| pubmed-article:17545594 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C1512409 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0752063 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0012854 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0311404 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0178499 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C1554963 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0079411 | lld:lifeskim |
| pubmed-article:17545594 | lifeskim:mentions | umls-concept:C0525129 | lld:lifeskim |
| pubmed-article:17545594 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:17545594 | pubmed:dateCreated | 2007-6-4 | lld:pubmed |
| pubmed-article:17545594 | pubmed:abstractText | Basal levels of endogenously generated oxidative DNA modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are present in apparently all mammalian cells, but their relevance for the generation of spontaneous cancers remains to be established. Both the 8-oxoG levels and the resulting spontaneous mutations are increased in the livers of Csb(m/m)/Ogg1(-/-) mice, which are deficient in the repair of 8-oxoG. In order to determine the consequences of these additional oxidative DNA modifications and mutations and thus assess the tumor initiating potency of this type of endogenous DNA damage, we treated Csb(m/m)/Ogg1(-/-) mice and repair-proficient controls with the peroxisome proliferator WY-14,643 (0.025% ad libitum), a potent inducer of liver cell proliferation. The treatment did not generate any additional oxidative DNA damage; the elevated levels of 8-oxoG in the Csb(m/m)/Ogg1(-/-) mice even decreased. Also, the spontaneous mutation frequencies observed in the lacI gene of BigBlue Csb(m/m)/Ogg1(-/-) mice, which were approximately 3-fold higher than in the repair-proficient mice, declined by 39% under the treatment, whereas the frequencies in the livers of the repair-proficient animals remained unchanged. Preneoplastic lesions (staining positive or negative for glucose-6-phoshatase) developed in the livers of both wild-type and Csb(m/m)/Ogg1(-/-) mice after 30 weeks. Both the numbers and the total volumes of the lesions were approximately 6-fold higher in the repair-deficient mice than in the wild-type mice. The results indicate that spontaneous mutations generated from endogenous oxidative DNA base damage efficiently translate into increased tumorigenesis when cell proliferation is stimulated. | lld:pubmed |
| pubmed-article:17545594 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17545594 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17545594 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17545594 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:17545594 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:17545594 | pubmed:author | pubmed-author:SchwarzMichae... | lld:pubmed |
| pubmed-article:17545594 | pubmed:author | pubmed-author:EpeBerndB | lld:pubmed |
| pubmed-article:17545594 | pubmed:author | pubmed-author:TrappChristia... | lld:pubmed |
| pubmed-article:17545594 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17545594 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:17545594 | pubmed:volume | 67 | lld:pubmed |
| pubmed-article:17545594 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17545594 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17545594 | pubmed:pagination | 5156-61 | lld:pubmed |
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| pubmed-article:17545594 | pubmed:meshHeading | pubmed-meshheading:17545594... | lld:pubmed |
| pubmed-article:17545594 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17545594 | pubmed:articleTitle | The peroxisome proliferator WY-14,643 promotes hepatocarcinogenesis caused by endogenously generated oxidative DNA base modifications in repair-deficient Csbm/m/Ogg1-/- mice. | lld:pubmed |
| pubmed-article:17545594 | pubmed:affiliation | Institute of Pharmacy, University of Mainz, Mainz, Germany. | lld:pubmed |
| pubmed-article:17545594 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17545594 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:18294 | entrezgene:pubmed | pubmed-article:17545594 | lld:entrezgene |
| entrez-gene:319955 | entrezgene:pubmed | pubmed-article:17545594 | lld:entrezgene |
