Linked Life Data

12531021

Source:http://linkedlifedata.com/resource/pubmed/id/12531021

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pubmed-article:12531021pubmed:abstractTextWe 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.lld:pubmed
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pubmed-article:12531021pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:12531021pubmed:articleTitleAdditive roles of XPA and MSH2 genes in UVB-induced skin tumorigenesis in mice.lld:pubmed
pubmed-article:12531021pubmed:affiliationLaboratories of Organismal Biosystems, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Japan.lld:pubmed
pubmed-article:12531021pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12531021pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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