Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-3-14
pubmed:abstractText
The effects of different liver tumor-promoting treatments (i.e., a choline-devoid, methionine-deficient (CMD) diet, phenobarbital (PB), or both) on Ha-ras and raf methylation status and expression were determined in mouse strains with different susceptibilities to liver tumor formation: the relatively sensitive B6C3F1 and the relatively resistant C57BL/6. Additionally, B6C3F1 mouse liver tumors, spontaneous or PB induced, were assessed for alterations in global DNA methylation status and expression of Ha-ras and raf. The CMD diet led to hypomethylation of Ha-ras and raf after 12 wk of administration in B6C3F1 and C57BL/6 mice. At this early phase of tumor promotion, the frequency of increased expression of both Ha-ras and raf mRNAs was higher in the B6C3F1 but not the C57BL/6 mice. This is a mechanism that may, in part, underlie the heightened sensitivity of the B6C3F1 mouse to liver tumorigenesis. Subpopulations of B6C3F1 mouse liver tumors displayed altered global methylation status, with both hypomethylation and hypermethylation evident. Carcinomas were significantly more hypomethylated than adenomas. The level of raf mRNA was not changed in spontaneous or PB-induced B6C3F1 mouse liver tumors. Increased expression of Ha-ras was evident in some spontaneous B6C3F1 liver tumors and in most of the PB-induced liver tumors. These experiments support the concept that altered DNA methylation plays a key role in tumorigenesis and indicate that the high propensity of the B6C3F1 mice to liver tumorigenesis may be due, in part, to a decreased ability to maintain normal methylation status.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0899-1987
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
97-106
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9049185-Animals, pubmed-meshheading:9049185-Blotting, Northern, pubmed-meshheading:9049185-Blotting, Southern, pubmed-meshheading:9049185-Cell Transformation, Neoplastic, pubmed-meshheading:9049185-DNA, Neoplasm, pubmed-meshheading:9049185-DNA Methylation, pubmed-meshheading:9049185-Gene Expression, pubmed-meshheading:9049185-Genes, ras, pubmed-meshheading:9049185-Liver Neoplasms, Experimental, pubmed-meshheading:9049185-Male, pubmed-meshheading:9049185-Mice, pubmed-meshheading:9049185-Mice, Inbred C57BL, pubmed-meshheading:9049185-Mice, Inbred Strains, pubmed-meshheading:9049185-Protein-Serine-Threonine Kinases, pubmed-meshheading:9049185-Proto-Oncogene Proteins, pubmed-meshheading:9049185-Proto-Oncogene Proteins c-raf, pubmed-meshheading:9049185-RNA, Messenger, pubmed-meshheading:9049185-RNA, Neoplasm
pubmed:year
1997
pubmed:articleTitle
Comparison of effect of tumor promoter treatments on DNA methylation status and gene expression in B6C3F1 and C57BL/6 mouse liver and in B6C3F1 mouse liver tumors.
pubmed:affiliation
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't