Gene expression profiling of chemically induced rat bladder tumors. Neoplasia 2007 Mar;9(3):207-21
Date
04/03/2007Pubmed ID
17401461Pubmed Central ID
PMC1838579DOI
10.1593/neo.06814Scopus ID
2-s2.0-33947375580 (requires institutional sign-in at Scopus site) 31 CitationsAbstract
A variety of genetic alterations and gene expression changes are involved in the pathogenesis of bladder tumors. To explore expression changes in 4-hydroxybutyl(butyl)nitrosamine-induced rat bladder tumors, microarray analysis was performed. Analysis yielded 1,138 known genes and 867 expressed sequence tags that were changed when comparing tumors to normal rat epithelia. Altered genes included cell cycle-related genes, EGFR-Ras signaling genes, apoptosis genes, growth factors, and oncogenes. Using the pathway visualization tool GenMAPP, we found that these genes can be grouped along several pathways that control apoptosis, cell cycle, and integrin-mediated cell adhesion. When comparing current data with previous mouse bladder tumor data, we found that > 280 of the same known genes were differentially expressed in both mouse and rat bladder tumors, including cell cycle-related genes, small G proteins, apoptosis genes, oncogenes, tumor-suppressor genes, and growth factors. These results suggest that multiple pathways are involved in rat bladder tumorigenesis, and a common molecular mechanism was found in both rat and mouse bladder tumors.
Author List
Yao R, Yi Y, Grubbs CJ, Lubet RA, You MMESH terms used to index this publication - Major topics in bold
AnimalsAnnexin A1
Apoptosis
Butylhydroxybutylnitrosamine
Cell Cycle
ErbB Receptors
Gene Expression Profiling
Immunohistochemistry
Mice
Oligonucleotide Array Sequence Analysis
Polymerase Chain Reaction
Rats
Rats, Sprague-Dawley
Urinary Bladder Neoplasms