| pubmed-article:15125777 | rdf:type | pubmed:Citation | lld:pubmed |
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| pubmed-article:15125777 | lifeskim:mentions | umls-concept:C0678226 | lld:lifeskim |
| pubmed-article:15125777 | lifeskim:mentions | umls-concept:C1424448 | lld:lifeskim |
| pubmed-article:15125777 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:15125777 | lifeskim:mentions | umls-concept:C0025723 | lld:lifeskim |
| pubmed-article:15125777 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:15125777 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:15125777 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:15125777 | pubmed:dateCreated | 2004-7-16 | lld:pubmed |
| pubmed-article:15125777 | pubmed:abstractText | CHK2 kinase is a tumor suppressor that plays important role in DNA damage signaling, cell cycle regulation and DNA damage induced apoptosis. CHK2 kinase expression was known to be ubiquitous in mammalian cells. CHK2-/- cells were remarkably resistant to DNA damage induced apoptosis, mimicking the clinical behavior of non-small cell lung cancer to conventional chemo and radiation therapy. | lld:pubmed |
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| pubmed-article:15125777 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15125777 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15125777 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15125777 | pubmed:month | May | lld:pubmed |
| pubmed-article:15125777 | pubmed:issn | 1476-4598 | lld:pubmed |
| pubmed-article:15125777 | pubmed:author | pubmed-author:RogersJohnJ | lld:pubmed |
| pubmed-article:15125777 | pubmed:author | pubmed-author:ReedEddieE | lld:pubmed |
| pubmed-article:15125777 | pubmed:author | pubmed-author:WangJieJ | lld:pubmed |
| pubmed-article:15125777 | pubmed:author | pubmed-author:YuanBao-ZhuBZ | lld:pubmed |
| pubmed-article:15125777 | pubmed:author | pubmed-author:ZhangPeilinP | lld:pubmed |
| pubmed-article:15125777 | pubmed:author | pubmed-author:GaoWeiyiW | lld:pubmed |
| pubmed-article:15125777 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:15125777 | pubmed:day | 4 | lld:pubmed |
| pubmed-article:15125777 | pubmed:volume | 3 | lld:pubmed |
| pubmed-article:15125777 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15125777 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15125777 | pubmed:pagination | 14 | lld:pubmed |
| pubmed-article:15125777 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:15125777 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15125777 | pubmed:articleTitle | CHK2 kinase expression is down-regulated due to promoter methylation in non-small cell lung cancer. | lld:pubmed |
| pubmed-article:15125777 | pubmed:affiliation | Department of Pathology, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26506-9203, USA. pzhang@hsc.wvu.edu | lld:pubmed |
| pubmed-article:15125777 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15125777 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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