Abstract
It is widely admitted that tumor induction occurs through a multistep process, the two first steps of which should be initiation and promotion (see Berenblum, 1975). Most carcinogens interact directly or indirectly with DNA to give rise to lesions on DNA which generally need to be repaired in order to permit the cell survival (Miller, 1978). The relationships between DNA repair and carcinogenesis become evident when studying some human syndromes such as xeroderma pigmentosum (XP), where patients develop skin cancer with a very high incidence after exposure to sun-light (Cleaver, 1968). The cells isolated from XP patients are unable to repair in vitro the DNA lesions, essentially pyrimidine dimers, made by UV-light. This result clearly indicates that unrepaired DNA lesions represent one of the first steps of carcinogenesis probably by giving rise to mutations due to incorrect base-pairing with the damaged base. Another way to get mutations is to use an error-prone repair pathway to repair lesions on DNA. Such an error-prone repair process has been well established in bacteria where it has been called the SOS repair pathway (Radman, 1975; Witkin, 1976; Devoret et al., 1977). Treatment of bacteria by various physical or chemical carcinogens, which inhibit DNA replication, induces the SOS repair pathway which will repair DNA lesions more efficiently but with a high rate of errors (Sarasin et al., 1977).
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Daya-Grosjean, L., Monier, R., Sarasin, A. (1983). Effects of Various Promoters on Cell Transformation by Simian Virus 40 Mutants. In: Castellani, A. (eds) The Use of Human Cells for the Evaluation of Risk from Physical and Chemical Agents. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1117-2_14
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DOI: https://doi.org/10.1007/978-1-4757-1117-2_14
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