Direct viral infection of solid tumors can cause tumor cell death, but these techniques offer the opportunity to express exogenous factors to enhance the antitumor response. We investigated the antitumor effects of a herpes simplex virus (HSV) amplicon expressing mouse granulocyte-macrophage colony-stimulating factor (mGM-CSF) using the replication-competent HSV type 1 mutant HF10 as a helper virus. HF10-packaged mGM-CSF-expressing amplicon (mGM-CSF amplicon) was used to infect subcutaneously inoculated murine colorectal tumor cells (CT26 cells) and the antitumor effects were compared to tumors treated with only HF10. The mGM-CSF amplicon efficiently replicated in CT26 cells with similar oncolytic activity to HF10 in vitro. However, when mice subcutaneously inoculated with CT26 cells were intratumorally injected with HF10 or mGM-CSF amplicon, greater tumor regression was seen in mGM-CSF amplicon-treated animals. Furthermore, mGM-CSF amplicon treatment prolonged mouse survival. Immunohistochemical analysis revealed increased inflammatory cell infiltration in the solid tumor in the mGM-CSF amplicon-treated animals. These results suggest that expression of GM-CSF enhances the antitumor effects of HF10, and HF10-packaged GM-CSF-expressing amplicon is a promising agent for the treatment of subcutaneous tumors.
Initial analysis of Pseudohynobius flavomaculatus chromosomes determined the chromosome number of this species to be 2n = 52. A re-examination of Ranodon shihi chromosomes detected 2n = 66 chromosomes, in contrast with a previous finding of 2n = 64. The C-banding patterns of these two species and that of Batrachuperus pinchonii were compared with each other. Regions of homoeology in the C-banding pattern among these three species represented 33.51-48.30% of the total length of their chromosomes. We also detected two types of chromosome rearrangement in hynobiid species based on the results of the present and previous cytogenetic studies.
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