| pubmed-article:17978477 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C1148756 | lld:lifeskim |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C0733521 | lld:lifeskim |
| pubmed-article:17978477 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:17978477 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:17978477 | pubmed:dateCreated | 2007-11-5 | lld:pubmed |
| pubmed-article:17978477 | pubmed:abstractText | Cytosine arabinoside (1-beta-D-arabinofuranosylcytosine; Ara-C) is the most important antimetabolite used to induce remission in acute leukemia, but cellular resistance to Ara-C reflects a poor prognosis in cancer chemotherapy. To further investigate the mechanisms of resistance to Ara-C, we have established Ara-C-resistant NALM-6 cells. The activation of nuclear factor kappaB (NF-kappaB) was accompanied by the acquisition of Ara-C resistance. Telomerase activity has also increased with the acquisition of Ara-C resistance. The expression of Bid, Bax, or p53 proteins have been shown to increase correlated with the acquisition of Ara-C resistance. In contrast to the increase in these proteins, Bcl-2, Bcl-x, and Bag-1 proteins remained unchanged with the acquisition of Ara-C resistance. Fas expression increased with the acquisition of Ara-C resistance in the late stage. The induction of apoptosis and reduction of cell viability by cytotoxic anti-Fas antibody was more susceptible in resistant cells than parental cells. In conclusion, this report has shown that resistance to Ara-C up-regulates the activation of NF-kappaB, telomerase activity and Fas expression. | lld:pubmed |
| pubmed-article:17978477 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17978477 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17978477 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17978477 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17978477 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17978477 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17978477 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17978477 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:17978477 | pubmed:issn | 0918-6158 | lld:pubmed |
| pubmed-article:17978477 | pubmed:author | pubmed-author:IshikawaMasaa... | lld:pubmed |
| pubmed-article:17978477 | pubmed:author | pubmed-author:ShoujiAiA | lld:pubmed |
| pubmed-article:17978477 | pubmed:author | pubmed-author:KannoSyu-ichi... | lld:pubmed |
| pubmed-article:17978477 | pubmed:author | pubmed-author:HiuraTakakoT | lld:pubmed |
| pubmed-article:17978477 | pubmed:author | pubmed-author:OsanaiYuuY | lld:pubmed |
| pubmed-article:17978477 | pubmed:author | pubmed-author:UjibeMayukoM | lld:pubmed |
| pubmed-article:17978477 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17978477 | pubmed:volume | 30 | lld:pubmed |
| pubmed-article:17978477 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17978477 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17978477 | pubmed:pagination | 2069-74 | lld:pubmed |
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| pubmed-article:17978477 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17978477 | pubmed:articleTitle | Resistance to Ara-C up-regulates the activation of NF-kappaB, telomerase activity and Fas expression in NALM-6 cells. | lld:pubmed |
| pubmed-article:17978477 | pubmed:affiliation | Department of Clinical Pharmacotherapeutics, Tohoku Pharmaceutical University, 4-4-1 Komatsushima, Aoba-ku, Sendai, Japan. syu-kan@tohoku-pharm.ac.jp | lld:pubmed |
| pubmed-article:17978477 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17978477 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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