Abstract
Gene therapy is based on restoring a missing or defective cellular function by delivering and expressing a gene encoding the protein responsible for that function. Initially, gene therapy was envisioned as a potential means to correct inherited mono-genic defects. This remains an active area of research, and a number of human clinical trials of this approach are ongoing (1–3). In addition to inherited monogenic defects, gene therapy is being applied to other types of diseases. This chapter describes gene therapy, as it is being used in the armamentarium of the war against cancer. More than 100 oncology-related clinical trials involving gene therapy have been approved worldwide (4). These therapeutic protocols include the expression of cytokines to enhance cellular immunogenicity, the expression of genes encoding prodrug activating enzymes, the expression of genes resulting in increased drug sensitivity (e.g., HSVTK/gancyclovir), or drug resistance (e.g., MDR-1 to protect normal bone marrow cells) (5) and the restoration of the function(s) of tumor suppressor genes. In addition to trials wherein an exogenous gene is being expressed with therapeutic intent, a number of other trials involving the suppression of gene expression (e.g., with antisense molecules targeting oncogenes) are also ongoing. The focus of the current chapter is the nonviral delivery of a functional tumor suppressor gene (encoding p53) to cancer cells.
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Chang, E.H., Xu, L., Pirollo, K.F. (2000). Targeted p53 Gene Therapy-Mediated Radiosensitization and Chemosensitization. In: Gutkind, J.S. (eds) Signaling Networks and Cell Cycle Control. Cancer Drug Discovery and Development. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-218-0_29
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