Since membrane-membrane fusion events are critical for all cell types and are important for maintaining the orderly movement of cargo proteins from one intracellular compartment to another, it is not surprising that there are a wide variety of distinct SNARE isoforms that reside on distinct intracellular compartments, thereby ensuring appropriate homotypic and heterotypic membrane fusion events. For example, there are a wide variety of syntaxin and VAMP isoforms in eukaryotic cells that are expressed on particular organelles in essentially all cell types. By contrast, SNAP-25 is only expressed in neuronal/neuroendocrine cells and the role of SNAP-25 in the SNARE complex in non-neuronal tissues is taken-over by the related protein SNAP-23. SNAP-23 is ubiquitiously expressed and has been shown to play a role in diverse protein trafficking events including GLUT4 transport in adipocytes, mast cell degranulation, dense core granule release in platelets, cholecystokinin-regulated exocytosis in pancreatic acinar cells, and surface expression/recycling of transferrin receptors, the glutamate transporter EAAC1,Diperodon and NMDA receptors. Genetic ablation of various syntaxin and VAMP isoforms does not significantly impair embryonic development, revealing the importance of genetic redundancy of SNARE function in development. Surprisingly, deletion of SNAP-25 does not affect embryo viability, although Snap25-null mice die at birth due to neuromuscular abnormalities. By contrast, the importance of SNAP-23 in mouse development and embryonic viability remains unknown. Bladder cancer is the fifth commonest malignancy in the United States with 70, 530 new cases and 14,680 deaths in 2010. The majority of tumors are Urothelial Cell Carcinoma. Clinicopathological data suggest this disease arises by two distinct pathways with low and high-grade cellular differentiation. The clinical phenotype and treatment of these two pathways differs considerably and molecular comparisons reveal few common events. The majority of UCC are low-grade tumors,Diniconazole which are characterized by FGFR3 mutation, chromosome 9 loss and relatively few other molecular alterations. In contrast, high-grade tumors have widespread chromosomal instability, numerous molecular changes and are best characterized by loss of p53 function. Molecular changes in cancer arise from either genetic or epigenetic events. The latter is defined as stable heritable changes in a chromosome without alterations in the DNA sequence. Epigenetic gene modulation occurs when a stimulus, termed epigenator, induces a change in gene expression that becomes maintained within the genome through cell replication and in terminally differentiated cells. Epigenetic maintainers induce an altered chromatin state by biochemical modification of DNA or histone proteins. Numerous histone modifications are described and these can be classified according location, biochemistry or associated gene expression. Of those that are repressive in nature, trimethylation of Histone 3 Lysine 9 and Histone 3 Lysine 27 are some of the best characterized. These epigenetic marks may occur independently or in combination with other modifications such as H3 lysine 4 methylation, H3K9 monomethylation and H2A.Z. At the nucleotide level DNA methylation mostly occurs at cytosine residues within CpG dinucleotides. These are concentrated into dense islands typically around the 59 end of genes. Most human genes contain a CpG island and the majority of these are unmethylated to allow associated gene transcription. Cytosine methylation may occur physiologically during development or aberrantly in carcinogenesis. Consequent tumor suppressor gene silencing or oncogene activation induces and promotes tumorogenesis.