Abstract
Spontaneous and induced mutation rates at two expanded simple tandem repeat (ESTR) loci were studied in the germ line of xeroderma pigmentosum group C (Xpc) knockout mice defective in global genome nucleotide excision repair. Spontaneous and radiation-induced mutation rates in homozygous Xpc-/- males were significantly higher than those in isogenic wild-type (Xpc +/+) and heterozygous (Xpc+/-) mice. In contrast, exposure to the monofunctional alkylating agent ethylnitrosourea resulted in similar increases in ESTR mutation rates across all genotypes. ESTR mutation spectra in the germ line of Xpc-/-, Xpc+/- and Xpc+/+ did not differ. Considering these data and the results of other publications, we propose that the Xpc-deficient mice possess a mutator phenotype in their germ line and somatic tissues that may significantly enhance carcinogenesis across multiple tissues.
Original language | English (US) |
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Pages (from-to) | 4695-4699 |
Number of pages | 5 |
Journal | Cancer research |
Volume | 67 |
Issue number | 10 |
DOIs | |
State | Published - May 15 2007 |
ASJC Scopus subject areas
- Oncology
- Cancer Research