Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Cancer appears to arise as a series of rate limiting steps, each of which represents the attainment of one cellular capability necessary for uncontrolled growth and invasion. As alterations in gene number or sequence can lead to the development of these cellular capabilities, the regulation of DNA fidelity is a vital homeostatic process. Mechanisms that disrupt DNA regulation lead to genomic instability and occur on two levels affecting either chromosomes (CIN; chromosomal instability) or individual DNA nucleotides (MSI; microsatellite instability). We conducted a search of the current literature to evaluate the evidence for the genomic instability in urothelial carcinoma (UC), and discuss the clinical role of the molecular pathways. Whilst CIN occurs more frequently in UC than MSI, the MSI molecular pathway is better understood. Distinct patterns of MSI occur in upper and lower urinary tract UC and produce tumours with a distinctive phenotype. Investigations into the mechanism of MSI in UC have revealed insights into the global pathogenesis of UC, similarities with other anatomically distant cancers and novel therapeutic strategies. The molecular mechanisms of CIN remain elusive. © 2005 Elsevier B.V. All rights reserved.

Original publication

DOI

10.1016/j.euus.2005.09.003

Type

Journal article

Journal

EAU Update Series

Publication Date

01/12/2005

Volume

3

Pages

180 - 188