DNA repair, cancer and gene therapy

Abstract

Fidelity of DNA synthesis is pivotal to our understanding of fundamental biological processes. An organism must replicate and repair its DNA with high accuracy and precision in order to maintain its genetic activity. DNA repair pathways enable cells to offer enhanced resistance to deleterious effects of chemicals and radiations (Lindahl, 1982). A number of pathways have been described e.g. the error-prone SOS repair (that lacks fidelity of repair process),the error-proof adaptive repair of alkylated DNA and inducible response to oxygen radical damage in DNA. These different circuits are under positive regulatory controls. However, the biochemical strategies employed to generate specific protein activators differ among the pathways. Although, the universally occurring repair activities seem to serve efficiently to counteract malignancy, error-prone polymerase and plasminogen activator have been instrumental in tumorigenesis, the process that proceeds by cascading of genetic errors (Sancar and Sancar, 1988).