pubmed-article:7908202 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C2698297 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0029016 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0023903 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0449438 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0025723 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C1515926 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:7908202 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:7908202 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:7908202 | pubmed:dateCreated | 1994-5-4 | lld:pubmed |
pubmed-article:7908202 | pubmed:abstractText | The liver tumor-prone B6C3F1 mouse (C57Bl/6 female x C3H/He male), in conjunction with the more susceptible C3H/He paternal strain and the resistant C57BL/6 maternal strain, is an excellent model for studying the mechanisms involved in carcinogenesis. The study reported here indicated that the B6C3F1 mouse inherited a maternal raf allele containing a methylated site not present in the paternal allele. Seven days after partial hepatectomy or after administration of a promoting dose of phenobarbital (PB) for 14 d; raf in B6C3F1 mouse liver was hypomethylated. The additional methylated site in the allele inherited from C57BL/6 was not maintained. The methylation status of raf in the liver of the C57BL/6 mouse was not affected by PB treatment. This indicates that the B6C3F1 mouse is less capable of maintaining methylation of raf than the C57BL/6 strain is. In both PB-induced and spontaneous B6C3F1 liver tumors, raf was hypomethylated in a nonrandom fashion. The level of raf mRNA increased in seven of 10 PB-induced tumors but in only one of five spontaneous tumors, whereas the level of Ha-ras mRNA increased in nine of 10 PB-induced tumors and in four of five spontaneous tumors. The results of our investigation (a) support the hypothesis that hypomethylation of DNA is a nongenotoxic mechanism involved in tumorigenesis, (b) support the notion that PB promotes liver tumors that develop along a pathway different from that leading to spontaneous tumors, and (c) indicate that differences in DNA methylation between C57BL/6 and B6C3F1 mice could, in part, account for the unusually high tendency of the latter strain to develop liver tumors. | lld:pubmed |
pubmed-article:7908202 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7908202 | pubmed:language | eng | lld:pubmed |
pubmed-article:7908202 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7908202 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:7908202 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7908202 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7908202 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7908202 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7908202 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7908202 | pubmed:month | Mar | lld:pubmed |
pubmed-article:7908202 | pubmed:issn | 0899-1987 | lld:pubmed |
pubmed-article:7908202 | pubmed:author | pubmed-author:RaoJ MJM | lld:pubmed |
pubmed-article:7908202 | pubmed:author | pubmed-author:GoodmanJ IJI | lld:pubmed |
pubmed-article:7908202 | pubmed:author | pubmed-author:McClainR MRM | lld:pubmed |
pubmed-article:7908202 | pubmed:author | pubmed-author:HarbisonM LML | lld:pubmed |
pubmed-article:7908202 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7908202 | pubmed:volume | 9 | lld:pubmed |
pubmed-article:7908202 | pubmed:geneSymbol | ras | lld:pubmed |
pubmed-article:7908202 | pubmed:geneSymbol | raf | lld:pubmed |
pubmed-article:7908202 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7908202 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7908202 | pubmed:pagination | 155-66 | lld:pubmed |
pubmed-article:7908202 | pubmed:dateRevised | 2011-10-27 | lld:pubmed |
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pubmed-article:7908202 | pubmed:meshHeading | pubmed-meshheading:7908202-... | lld:pubmed |
pubmed-article:7908202 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7908202 | pubmed:articleTitle | Alterations in the methylation status and expression of the raf oncogene in phenobarbital-induced and spontaneous B6C3F1 mouse liver tumors. | lld:pubmed |
pubmed-article:7908202 | pubmed:affiliation | Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824. | lld:pubmed |
pubmed-article:7908202 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7908202 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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