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rdf:type |
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lifeskim:mentions |
umls-concept:C0001430,
umls-concept:C0002085,
umls-concept:C0018270,
umls-concept:C0021853,
umls-concept:C0025918,
umls-concept:C0025921,
umls-concept:C0026809,
umls-concept:C0027651,
umls-concept:C0079419,
umls-concept:C0392756,
umls-concept:C0439232,
umls-concept:C0442821,
umls-concept:C0449822,
umls-concept:C0683598,
umls-concept:C0815327,
umls-concept:C1514623,
umls-concept:C1516451,
umls-concept:C1521828
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pubmed:issue |
14
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pubmed:dateCreated |
2000-8-24
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pubmed:abstractText |
Altered patterns of the 5-cytosine methylation of genomic DNA are associated with the development of a wide range of human cancers. We have studied the mechanisms and genetic pathways by which a targeted heterozygous deficiency in the murine 5-cytosine DNA methyltransferase gene (Dnmt1(N/+)) diminishes intestinal tumorigenesis in C57BL/6-multiple intestinal neoplasia (Min)/+ mice. We found that Dnmt1(N/+) retards the net growth rate of intestinal adenomas and reduces tumor multiplicity by approximately 50%. This tumor resistance affects the entire intestinal tract and is independent of the status of modifier of Min 1 and p53, two loci that have been found to confer strong resistance to Min-induced neoplasia Interestingly, Dnmt/(N/+) and modifier of Min 1 resistance interact synergistically, together virtually eliminating tumor incidence. This finding may provide an insight into potential combinatorial therapeutic approaches for treating human colon cancer.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0008-5472
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
60
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3965-70
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10919675-Adenoma,
pubmed-meshheading:10919675-Age Factors,
pubmed-meshheading:10919675-Alleles,
pubmed-meshheading:10919675-Animals,
pubmed-meshheading:10919675-Apoptosis,
pubmed-meshheading:10919675-Bromodeoxyuridine,
pubmed-meshheading:10919675-Cell Division,
pubmed-meshheading:10919675-DNA (Cytosine-5-)-Methyltransferase,
pubmed-meshheading:10919675-DNA Methylation,
pubmed-meshheading:10919675-DNA Replication,
pubmed-meshheading:10919675-Female,
pubmed-meshheading:10919675-Genes, p53,
pubmed-meshheading:10919675-Genotype,
pubmed-meshheading:10919675-Germ-Line Mutation,
pubmed-meshheading:10919675-Intestinal Neoplasms,
pubmed-meshheading:10919675-Male,
pubmed-meshheading:10919675-Mice,
pubmed-meshheading:10919675-Mice, Inbred C57BL,
pubmed-meshheading:10919675-Mice, Mutant Strains,
pubmed-meshheading:10919675-Mitosis,
pubmed-meshheading:10919675-Mutagenesis, Site-Directed,
pubmed-meshheading:10919675-Neoplasms, Experimental
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pubmed:year |
2000
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pubmed:articleTitle |
Dnmt1N/+ reduces the net growth rate and multiplicity of intestinal adenomas in C57BL/6-multiple intestinal neoplasia (Min)/+ mice independently of p53 but demonstrates strong synergy with the modifier of Min 1(AKR) resistance allele.
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pubmed:affiliation |
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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