| pubmed-article:16424029 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0007600 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0684249 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0042172 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0312418 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C2916831 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0036667 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:16424029 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:16424029 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:16424029 | pubmed:dateCreated | 2006-1-20 | lld:pubmed |
| pubmed-article:16424029 | pubmed:abstractText | The epidermal growth factor receptor (EGFR) is overexpressed in the majority of non-small cell lung cancers (NSCLC). EGFR tyrosine kinase inhibitors, such as gefitinib and erlotinib, produce 9% to 27% response rates in NSCLC patients. E-Cadherin, a calcium-dependent adhesion molecule, plays an important role in NSCLC prognosis and progression, and interacts with EGFR. The zinc finger transcriptional repressor, ZEB1, inhibits E-cadherin expression by recruiting histone deacetylases (HDAC). We identified a significant correlation between sensitivity to gefitinib and expression of E-cadherin, and ZEB1, suggesting their predictive value for responsiveness to EGFR-tyrosine kinase inhibitors. E-Cadherin transfection into a gefitinib-resistant line increased its sensitivity to gefitinib. Pretreating resistant cell lines with the HDAC inhibitor, MS-275, induced E-cadherin along with EGFR and led to a growth-inhibitory and apoptotic effect of gefitinib similar to that in gefitinib-sensitive NSCLC cell lines including those harboring EGFR mutations. Thus, combined HDAC inhibitor and gefitinib treatment represents a novel pharmacologic strategy for overcoming resistance to EGFR inhibitors in patients with lung cancer. | lld:pubmed |
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| pubmed-article:16424029 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16424029 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16424029 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16424029 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16424029 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:16424029 | pubmed:author | pubmed-author:GazdarAdi FAF | lld:pubmed |
| pubmed-article:16424029 | pubmed:author | pubmed-author:MinnaJohn DJD | lld:pubmed |
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| pubmed-article:16424029 | pubmed:author | pubmed-author:ZengChanC | lld:pubmed |
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| pubmed-article:16424029 | pubmed:author | pubmed-author:WittaSamir... | lld:pubmed |
| pubmed-article:16424029 | pubmed:author | pubmed-author:RavdelLarisaL | lld:pubmed |
| pubmed-article:16424029 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16424029 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:16424029 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:16424029 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16424029 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16424029 | pubmed:pagination | 944-50 | lld:pubmed |
| pubmed-article:16424029 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16424029 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16424029 | pubmed:articleTitle | Restoring E-cadherin expression increases sensitivity to epidermal growth factor receptor inhibitors in lung cancer cell lines. | lld:pubmed |
| pubmed-article:16424029 | pubmed:affiliation | Department of Medicine/Medical Oncology, University of Colorado Health Sciences Center and University of Colorado Cancer Center, Campus Box 8117, PO Box 6511, Aurora, CO 80045, USA. Samir.Witta@uchsc.edu | lld:pubmed |
| pubmed-article:16424029 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16424029 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16424029 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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