Format

Send to

Choose Destination
See comment in PubMed Commons below
Expert Rev Mol Med. 2010 Mar 25;12:e10. doi: 10.1017/S1462399410001407.

Molecular genesis of non-muscle-invasive urothelial carcinoma (NMIUC).

Author information

1
Department of Molecular Physiology, University of Virginia, Charlottesville, VA 22908, USA.

Abstract

Urothelial carcinoma (UC) is the most common type of bladder cancer in Western nations. Most patients present with the non-muscle-invasive (NMIUC) form of the disease, while up to a third harbour the invasive form (MIUC). Specifically, the aetiology of NMIUC appears to be multifactorial and very different from that of MIUC. Loss of specific tumour suppressor genes as well as gain-of-function mutations in proteins within defined cellular signalling pathways have been implicated in NMIUC aetiology. The regions of chromosome 9 that harbour CDKN2A, CDKN2B, TSC1, PTCH1 and DBC1 are frequently mutated in NMIUC, resulting in functional loss; in addition, HRAS and FGFR3, which are both proto-oncogenes encoding components of the Ras-MAPK signalling pathway, have been found to harbour activating mutations in a large number of NMIUCs. Interestingly, some of these molecular events are mutually exclusive, suggesting functional equivalence. Since several of these driving changes are amenable to therapeutic targeting, understanding the signalling events in NMIUC may offer novel approaches to manage the recurrence and progression of this disease.

PMID:
20334706
PMCID:
PMC3025483
DOI:
10.1017/S1462399410001407
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Cambridge University Press Icon for PubMed Central
    Loading ...
    Support Center