pubmed-article:17183066 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17183066 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:17183066 | lifeskim:mentions | umls-concept:C1512409 | lld:lifeskim |
pubmed-article:17183066 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
pubmed-article:17183066 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:17183066 | pubmed:dateCreated | 2007-4-26 | lld:pubmed |
pubmed-article:17183066 | pubmed:abstractText | The farnesoid X receptor (FXR) controls the synthesis and transport of bile acids (BAs). Mice lacking expression of FXR, designated Fxr-null, have elevated levels of serum and hepatic BAs and an increase in BA pool size. Surprisingly, at 12 months of age, male and female Fxr-null mice had a high incidence of degenerative hepatic lesions, altered cell foci and liver tumors including hepatocellular adenoma, carcinoma and hepatocholangiocellular carcinoma, the latter of which is rarely observed in mice. At 3 months, Fxr-null mice had increased expression of the proinflammatory cytokine IL-1beta mRNA and elevated beta-catenin and its target gene c-myc. They also had increased cell proliferation as revealed by increased PCNA mRNA and BrdU incorporation. These studies reveal a potential role for FXR and BAs in hepatocarcinogenesis. | lld:pubmed |
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pubmed-article:17183066 | pubmed:language | eng | lld:pubmed |
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pubmed-article:17183066 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17183066 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17183066 | pubmed:month | May | lld:pubmed |
pubmed-article:17183066 | pubmed:issn | 0143-3334 | lld:pubmed |
pubmed-article:17183066 | pubmed:author | pubmed-author:MorimuraKeiic... | lld:pubmed |
pubmed-article:17183066 | pubmed:author | pubmed-author:GonzalezFrank... | lld:pubmed |
pubmed-article:17183066 | pubmed:author | pubmed-author:WardJerrold... | lld:pubmed |
pubmed-article:17183066 | pubmed:author | pubmed-author:YangQianQ | lld:pubmed |
pubmed-article:17183066 | pubmed:author | pubmed-author:KimInsookI | lld:pubmed |
pubmed-article:17183066 | pubmed:author | pubmed-author:ShahYatrikY | lld:pubmed |
pubmed-article:17183066 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17183066 | pubmed:volume | 28 | lld:pubmed |
pubmed-article:17183066 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17183066 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17183066 | pubmed:pagination | 940-6 | lld:pubmed |
pubmed-article:17183066 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:17183066 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17183066 | pubmed:articleTitle | Spontaneous hepatocarcinogenesis in farnesoid X receptor-null mice. | lld:pubmed |
pubmed-article:17183066 | pubmed:affiliation | Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. | lld:pubmed |
pubmed-article:17183066 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17183066 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
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