What we could do now: molecular pathology of bladder cancer

Authors
Citation
Ma. Knowles, What we could do now: molecular pathology of bladder cancer, J CL PATH-M, 54(4), 2001, pp. 215-221
Citations number
81
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF CLINICAL PATHOLOGY-MOLECULAR PATHOLOGY
ISSN journal
13668714 → ACNP
Volume
54
Issue
4
Year of publication
2001
Pages
215 - 221
Database
ISI
SICI code
1366-8714(200108)54:4<215:WWCDNM>2.0.ZU;2-X
Abstract
There is much information on the genetic alterations that contribute to the development of bladder cancer. Because it is hypothesised that the genotyp e of the cancer cell plays a major role in determining phenotype, this gene tic information should impact on clinical practice. To date however, this h as not happened. Some of the alterations identified in bladder cancer have clear associations with outcome for example, mutational inactivation of the cell cycle regulator proteins p53 and the retinoblastoma protein (Rb). How ever, as single markers, these events have insufficient predictive power to be applied in the management of individual patients. The use of panels of markers is a potential solution to this problem. Examples of suitable panel s include those genes/ proteins with known impact on specific cell cycle ch eckpoints or with impact on cellular phenotypes, such as immortalisation, i nvasion, or metastasis. To evaluate such marker panels, large tumour series will be needed-for example, archival samples from completed clinical trial s. The use of these valuable resources will require coordination of sample provision. This might involve central collection and distribution of tissue blocks, sections, or tissue arrays and the provision of patient follow up information to laboratories participating in a study. With the availability of microarray technologies, including cDNA and comparative genomic hybridi sation arrays, the transcriptome and genome of transitional cell carcinomas of different phenotypes can be compared and will undoubtedly provide a wea lth of information with potential diagnostic and prognostic uses. Although these studies can be initiated using small local tissue collections, high q uality collection of fresh tissues from new clinical trials will be crucial for proper evaluation of associations with clinical outcome. Funding for m olecular pathological studies to date has been poor. To begin to translate molecular information from the laboratory to the clinic and to make maximum use of valuable urological patient resources in the UK, adequate funding a nd scientific energy are required. Whereas the latter is not in doubt, pres ent funding for this type of translational research is inadequate.