Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases

Maria Teresa Russo, Gabriele De Luca, Paolo Degan, Eleonora Parlanti, Eugenia Dogliotti, Deborah E. Barnes, Tomas Lindahl, Hanjing Yang, Jeffrey H. Miller, Margherita Bignami

Research output: Contribution to journalArticlepeer-review

Abstract

The OGG1 and MYH DNA glycosylases prevent the accumulation of DNA 8-hydroxyguanine. In Myh -/- mice, there was no time-dependent accumulation of DNA 8-hydroxyguanine in brain, small intestine, lung, spleen, or kidney. Liver was an exception to this general pattern. Inactivation of both MYH and OGG1 caused an age-associated accumulation of DNA 8-hydroxyguanine in lung and small intestine. The effects of abrogated OGG1 and MYH on hepatic DNA 8-hydroxyguanine levels were additive. Because there is an increased incidence of lung and small intestine cancer in Myh -/-/Ogg1 -/- mice, these findings support a causal role for unrepaired oxidized DNA bases in cancer development.

Original languageEnglish
Pages (from-to)4411-4414
Number of pages4
JournalCancer Research
Volume64
Issue number13
DOIs
Publication statusPublished - Jul 1 2004

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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