Abstract
Many diseases in humans are the result of specific genetic mutations. In the etiology of cancer, mutagenesis plays a critical and complex role. DNA damage by chemicals or radiation usually increases the rate of polymerase errors, but the types and frequencies of mutations depend on the structure and conformation of the DNA lesion, the cells in which it is replicated, and the DNA sequence context. A survey of the research in this area is presented here.
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Notes
- 1.
Abbreviations: MF mutational frequency; TFT trifluorothymidine; AFB 1 aflatoxin B1; Fapy formamidopyrimidine; PAH polycyclic aromatic hydrocarbon; BP benzo[a]pyrene; DMN dimethylnitrosamine; AF 2-aminofluorene; AAF N-acetyl-2-aminofluorene; AP 1-aminopyrene; εA 1,N 6-ethenoadenine; εC3,N  4-ethenocytosine; M 1 G pyrimido[1,2-α]purin-10(3H)-one; m C 5-methylcytosine; NNK 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone; TLS translesion synthesis.
- 2.
 SOS response: In addition to excision of the damaged nucleotide or base by DNA repair proteins, strategies have evolved for a cell to survive when its DNA is damaged. The SOS response is an extensively studied DNA damage tolerance mechanism first discovered in Escherichia coli. The SOS response is discussed extensively in Chap.  16.
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Acknowledgments
Research in the author’s laboratory was supported by the National Institute of Environmental Health Sciences, NIH (grants ES009127 and ES013324).
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Basu, A.K. (2011). Mutagenesis: The Outcome of Faulty Replication of DNA. In: Penning, T. (eds) Chemical Carcinogenesis. Current Cancer Research. Humana Press. https://doi.org/10.1007/978-1-61737-995-6_17
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