Solid tissues removed from Atm homozygous deficient mice do not exhibit a mutator phenotype for second-step autosomal mutations

Mitchell S. Turker, Blythe M. Gage, Jennifer A. Rose, Olga N. Ponomareva, Jay A. Tischfield, Peter J. Stambrook, Carrolee Barlow, Anthony Wynshaw-Boris

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

The presence of increased frequencies of blood-derived and solid tumors in ataxia-telangiectasia (A-T) patients, coupled with a role for the ATM (A-T mutation) protein in detecting specific forms of DNA damage, has led to the assumption of a mutator phenotype in A TM-deficient cells. Supporting this assumption are observations of increased rates of chromosomal aberrations and intrachromosomal homologous recombinational events in the cells of A-T patients. We have bred mice with knockout mutations for the selectable Aprt (adenine phosphoribosyltransferase) locus and the Atm locus to examine the frequency of second-step autosomal mutations in Amt-deficient cells. Two solid tissues were examined: (a) the ear, which yields predominately mesenchymal cells; and (b) the kidney, which yields predominately epithelial cells. We report here the lack of a mutator phenotype for inactivating autosomal mutations in solid tissues of the Atm-deficient mice.

Original languageEnglish (US)
Pages (from-to)4781-4783
Number of pages3
JournalCancer Research
Volume59
Issue number19
StatePublished - Oct 1 1999

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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    Turker, M. S., Gage, B. M., Rose, J. A., Ponomareva, O. N., Tischfield, J. A., Stambrook, P. J., Barlow, C., & Wynshaw-Boris, A. (1999). Solid tissues removed from Atm homozygous deficient mice do not exhibit a mutator phenotype for second-step autosomal mutations. Cancer Research, 59(19), 4781-4783.