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Updated: Jul 15, 2026
Magnetic Resonance Imaging Assessment of Carcinogen-induced Murine Bladder Tumors
Published on: March 29, 2019
Gene expression profiling of chemically induced rat bladder tumors
Ruisheng Yao1, Yijun Yi, Clinton J Grubbs
1Department of Surgery and The Alvin J. Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
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.
Insights
This study investigated gene expression changes in rat bladder tumors, revealing alterations in cell cycle, signaling pathways, and apoptosis. Common molecular mechanisms were identified between rat and mouse bladder tumors, suggesting conserved pathways in tumorigenesis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Bladder tumor development involves genetic alterations and gene expression changes.
- Understanding these molecular changes is crucial for identifying therapeutic targets.
Purpose of the Study:
- To explore gene expression changes in 4-hydroxybutyl(butyl)nitrosamine-induced rat bladder tumors using microarray analysis.
- To compare gene expression profiles with existing mouse bladder tumor data.
Main Methods:
- Microarray analysis was performed on rat bladder tumors and normal epithelia.
- Gene expression data was analyzed to identify differentially expressed genes.
- Pathway analysis was conducted using GenMAPP to visualize affected biological pathways.
- Comparative analysis was performed with previously published mouse bladder tumor data.
Main Results:
- Microarray analysis identified 1,138 known genes and 867 expressed sequence tags with altered expression in rat bladder tumors.
- Affected genes were involved in cell cycle regulation, EGFR-Ras signaling, apoptosis, growth factors, and oncogenes.
- Pathway analysis revealed involvement of apoptosis, cell cycle, and integrin-mediated cell adhesion pathways.
- Over 280 common differentially expressed genes were found in both rat and mouse bladder tumors, including genes related to cell cycle, apoptosis, oncogenes, and tumor suppressors.
Conclusions:
- Multiple molecular pathways are implicated in rat bladder tumorigenesis.
- A common molecular mechanism underlies bladder tumor development in both rat and mouse models.
- These findings highlight conserved pathways in bladder cancer progression across species.
