Is base excision repair a tumor suppressor mechanism?

Joann B. Sweasy, Tieming Lang, Daniel DiMaio

Research output: Contribution to journalReview articlepeer-review

62 Scopus citations

Abstract

The base excision repair pathway is critical for the removal of oxidized and methylated bases from the DNA. Much of this DNA damage arises endogenously, as a result of oxygen metabolism. Several proteins including DNA glycosylases, the APE1 endonuclease, DNA polymerase β and DNA ligase, act in a highly regulated and coordinated manner during base excision repair to excise the base adducts from the DNA and restore the normal DNA sequence. Both germline and tumor-associated variants of genes encoding these proteins have been identified in humans. In many cases, the protein variant has been shown to have properties that could contribute to the development of cancer, suggesting that base excision repair acts as a tumor suppressor mechanism in humans. Limited epidemiological studies are consistent with this view. Our review of the literature indicates that additional laboratory and epidemiological studies of the role of base excision repair in cancer etiology is warranted.

Original languageEnglish (US)
Pages (from-to)250-259
Number of pages10
JournalCell Cycle
Volume5
Issue number3
DOIs
StatePublished - Feb 1 2006
Externally publishedYes

Keywords

  • Base exciasion repair
  • Cancer
  • DNA glycosylase
  • DNA ligase
  • Genomic instability
  • XRCC1
  • dRP lyase

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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