pubmed-article:12810624 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12810624 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:12810624 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
pubmed-article:12810624 | lifeskim:mentions | umls-concept:C0596263 | lld:lifeskim |
pubmed-article:12810624 | lifeskim:mentions | umls-concept:C1420045 | lld:lifeskim |
pubmed-article:12810624 | lifeskim:mentions | umls-concept:C1422341 | lld:lifeskim |
pubmed-article:12810624 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:12810624 | lifeskim:mentions | umls-concept:C2697585 | lld:lifeskim |
pubmed-article:12810624 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:12810624 | pubmed:dateCreated | 2003-6-17 | lld:pubmed |
pubmed-article:12810624 | pubmed:abstractText | Through a genome-wide cDNA microarray, we identified that the paternally expressed gene 10 (PEG10) was highly expressed in a great majority of hepatocellular carcinomas, although its expression was absent in normal liver cells. Exogenous expression of PEG10 conferred oncogenic activity and transfection of hepatoma cells with antisense S-oligonucleotides suppressing PEG10 resulted in their growth inhibition. Additional experiments revealed that PEG10 protein associated with SIAH1, a mediator of apoptosis, and that overexpression of PEG10 decreased the cell death mediated by SIAH1. These findings suggested that development of drug(s) inhibiting PEG10 activity could be a novel approach for the treatment of hepatocellular carcinomas. | lld:pubmed |
pubmed-article:12810624 | pubmed:language | eng | lld:pubmed |
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pubmed-article:12810624 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12810624 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12810624 | pubmed:month | Jun | lld:pubmed |
pubmed-article:12810624 | pubmed:issn | 0008-5472 | lld:pubmed |
pubmed-article:12810624 | pubmed:author | pubmed-author:NakamuraYusuk... | lld:pubmed |
pubmed-article:12810624 | pubmed:author | pubmed-author:YamaokaYoshio... | lld:pubmed |
pubmed-article:12810624 | pubmed:author | pubmed-author:FurukawaYoich... | lld:pubmed |
pubmed-article:12810624 | pubmed:author | pubmed-author:HasegawaSugur... | lld:pubmed |
pubmed-article:12810624 | pubmed:author | pubmed-author:OkabeHiroshiH | lld:pubmed |
pubmed-article:12810624 | pubmed:author | pubmed-author:SatohSeijiS | lld:pubmed |
pubmed-article:12810624 | pubmed:author | pubmed-author:KatoTatsushiT | lld:pubmed |
pubmed-article:12810624 | pubmed:author | pubmed-author:NakajimaYumiY | lld:pubmed |
pubmed-article:12810624 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12810624 | pubmed:day | 15 | lld:pubmed |
pubmed-article:12810624 | pubmed:volume | 63 | lld:pubmed |
pubmed-article:12810624 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12810624 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12810624 | pubmed:pagination | 3043-8 | lld:pubmed |
pubmed-article:12810624 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:12810624 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12810624 | pubmed:articleTitle | Involvement of PEG10 in human hepatocellular carcinogenesis through interaction with SIAH1. | lld:pubmed |
pubmed-article:12810624 | pubmed:affiliation | Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. | lld:pubmed |
pubmed-article:12810624 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12810624 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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