Project description:Urogenital schistosomiasis (caused by Schistosoma haematobium) remains a major public health concern worldwide. In response to parasite egg deposition, the host bladder undergoes gross and molecular morphological changes relevant for disease manifestation. However, limited mechanistic studies to date imply that the molecular mechanisms underlying pathology have not been well-defined. We leveraged a mouse model of urogenital schistosomiasis to perform for the first time, proteome profiling of the early molecular events that occur in the bladder after exposure to S. haematobium eggs, and to elucidate the protein pathways involved in urogenital schistosomiasis-induced pathology. Purified S. haematobium eggs or control vehicle were microinjected into the bladder walls of mice. Mice were sacrificed seven days post-injection and bladder proteins isolated and processed for proteome profiling using mass spectrometry.
Project description:The objective of this study was to evaluate the efficacy of nicotinamide in a N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN)-induced urinary bladder cancer model in mice, and to identify through gene expression profiling the molecular signatures of cancer prevention by nicotinamide. We used 20 mice for microarray experiments: five mice with normal bladders (group I), five with nicotinamide-treated bladders (group II), five with BBN-induced mouse bladder tumors (group III), and five with non-tumorigenic bladders treated with BBN and nicotinamide (group IV). Keywords: Gene expression, Mouse bladder cancer, Cancer prevention
Project description:Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells. Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells.
Project description:We investigated the genetic characteristics of the mouse tumors. First, we investigated whether mouse BBN-induced bladder cancers displayed distinct gene expression profiles according to the cell of origin or pre-induced Trp53 mutation. Gene expression profiles based on cDNA microarray data were analyzed using non-hierarchical clustering, which revealed that none of the mouse bladder tumors were differentially clustered based on the genotypes.
Project description:Attenuation of Hedgehog (Hh) pathway activity leads to accelerated tumor progression in a mouse model of N-butyl-N-4-hydroxybutyl nitrosamine (BBN) – induced bladder carcinoma. In order to identify genes regulated by the Hh pathway that might be involved in bladder cancer progression, we performed transcriptional profiling of bladders harvested from mice after BBN-exposure, comparing Gli1CreER/WT; Smoflox/WT mice to Gli1CreER/WT; Smoflox/flox mice, which express CreER under control of the Gli1 promoter and carry one or two floxed alleles of the essential Hh pathway transductory component Smoothened (Smo) respectively. Administration of Tamoxifen to these mice results in attenuation of Hh pathway activty to a greater extent in the Gli1CreER/WT;Smoflox/flox mice as compared to Gli1CreER/WT;Smoflox/WT mice, allowing identification of Hh-pathway regulated genes. 6 total samples were analyzed. 3 bladders from Gli1CreER/WT; Smoflox/WT mice and 3 bladders from Gli1CreER/WT; Smoflox/flox mice were analyzed.