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Suicide Gene Therapy
Despite the development of new therapeutic strategies, cancer remains incurable in most patients with advanced disease. A recent potential improvement in therapeutic strategies is the concept of suicide gene therapy.
After transfection with a suicide gene, cells can convert a harmless prodrug into its toxic metabolite, resulting in selective elimination of these cells.
One of the most frequently studied therapeutic strategies is based on transfection with the herpes simplex virus 1 thymidine kinase gene (HSV1-tk), followed by ganciclovir administration.
Despite promising results in vitro and in vivo, the antitumor effect in clinical trials remains poor, due to very low transfection efficiency. However, high percentages of transfected cells are not mandatory for complete eradication of a tumor in vivo. Transfected tumor cells appear to be capable of inducing the death of neighboring untransfected cells. This cell killing is called the “bystander effect”. The bystander effect can be enhanced by the introduction of gap junction proteins into cells. A substantial bystander effect could overcome the limitations of low transfection efficiency and result in an enhanced and possibly clinically worthwhile antitumor effect in patients.
Suicide Genes and Connexin Genes
Suicide genes code for enzymes that convert non-toxic compounds (prodrugs) into toxic products. The most potent and widely used are the genes encoding for thymidine kinases and cytosine deaminases.
Connexins are transmembrane proteins forming gap junctions allowing the passage of small molecules between cells. The restoration of connexin expression in tumor cells often restores the bystander effect by enabling the passage of toxic products.
InvivoGen provides the prodrugs paired with the suicide genes. These prodrugs are FDA approved for human treatment but are suitable for research purposes only : 5-Fluorocytosine (5-FC), 5-Fluorouracil (5-FU) and Ganciclovir (GCV).