XXXX treatment of metastatic @entity0 .

@entity1 @entity778 @entity137 @entity0 @entity5 @entity19 @entity2 @entity281
The high prevalence and poor prognosis of @entity0 provides a strong rationale for developing new treatment strategies and preventive and therapeutic agents. @entity778 (HSV) can @entity5 cells, replicating and killing the cells by direct cytopathic effect and then spreading within the @entity5 . Replication of oncolytic HSV leads to the destruction of the infected @entity5 cell and release of new virions, which are able to infect adjacent cells until potentially all @entity5 cells are destroyed. In this study, the @entity137 of a third-generation oncolytic HSV vector, designated G47/\, was examined in @entity1 @entity0 cell lines, as well as in immortalized and normal breast cells. A pulmonary metastatic model of @entity0 established in Balb/c @entity19 was used to evaluate the efficacy of G47/\ treatment. Systemic treatment by intravenous administration of G47/\ for metastatic @entity2 was initiated 14 days after injection of @entity5 cells. On Day 56, the @entity19 were sacrificed and @entity5 nodules on the surface of the lung were counted. G47/\ was highly cytotoxic to @entity0 and immortalized breast cells in vitro at low multiplicities of @entity281 (MOI), while normal breast cells remained viable 5 days after @entity281 . In the pulmonary metastatic model, the average number of surface @entity2 nodules in the G47/\-treated group was approximately 9  -fold less than in the control-treated group. X-gal staining illustrated viral replication and spread in the @entity5 cells in vitro and in vivo. In conclusion, G47/\ effectively killed @entity1 @entity0 cells and immortalized breast cells but not normal breast cells. Systemic administration of G47/\ by tail vein injection was effective in inhibiting the growth of established @entity0 .
