pubmed-article:19563669 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19563669 | lifeskim:mentions | umls-concept:C0006142 | lld:lifeskim |
pubmed-article:19563669 | lifeskim:mentions | umls-concept:C0893445 | lld:lifeskim |
pubmed-article:19563669 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
pubmed-article:19563669 | lifeskim:mentions | umls-concept:C0243076 | lld:lifeskim |
pubmed-article:19563669 | lifeskim:mentions | umls-concept:C0205195 | lld:lifeskim |
pubmed-article:19563669 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:19563669 | pubmed:dateCreated | 2009-7-28 | lld:pubmed |
pubmed-article:19563669 | pubmed:abstractText | Inhibitor of apoptosis (IAPs) proteins are a family of proteins that can block apoptosis in normal cells and have been suggested to cause resistance to apoptosis in cancer. Overexpression of oncogenic receptor tyrosine kinases is common in breast cancer; in particular 20% of all cases show elevated Her2. Despite clinical success with the use of targeted therapies, such as Trastuzumab, only up to 35% of Her2-positive patients initially respond. We reasoned that IAP-mediated apoptosis resistance might contribute to this insensitivity to receptor tyrosine kinase therapy, in particular ErbB antagonists. Here we examine the levels of IAPs in breast cancer and evaluate whether targeting IAPs can enhance apoptosis in response to growth factor receptor antagonists and TRAIL. | lld:pubmed |
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pubmed-article:19563669 | pubmed:language | eng | lld:pubmed |
pubmed-article:19563669 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563669 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19563669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19563669 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19563669 | pubmed:issn | 1465-542X | lld:pubmed |
pubmed-article:19563669 | pubmed:author | pubmed-author:BundredNigel... | lld:pubmed |
pubmed-article:19563669 | pubmed:author | pubmed-author:StreuliCharle... | lld:pubmed |
pubmed-article:19563669 | pubmed:author | pubmed-author:BrennanKeithK | lld:pubmed |
pubmed-article:19563669 | pubmed:author | pubmed-author:ClarkeRobert... | lld:pubmed |
pubmed-article:19563669 | pubmed:author | pubmed-author:FosterFiona... | lld:pubmed |
pubmed-article:19563669 | pubmed:author | pubmed-author:Tanianis-Hugh... | lld:pubmed |
pubmed-article:19563669 | pubmed:author | pubmed-author:OwensThomas... | lld:pubmed |
pubmed-article:19563669 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19563669 | pubmed:volume | 11 | lld:pubmed |
pubmed-article:19563669 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19563669 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19563669 | pubmed:pagination | R41 | lld:pubmed |
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