DNA damage-induced mutagenesis: a novel target for cancer prevention.

Z. Wang

Research output: Contribution to journalReview articlepeer-review

38 Scopus citations


Tolerance to some degree of unrepaired DNA damage is crucial for cell survival-more specifically, for the sustained functionality of the DNA replication machinery-in the presence of adverse (genotoxic) conditions. At least two mechanisms ensure such tolerance: template switching and lesion bypass. Lesion bypass, whereby unrepaired damaged DNA serves as template, involves the Y family of DNA polymerases; lesion bypass can be error-free or error-prone, depending on the nucleotide incorporated during translesion synthesis. Error-prone lesion bypass constitutes a major mechanism of mutagenesis and, in eukaryotes, is primarily effected by the DNA polymerase zeta (Polzeta) pathway. A relationship between the Y family polymerases and the Polzeta pathway is thus implicated, and conforms to the two-polymerase two-step model of lesion bypass. Based on the mutagenesis hypothesis of cancer formation, DNA damage-induced mutagenesis and its underlying molecular biology offer an intriguing potential target for cancer prevention.

Original languageEnglish
Pages (from-to)269-281
Number of pages13
JournalMolecular Interventions
Issue number5
StatePublished - Dec 2001

ASJC Scopus subject areas

  • Molecular Medicine


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