| First Author | Sands AT | Year | 1995 |
| Journal | Nature | Volume | 377 |
| Issue | 6545 | Pages | 162-5 |
| PubMed ID | 7675084 | Mgi Jnum | J:28708 |
| Mgi Id | MGI:76252 | Doi | 10.1038/377162a0 |
| Citation | Sands AT, et al. (1995) High susceptibility to ultraviolet-induced carcinogenesis in mice lacking XPC. Nature 377(6545):162-5 |
| abstractText | Compromise of genetic information by mutation may result in the dysregulation of cellular growth control and subsequent tumour formation. Xeroderma pigmentosum (XP) is a rare autosomal disease characterized by hypersensitivity of the skin to sunlight and > 1,000-fold increased risk of skin cancers in sun-exposed parts of the body. Cell fusion studies have revealed eight complementation groups in XP (A-G, and an XP-variant form); group C is one of the most common forms of the disease. We have isolated a mouse homologue of the human gene for XP group C and generated XPC-deficient mice by using embryonic stem cell technology. Mice homozygous for the XPC mutant allele (xpcm1/xpcm1) are viable and do not exhibit an increased susceptibility to spontaneous tumour generation at one year of age. However, xpcm1/xpcm1 mice were found to be highly susceptible to ultraviolet-induced carcinogenesis compared with mice heterozygous for the mutant allele (xpcm1/+) and wild-type controls. Homozygous xpcm1 mutant mice also display a spectrum of ultraviolet-exposure-related pathological skin and eye changes consistent with the human disease xeroderma pigmentosum group C. |
