| First Author | Yoshino M | Year | 2002 |
| Journal | DNA Repair (Amst) | Volume | 1 |
| Issue | 11 | Pages | 935-40 |
| PubMed ID | 12531021 | Mgi Jnum | J:79734 |
| Mgi Id | MGI:2388859 | Doi | 10.1016/s1568-7864(02)00144-1 |
| Citation | Yoshino M, et al. (2002) Additive roles of XPA and MSH2 genes in UVB-induced skin tumorigenesis in mice. DNA Repair (Amst) 1(11):935-40 |
| abstractText | We have made xeroderma pigmentosum group A gene (XPA)-knockout mice (XPA(-/-) mice). The XPA(-/-) mice had no detectable activity for nucleotide excision repair (NER) and showed a high incidence of UVB-induced skin tumorigenesis. We have also found that cell lines derived from skin cancers in UVB-irradiated XPA(-/-) mice become tolerant to UV-irradiation and showed abnormal UV-induced cell cycle checkpoints and decreased mismatch repair (MMR) activity. These results suggested that the MMR-downregulation may help cells escape killing by UV-irradiation and thus MMR-deficient clones are selected for during the tumorigenic transformation of XPA(-/-) cells. In this report, we examined whether the incidence of UVB-induced skin tumorigenesis is enhanced in XPA(-/-)MSH2(-/-), XPA(-/-) and MSH2(-/-) mice when compared with that in wild-type mice. Our results indicate that the MSH2-deficiency caused a high incidence of spontaneous and UVB-induced skin tumorigenesis and the XPA and MSH2 genes have additive roles in the UV-induced skin tumorigenesis. |
