pubmed-article:20668531 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20668531 | lifeskim:mentions | umls-concept:C1335274 | lld:lifeskim |
pubmed-article:20668531 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
pubmed-article:20668531 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:20668531 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:20668531 | pubmed:dateCreated | 2010-7-29 | lld:pubmed |
pubmed-article:20668531 | pubmed:abstractText | Proteins that are required for anchorage-independent survival of tumor cells represent attractive targets for therapeutic intervention since this property is believed to be critical for survival of tumor cells displaced from their natural niches. Anchorage-independent survival is induced by growth factor receptor hyperactivation in many cell types. We aimed to identify molecules that critically regulate IGF-1-induced anchorage-independent survival. | lld:pubmed |
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pubmed-article:20668531 | pubmed:language | eng | lld:pubmed |
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pubmed-article:20668531 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20668531 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20668531 | pubmed:issn | 1932-6203 | lld:pubmed |
pubmed-article:20668531 | pubmed:author | pubmed-author:RodT OTO | lld:pubmed |
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pubmed-article:20668531 | pubmed:author | pubmed-author:IidaNaokoN | lld:pubmed |
pubmed-article:20668531 | pubmed:author | pubmed-author:EpsteinCharle... | lld:pubmed |
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pubmed-article:20668531 | pubmed:author | pubmed-author:SelforsLaura... | lld:pubmed |
pubmed-article:20668531 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20668531 | pubmed:volume | 5 | lld:pubmed |
pubmed-article:20668531 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20668531 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20668531 | pubmed:pagination | e11729 | lld:pubmed |