| pubmed-article:19350262 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19350262 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:19350262 | lifeskim:mentions | umls-concept:C2239176 | lld:lifeskim |
| pubmed-article:19350262 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:19350262 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:19350262 | lifeskim:mentions | umls-concept:C0449774 | lld:lifeskim |
| pubmed-article:19350262 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:19350262 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:19350262 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19350262 | pubmed:dateCreated | 2009-6-9 | lld:pubmed |
| pubmed-article:19350262 | pubmed:abstractText | Hepatocellular carcinoma (HCC) represents the sixth most frequent human cancer worldwide and is characterized by rapid progression as well as resistance to systemic chemotherapy. Recently, glycolysis has emerged as a potent driving force of tumor growth and therapy failure. The precise role of glycolysis for the pathogenesis of human HCC has not been elucidated thus far. Therefore, we have conducted a comprehensive analysis of the expression patterns of central glycolysis-related factors [glucose transporter-1 and -2 (Glut-1 and Glut-2), phosphoglycerate kinase-1 (PGK-1) and hypoxia-inducible factor-1alpha (HIF-1alpha)] in a large cohort of benign and malignant human liver samples. PGK-1 protein and gene expression was scant in normal liver, elevated in cirrhotic livers and most intense in HCC. Strong immunoreactivity of Glut-2 was noted in cirrhotic livers, whereas in HCC it was only expressed in 50% of examined cases. Strikingly, PGK-1 as well as Glut-2 protein expression was indicative of poor patient prognosis. Glut-1 protein was absent in neoplastic hepatocytes but prominent in tumor-associated endothelial cells. Specific nuclear staining of HIF-1alpha was noted in only 12% of HCC samples. Our data point toward a tumor-promoting function of glycolysis in HCC and establish PGK-1 as an independent prognostic parameter. Furthermore, the endothelial-specific expression of Glut-1 makes a special dependence of vessels on glucose reasonable to assume. In summary, we believe our analysis warrants the validation of glycolytic inhibitors as innovative treatment approaches of human HCC. | lld:pubmed |
| pubmed-article:19350262 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19350262 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19350262 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19350262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19350262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19350262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19350262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19350262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19350262 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19350262 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:19350262 | pubmed:issn | 1432-119X | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:NeuhausPeterP | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:WiedenmannBer... | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:JonasSvenS | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:CramerThorste... | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:ThelenArminA | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:BenckertChris... | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:PfanderDavidD | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:WeichertWilko... | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:DaskalowKatja... | lld:pubmed |
| pubmed-article:19350262 | pubmed:author | pubmed-author:RohwerNadineN | lld:pubmed |
| pubmed-article:19350262 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19350262 | pubmed:volume | 132 | lld:pubmed |
| pubmed-article:19350262 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19350262 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19350262 | pubmed:pagination | 21-31 | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:meshHeading | pubmed-meshheading:19350262... | lld:pubmed |
| pubmed-article:19350262 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19350262 | pubmed:articleTitle | Distinct temporospatial expression patterns of glycolysis-related proteins in human hepatocellular carcinoma. | lld:pubmed |
| pubmed-article:19350262 | pubmed:affiliation | Medizinische Klink mit Schwerpunkt Hepatologie und Gastroenterologie, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany. | lld:pubmed |
| pubmed-article:19350262 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19350262 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19350262 | lld:pubmed |
