cDNA microarrays. For selected genes their expressions were verified on a cohort of 251 bladder cancer patients using tissue microarray and immunohistochemistry and were related to clinicopathological parameters including follow-up data. We identified alterations in seven gene clusters controlling proliferation, differentiation, and programmed cell death that were common for papillary and nonpapillary cancer. In contrast, genes controlling cellular and stromal interactions were altered in the nonpapillary cancer. The expression levels of only two genes from this group could be used to define an aggressive form of the disease. Tumors characterized by the low expression of e-cadherin and the high expression of DNA alpha-topoisomerase II had a high propensity for distant metastasis and were associated with poor survival. Editorial Comment: The authors show differences in gene alterations between papillary and nonpapillary pathways, and also identify candidate aggressive behavior genes in bladder cancer. Timothy L. Ratliff, Ph.D.
Recent Advances in Understanding the Biology of Diabetes-Associated Bladder Complications and Novel Therapy N. YOSHIMURA, M. B. CHANCELLOR, K. E. ANDERSSON AND G. J. CHRIST, Department of Urology and Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania BJU Int, 95: 733–738, 2005 No Abstract
Molecular Prognostic Factors in Bladder Cancer M. BUSCARINI, M. L. QUEK, P. GILL, G. XIA, D. I. QUINN AND J. P. STEIN, Department of Urology, Kenneth Norris, Jr. Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, California BJU Int, 95: 739 –742, 2005 No Abstract
Cell Responses to FGFR3 Signaling: Growth, Differentiation and Apoptosis C. G. L’HOTE AND M. A. KNOWLES, Cancer Research UK Clinical Centre, St. James’s University Hospital, Leeds, United Kingdom Exp Cell Res, 304: 417– 431, 2005 FGFR3 is a receptor tyrosine kinase (RTK) of the FGF receptor family, known to have a negative regulatory effect on long bone growth. Fgfr3 knockout mice display longer bones and, accordingly, most 1497