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Archive - Mar 20, 2012


VSV Viruses Kill Pancreatic Tumors in Preclinical Model

An intra-tumor injection of a virus prevented further growth of some pancreatic tumors and eradicated others in mouse models of pancreatic ductal adenocarcinoma. However, some tumors continued growing despite this treatment, proving resistant to the viruses. The research is published in the March 2012 Journal of Virology. About 95 percent of pancreatic cancers are pancreatic ductal adenocarcinomas (PDAs). PDA is considered to be one of the most lethal malignancies, resulting in a five-year survival rate of only 8-20 percent. In this study, the researchers, led by Dr. Valery Z. Grdzelishvili of the University of North Carolina, Charlotte, tested several species of virus against pancreatic tumors, most notably vesicular stomatitis virus (VSV), a type of virus that is commonly used in the laboratory. Previous studies had demonstrated that some other viruses, including adenoviruses, herpesviruses, and reoviruses, could be used to kill pancreatic cancer cells in some animal models of pancreatic cancer. VSV has several qualities which make it attractive as a potential oncolytic (cancer killing) agent. First, unlike some other viruses (including adenoviruses), VSV replication does not require the cancer cell to express a specific receptor in order to infect that cell, and therefore it can infect most any cancer cell. Second, replication occurs in the cytoplasm of host cells, which means that there is no risk that it will cause healthy host cells to become cancerous, says Dr. Grdzelishvili. Third, this virus's genome is easily manipulated, which would make it fairly practical to adjust levels of foreign gene expression to enhance the virus's specificity for particular cancers, and its ability to kill them. Fourth, unlike with some other viruses, humans have no preexisting immunity to VSV.