Related Experiment Video
Updated: Aug 9, 2026
11:02
Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
Published on: October 31, 2013
Altered gene expression profile in mouse bladder cancers induced by hydroxybutyl(butyl)nitrosamine
Ruisheng Yao1, William J Lemon, Yian Wang
1Department of Surgery and The Alvin J. Siteman Cancer Center, Campus Box 8109, Washington University School of Medicine, St. Louis, MO 63110, USA.
Neoplasia (New York, N.Y.)
|November 19, 2004
Summary
Gene expression profiling reveals key molecular changes in mouse bladder tumors. These alterations in pathways like EGFR-Ras and TGF-beta are crucial for tumor development.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Bladder tumor development involves complex genetic and gene expression alterations.
- Understanding these molecular changes is crucial for identifying therapeutic targets.
Purpose of the Study:
- To comprehensively analyze gene expression profiles in carcinogen-induced mouse bladder tumors.
- To identify specific genes and signaling pathways dysregulated during bladder tumorigenesis.
Main Methods:
- Oligonucleotide array analysis using Affymetrix GeneChips on RNA from normal and tumor mouse bladder epithelia.
- Pathway analysis using GenMAPP to visualize differentially expressed genes in biological pathways.
Main Results:
- Identified 1164 known genes with altered expression in bladder tumors.
- Upregulated genes include EGFR-Ras signaling, transcription factors, and cell cycle regulators.
- Downregulated genes include mitogen-activated protein kinases, cell cycle checkpoints, and Rho/Rab subfamily genes.
- Differential expression observed in TGF-beta and G13 signaling pathways involving genes like Smad1, Smad2, NFkappaB, and RhoGEF.
Conclusions:
- Mouse bladder tumorigenesis is characterized by distinct gene expression profiles.
- Activation of EGFR-Ras, uncontrolled cell cycle, aberrant transcription factors, and dysregulated TGF-beta and G13 pathways are implicated.
- Cross-talk between these signaling pathways plays a significant role in bladder tumor progression.
