| http://purl.uniprot.org/citations/21156972 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21156972 | http://www.w3.org/2000/01/rdf-schema#comment | "The causal metabolic pathways underlying associations between folate and risk for colorectal cancer (CRC) have yet to be established. Folate-mediated one-carbon metabolism is required for the de novo synthesis of purines, thymidylate and methionine. Methionine is converted to S-adenosylmethionine (AdoMet), the major one-carbon donor for cellular methylation reactions. Impairments in folate metabolism can modify DNA synthesis, genomic stability and gene expression, characteristics associated with tumorigenesis. The Mthfd1 gene product, C1-tetrahydrofolate synthase, is a trifunctional enzyme that generates one-carbon substituted tetrahydrofolate cofactors for one-carbon metabolism. In this study, we use Mthfd1(gt/+) mice, which demonstrate a 50% reduction in C1-tetrahydrofolate synthase, to determine its influence on tumor development in two mouse models of intestinal cancer, crosses between Mthfd1(gt/+) and Apc(min)(/+) mice and azoxymethane (AOM)-induced colon cancer in Mthfd1(gt/+) mice. Mthfd1 hemizygosity did not affect colon tumor incidence, number or load in Apc(min/+) mice. However, Mthfd1 deficiency increased tumor incidence 2.5-fold, tumor number 3.5-fold and tumor load 2-fold in AOM-treated mice. DNA uracil content in the colon was lower in Mthfd1(gt/+) mice, indicating that thymidylate biosynthesis capacity does not play a significant role in AOM-induced colon tumorigenesis. Mthfd1 deficiency-modified cellular methylation potential, as indicated by the AdoMet: S-adenosylhomocysteine ratio and gene expression profiles, suggesting that changes in the transcriptome and/or decreased de novo purine biosynthesis and associated mutability cause cellular transformation in the AOM CRC model. This study emphasizes the impact and complexity of gene-nutrient interactions with respect to the relationships among folate metabolism and colon cancer initiation and progression."xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.org/dc/terms/identifier | "doi:10.1093/carcin/bgq270"xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/author | "Perry C.A."xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/author | "Stover P.J."xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/author | "Lin D.M."xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/author | "MacFarlane A.J."xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/author | "McEntee M.F."xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/name | "Carcinogenesis"xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/pages | "427-433"xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/title | "Mthfd1 is a modifier of chemically induced intestinal carcinogenesis."xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://purl.uniprot.org/core/volume | "32"xsd:string |
| http://purl.uniprot.org/citations/21156972 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21156972 |
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