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The bystander effect (BSE) is an interesting and important communication. We confirmed that mixtures of tumor cells property of the herpes thymidine kinase/ganciclovir resistant to the BSE did not show dye transfer from cell to (hTK/GCV) system of gene therapy for cancer. With the cell while bystander-sensitive tumor cells did. Dieldrin, a BSE, not only are the hTK expressing cells killed upon gandrug known to decrease GJ communication, diminished ciclovir (GCV) exposure but also neighboring wild-type dye transfer and also inhibited the BSE. Forskolin, an uptumor cells. On testing a large number of tumor cell lines regulator of cAMP did increase GJ, but directly inhibited in vitro, a wide range of sensitivity to bystander killing was hTK and therefore its effect on BSE could not be deterfound. Since transfer of toxic GCV metabolites from hTKmined. We conclude that these observations further supmodified to wild-type tumor cells via gap junctions (GJ) port the concept that functional GJ play an important role seemed to be a likely mechanism of the BSE, we tested in the BSE and further suggest that pharmacological GJ function in these various tumors with a dye transfer manipulation of GJ may influence the outcome of cancer technique and pharmacological agents known to affect GJ therapy with hTK/GCV.

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