| First Author | van Steeg H | Year | 2000 |
| Journal | Mutat Res | Volume | 450 |
| Issue | 1-2 | Pages | 167-80 |
| PubMed ID | 10838141 | Mgi Jnum | J:62684 |
| Mgi Id | MGI:1859454 | Doi | 10.1016/s0027-5107(00)00023-3 |
| Citation | van Steeg H, et al. (2000) Mutagenesis and carcinogenesis in nucleotide excision repair-deficient XPA knock out mice. Mutat Res 450(1-2):167-80 |
| abstractText | Mice with a defect in the xeroderma pigmentosum group A (XPA) gene have a complete deficiency in nucleotide excision repair (NER). As such, these mice mimic the human XP phenotype in that they have a >1000-fold higher risk of developing UV-induced skin cancer. Besides being UV-sensitive, XPA(-/-) mice also develop internal tumors when they are exposed to chemical carcinogens. To investigate the effect of a total NER deficiency on the induction of gene mutations and tumor development, we crossed XPA(-/-) mice with transgenic lacZ/pUR288 mutation-indicator mice. The mice were treated with various agents and chemicals like UV-B, benzo[a]pyrene and 2-aceto-amino-fluorene. Gene mutation induction in several tumor target- and non-target tissues was determined in both the bacterial lacZ reporter gene and in the endogenous Hprt gene. Furthermore, alterations in the p53- and ras genes were determined in UV-induced skin tumors of XPA(-/-) mice. In this work, we review these results and discuss the applicability and reliability of enhanced gene mutant frequencies as early indicators of tumorigenesis. |
