8-Hydroxyguanosine repair is defective in some microsatellite stable colorectal cancer cells

Antony R. Parker, Robert N. O'Meally, Dwight H. Oliver, Li Hua, William G. Nelson, Theodore L. DeWeese, James R. Eshleman

Research output: Contribution to journalArticle

Abstract

Mutator phenotypes are involved in the carcinogenesis of some cancers, e.g., defects in mismatch repair produce a mutator phenotype that drives carcinogenesis and causes microsatellite instability in hereditary nonpolyposis colon cancers and some sporadic colorectal cancers (CRC). Less understood, however, is the potential role of mutator phenotypes in microsatellite stable (MSS) CRC carcinogenesis. A novel transversion mutator phenotype was reported recently in an MSS CRC cell line. We hypothesized that 8-hydroxyguanosine could be involved and found elevations in 5 of 15 (33%) MSS CRC cell lines analyzed. Repair of an adenine·8-hydroxyguanosine mispair was functionally defective in the same five cell lines. The human MutY homologue transcript and MutY homologue protein levels were also decreased. These findings may reflect a MSS mutator phenotype contributing to the development of CRC.

Original languageEnglish (US)
Pages (from-to)7230-7233
Number of pages4
JournalCancer Research
Volume62
Issue number24
StatePublished - Dec 15 2002

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of '8-Hydroxyguanosine repair is defective in some microsatellite stable colorectal cancer cells'. Together they form a unique fingerprint.

  • Cite this