Medical College of Wisconsin
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Gene expression profiling of chemically induced rat bladder tumors. Neoplasia 2007 Mar;9(3):207-21

Date

04/03/2007

Pubmed ID

17401461

Pubmed Central ID

PMC1838579

DOI

10.1593/neo.06814

Scopus ID

2-s2.0-33947375580 (requires institutional sign-in at Scopus site)   31 Citations

Abstract

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 M



MESH terms used to index this publication - Major topics in bold

Animals
Annexin 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