Increased transversions in a novel mutator colon cancer cell line

James R. Eshleman, P. Scott Donover, Susan J. Littman, Sandra E. Swinler, Guo Min Li, James D. Lutterbaugh, James K V Willson, Paul Modrich, W. David Sedwick, Sanford D. Markowitz, Martina L. Veigl

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

We describe a novel mutator phenotype in the Vaco411 colon cancer cell line which increases the spontaneous mutation rate 10-100-fold over background. This mutator results primarily in transversion base substitutions which are found infrequently in repair competent cells. Of the four possible types of transversions, only three were principally recovered. Spontaneous mutations recovered also included transitions and large deletions, but very few frameshifts were recovered. When compared to known mismatch repair defective colon cancer mutators, the distribution of mutations in Vaco411 is significantly different. Consistent with this difference, Vaco411 extracts are proficient in assays of mismatch repair. The Vaco411 mutator appears to be novel, and is not an obvious human homologue of any of the previously characterized bacterial or yeast transversion phenotypes. Several hypotheses by which this mutator may produce transversions are presented.

Original languageEnglish (US)
Pages (from-to)1125-1130
Number of pages6
JournalOncogene
Volume16
Issue number9
DOIs
StatePublished - Mar 5 1998

Keywords

  • Colon cancer
  • HPRT
  • Mutator phenotype
  • Transversions

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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