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• W2035867525 endingPage "11075" @default.
• W2035867525 startingPage "11071" @default.
• W2035867525 abstract "Herpes simplex virus thymidine kinase (HSV-tk)/ganciclovir (GCV) viral-directed enzyme prodrug gene therapy causes potent, tumor-selective cytotoxicity in animal models in which HSV-tk gene transduction is limited to a minority of tumor cells. The passage of toxic molecules from HSV-tk+ cells to neighboring HSV-tk- cells during GCV therapy is one mechanism that may account for this bystander cytotoxicity. To investigate whether gap junction-mediated intercellular coupling could mediate this bystander effect, we used a flow cytometry assay to quantitate the extent of heterocellular coupling between HSV-tk+ murine fibroblasts and both rodent and human tumor cell lines. Bystander tumor cytotoxicity during GCV treatment in a coculture assay was highly correlated (P < 0.001) with the extent of gap junction-mediated coupling. These findings show that gap junction-mediated intercellular coupling contributes to the in vitro bystander effect during HSV-tk/GCV therapy and that retroviral transduction of tumor cells is not required for bystander cytotoxicity." @default.
• W2035867525 created "2016-06-24" @default.
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• W2035867525 date "1995-11-21" @default.
• W2035867525 modified "2023-10-13" @default.
• W2035867525 title "The extent of heterocellular communication mediated by gap junctions is predictive of bystander tumor cytotoxicity in vitro." @default.
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• W2035867525 doi "https://doi.org/10.1073/pnas.92.24.11071" @default.
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