Molecular credentialing of rodent bladder carcinogenesis models

PD Williams, JK Lee, D Theodorescu - Neoplasia, 2008 - Elsevier
PD Williams, JK Lee, D Theodorescu
Neoplasia, 2008Elsevier
Cancer of the urinary bladder is often a result of exposure to chemical carcinogens. Models
of this disease have been developed by exposing rodents to N-butyl-N-(4-hydroxybutyl)-
nitrosamine (OH-BBN). The resultant tumors are histologically similar to human disease, but
little is known about genetic similarities to the latter. Such knowledge would help identify or
corroborate genes found important in human bladder cancer and suggest biologically
appropriate mechanistic studies. We address this need by comparing gene expression …
Abstract
Cancer of the urinary bladder is often a result of exposure to chemical carcinogens. Models of this disease have been developed by exposing rodents to N-butyl-N-(4-hydroxybutyl)-nitrosamine (OH-BBN). The resultant tumors are histologically similar to human disease, but little is known about genetic similarities to the latter. Such knowledge would help identify or corroborate genes found important in human bladder cancer and suggest biologically appropriate mechanistic studies. We address this need by comparing gene expression profiles associated with urothelial carcinoma for three different species: mouse, rat, and human. We find that many human genes homologous to those differentially expressed in carcinogen-induced rodent tumors are also differentially expressed in human disease and are preferentially associated with progression from non-muscle-invasive to muscle-invasive disease. We also find that overall gene expression profiles of rodent tumors correspond more closely with those of invasive human tumors rather than non-muscle-invasive tumors. Finally, we provide a list of genes that are likely candidates for driving this disease process by virtue of their concordant regulation in tumors of all three species.
Elsevier