Released by affected animals into their environment can survive for extended periods of time outside the amphibian host; ranging from at least three to seven weeks respectively, and potentially longer under optimal conditions. If untreated disposal of contaminated water were to occur. Moreover, these databases for which both LNCaP and C4-2B cells are being used. They can also be used to generate hypotheses on the metastatic process, as exemplified for the MLCK pathway. C4-2B cells as well as LNCaP cells have a surprisingly high number of point mutations: 4373 and 2790 mutations respectively. Like in primary PCa and castration-resistant PCa samples, the mutational spectrum is dominated by G-to-A and C-to-T transitions. It is known that mismatch repair defects cause transition mutations, particularly G-to-A and C-to-T substitutions. Hence, most mutations might be caused by the defective mismatch repair system in LNCaP cells, due to the homozygous deletion of the 39 end of the MSH2 gene. Chen et al. already described a correlating high instability of satellite DNA in LNCaP cells. The number of point mutations in our cell lines is much higher than the average 16–33 mutations detected in whole LY2835219 exomes of PCa samples. These cell lines are therefore atypical, but might be considered a model for cases of PCa in which mismatch repair is defective as described for instance by Barbieri et al., where a Screening Libraries single PCa tumor harbored a frameshift mutation of the MSH6 gene among 996 other mutations. Obviously, such higher mutation rates would explain the even higher number of mutations we found in C4-2B compared to LNCaP. Unfortunately, this will also obscure the driver mutations that may have conferred a survival advantage during the metastatic process. Our data can clearly lead to the hypothesis on the metastatic process that took place during the conversion of LNCaP to C4-2B cells. This is exemplified by the convergence of a number of affected pathways to an upregulation of MLCK. Indeed, there are several published links between MLCK and the metastatic process. Discriminant analysis of microarrays identified the MLCK gene as the most informative gene for the PCa genesis process, and inhibition of MLCK in rat PCa cells results in reduction of invasiveness, which was principally due to impaired cellular motility. Inhibiting MLCK in fibrosarcoma, pancreatic cancer and breast cancer cells also results in decreased adhesion, migration and invasion and increased apoptosis. Conversely, activating MLCK leads to an increase in invasion in breast cancer cells and an increased metastatic potential in non-small cell lung cancer. The differential expression of the MLCK gene in the two cell lines investigated here might therefore correlate with the higher metastatic capacity of the C4-2B cells. Persistent neurogenesis has been identified in two restricted regions, namely the subventricular zone of the lateral ventricle and the subgranular zone of the hippocampal dentate gyrus, in the adult mammalian brain, including humans, not only in developing ones. Many stimuli, exogenously applied agents, and endogenous factors or states appear to regulate adult neurogenesis.