**1. Introduction**

292 Selected Topics in DNA Repair

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Genotoxic stress induces cell cycle arrest, DNA repair, and apoptotic cell death. The decision by cells either to repair DNA lesions and continue through the cell cycle or to undergo apoptosis is relevant to the incidence of mutagenesis and, subsequently, carcinogenesis. In this regard, incomplete repair of DNA damage prior to replication or mitosis can result in the accumulation of heritable genetic changes. Therapeutic anti-cancer treatments that use genotoxic agents must strike a balance between induction of repair and apoptosis in order to maximize the therapeutic effect. However, the nature of the cellular signaling response that determines cell fate such as survival or death is far from being understood. Certain insights have been derived from the finding that diverse isozymes of the protein kinase C (PKC) family are activated in response to DNA damage. PKC-mediated signaling pathway modulates destiny of cells following genotoxic insults (Yoshida 2007a, Yoshida 2008a). In particular, recent studies have shown that certain isozyme of PKC controls function of the p53 tumor suppressor in induction of cell cycle arrest, DNA repair, and apoptosis. In the past 10 years, understanding the molecular mechanisms of apoptosis mediated by PKC has advanced considerably, and the primary focus of this review is to provide an overview of PKC and p53, its mode of action and its physiological role in DNA damage-induced apoptosis.
