Abstract
The most established suicide gene therapy system is the herpes simplex virus thymidine kinase (GSVtk)=gancyclovir (GCV) axis. On expression of the enzyme HSVtk, the cell metabolizes gancyclovir into toxic metabolites, destroying the cell. The killing of these cells is spread to nearby cells by a bystander effect. The mechanism of this effect is not understood, but it is thought to involve gap junctions locally and the immune system at distant sites. We have explored the role of this suicide gene system in the rat model of prostate cancer.
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