Carcinogenesis Advance Access published online on December 13, 2005
Carcinogenesis, doi:10.1093/carcin/bgi310
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Cancer Research UK Clinical Centre, St James's University Hospital, Beckett Street, Leeds, LS9 7TF, United Kingdom
* To whom correspondence should be addressed. Cancer of the bladder shows divergent clinical behaviour following diagnosis and it has been proposed that 2 major groups of tumours exist that develop via different molecular pathways. Low-grade, non-invasive papillary tumours recur frequently, but patients with these tumours do not often suffer progression of disease to muscle invasion. In contrast, tumours that are invading muscle at diagnosis are aggressive and associated with significant mortality. Molecular studies have identified distinct genetic, epigenetic and expression changes in these groups. However, it is not yet clear whether there is direct progression of low-grade superficial tumours to become invasive (a Jeckell and Hyde scenario) or whether in those patients who apparently progress from one form of the disease to the other, different tumour clones are involved and that the two tumours groups are mutually exclusive ("chalk and cheese"). If the latter is true, then attempts to identify molecular markers to predict progression of low-grade superficial bladder tumours may be fruitless. Similarly, it is not clear whether other sub-groups of tumours exist that arise via other molecular pathways. There is now a large amount of molecular information about bladder cancer that facilitates examination of these possibilities. Some recent studies provide evidence for the existence of at least one further group of tumours, high-grade superficial papillary tumours, which may develop via a distinct molecular pathway. Patients with such tumours do show increased risk of disease progression and for these there may exist a real progression continuum from non-invasive to invasive. If this is the case, definition of the molecular signature of this pathway and improved understanding of the biological consequences of the events involved will be pivotal in disease management.
Received September 30, 2005
Revised November 12, 2005
Accepted December 6, 2005
REVIEW
Molecular subtypes of bladder cancer: Jekyll and Hyde or chalk and cheese?
Margaret A. Knowles 1 *
Margaret A. Knowles, E-mail: margaret.knowles{at}cancer.org.uk
Abstract 
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J. W.F. Catto, S. Miah, H. C. Owen, H. Bryant, K. Myers, E. Dudziec, S. Larre, M. Milo, I. Rehman, D. J. Rosario, et al. Distinct MicroRNA Alterations Characterize High- and Low-Grade Bladder Cancer Cancer Res., November 1, 2009; 69(21): 8472 - 8481. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. C. Tomlinson, F. R. Lamont, S. D. Shnyder, and M. A. Knowles Fibroblast Growth Factor Receptor 1 Promotes Proliferation and Survival via Activation of the Mitogen-Activated Protein Kinase Pathway in Bladder Cancer Cancer Res., June 1, 2009; 69(11): 4613 - 4620. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. M. Gallagher, D. M. O'Shea, P. Fitzpatrick, M. Harrison, B. Gilmartin, J. A. Watson, T. Clarke, M. O. Leonard, A. McGoldrick, M. Meehan, et al. Recurrence of Urothelial Carcinoma of the Bladder: A Role for Insulin-Like Growth Factor-II Loss of Imprinting and Cytoplasmic E-Cadherin Immunolocalization Clin. Cancer Res., November 1, 2008; 14(21): 6829 - 6838. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Kawanishi, Y. Matsui, M. Ito, J. Watanabe, T. Takahashi, K. Nishizawa, H. Nishiyama, T. Kamoto, Y. Mikami, Y. Tanaka, et al. Secreted CXCL1 Is a Potential Mediator and Marker of the Tumor Invasion of Bladder Cancer Clin. Cancer Res., May 1, 2008; 14(9): 2579 - 2587. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S Schwarz, M Rechenmacher, T Filbeck, R Knuechel, H Blaszyk, A Hartmann, and G Brockhoff Value of multicolour fluorescence in situ hybridisation (UroVysion) in the differential diagnosis of flat urothelial lesions J. Clin. Pathol., March 1, 2008; 61(3): 272 - 277. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Lee, J. Jeong, T. Majewski, S. E. Scherer, M.-S. Kim, T. Tuziak, K. S. Tang, K. Baggerly, H. B. Grossman, J.-H. Zhou, et al. Forerunner genes contiguous to RB1 contribute to the development of in situ neoplasia PNAS, August 21, 2007; 104(34): 13732 - 13737. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. P. Mitra, R. H. Datar, and R. J. Cote Molecular Pathways in Invasive Bladder Cancer: New Insights Into Mechanisms, Progression, and Target Identification J. Clin. Oncol., December 10, 2006; 24(35): 5552 - 5564. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. D. Zhou, M. A. Sens, S. H. Garrett, S. Somji, S. Park, V. Gurel, and D. A. Sens Enhanced Expression of Metallothionein Isoform 3 Protein in Tumor Heterotransplants Derived from As+3- and Cd+2-Transformed Human Urothelial Cells Toxicol. Sci., October 1, 2006; 93(2): 322 - 330. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Hernandez, E. Lopez-Knowles, J. Lloreta, M. Kogevinas, A. Amoros, A. Tardon, A. Carrato, C. Serra, N. Malats, and F. X. Real Prospective Study of FGFR3 Mutations As a Prognostic Factor in Nonmuscle Invasive Urothelial Bladder Carcinomas J. Clin. Oncol., August 1, 2006; 24(22): 3664 - 3671. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Lopez-Knowles, S. Hernandez, N. Malats, M. Kogevinas, J. Lloreta, A. Carrato, A. Tardon, C. Serra, F. X. Real, and EPICURO Study Group Investigators PIK3CA Mutations Are an Early Genetic Alteration Associated with FGFR3 Mutations in Superficial Papillary Bladder Tumors. Cancer Res., August 1, 2006; 66(15): 7401 - 7404. [Abstract] [Full Text] [PDF]
|
|