MathewsDeoxyribonucleotideMetabolismMutagenesisAndCancer.pdf

Citeable URL: https://ir.library.oregonstate.edu/concern/articles/v118rg38r

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Creator	Mathews, Christopher K.
Abstract	Cancer was recognized as a genetic disease at least four decades ago, with the realization that the spontaneous mutation rate must increase early in tumorigenesis, to account for the many mutations in tumor cells as compared with their progenitor normal cells. The genetic basis for cancer was established also from the finding that viral oncogenes have cellular counterparts, expression of which could transform cells. Deoxyribonucleotide pool abnormalities have long been recognized as determinants of DNA replication fidelity, and hence, may contribute to mutagenic processes involved in carcinogenesis. In addition, many anticancer agents act as antagonists of deoxyribonucleotide metabolism. To what extent may aspects of deoxyribonucleotide metabolism contribute to our understanding of both carcinogenesis and the effective use of anticancer agents? Keywords: DNA mismatch repair, Base excision repair, Genomic instability, DNA metabolism, Biochemistry, DNA replication Keywords: DNA mismatch repair, Base excision repair, Genomic instability, DNA metabolism, Biochemistry, DNA replication
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