| pubmed-article:18692501 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18692501 | lifeskim:mentions | umls-concept:C0013216 | lld:lifeskim |
| pubmed-article:18692501 | lifeskim:mentions | umls-concept:C1417701 | lld:lifeskim |
| pubmed-article:18692501 | lifeskim:mentions | umls-concept:C0153452 | lld:lifeskim |
| pubmed-article:18692501 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:18692501 | lifeskim:mentions | umls-concept:C1427969 | lld:lifeskim |
| pubmed-article:18692501 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:18692501 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:18692501 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:18692501 | pubmed:dateCreated | 2008-10-20 | lld:pubmed |
| pubmed-article:18692501 | pubmed:abstractText | Biliary tract cancer (BTC) is a highly malignant tumor, and identification of effective therapeutic targets to improve prognosis is urgently required. Oncogenic activation of survival genes is important for cancer cells to overcome oxidative stresses induced by their microenvironments that include chronic inflammation or exposure to anticancer drugs. We attempted to examine whether deregulation of Nrf2, a master transcriptional factor of various cytoprotective genes against oxidative stress, plays a role in the carcinogenesis of BTC. | lld:pubmed |
| pubmed-article:18692501 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18692501 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18692501 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:18692501 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18692501 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18692501 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18692501 | pubmed:issn | 1528-0012 | lld:pubmed |
| pubmed-article:18692501 | pubmed:author | pubmed-author:YamamotoMasay... | lld:pubmed |
| pubmed-article:18692501 | pubmed:author | pubmed-author:GotohMasahiro... | lld:pubmed |
| pubmed-article:18692501 | pubmed:author | pubmed-author:HirohashiSets... | lld:pubmed |
| pubmed-article:18692501 | pubmed:author | pubmed-author:KokubuAkikoA | lld:pubmed |
| pubmed-article:18692501 | pubmed:author | pubmed-author:ShibataTatsuh... | lld:pubmed |
| pubmed-article:18692501 | pubmed:author | pubmed-author:OhtaTsutomuT | lld:pubmed |
| pubmed-article:18692501 | pubmed:author | pubmed-author:OjimaHidenori... | lld:pubmed |
| pubmed-article:18692501 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18692501 | pubmed:volume | 135 | lld:pubmed |
| pubmed-article:18692501 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18692501 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18692501 | pubmed:pagination | 1358-1368, 1368.e1-4 | lld:pubmed |
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| pubmed-article:18692501 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18692501 | pubmed:articleTitle | Genetic alteration of Keap1 confers constitutive Nrf2 activation and resistance to chemotherapy in gallbladder cancer. | lld:pubmed |
| pubmed-article:18692501 | pubmed:affiliation | Cancer Genomics Project, National Cancer Center Research Institute, Tokyo, Japan; Pathology Division, National Cancer Center Research Institute, Tokyo, Japan. tashibat@ncc.go.jp | lld:pubmed |
| pubmed-article:18692501 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18692501 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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