pubmed-article:18973272 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18973272 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
pubmed-article:18973272 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
pubmed-article:18973272 | lifeskim:mentions | umls-concept:C0162714 | lld:lifeskim |
pubmed-article:18973272 | lifeskim:mentions | umls-concept:C0292818 | lld:lifeskim |
pubmed-article:18973272 | lifeskim:mentions | umls-concept:C0332448 | lld:lifeskim |
pubmed-article:18973272 | lifeskim:mentions | umls-concept:C0598934 | lld:lifeskim |
pubmed-article:18973272 | lifeskim:mentions | umls-concept:C2266986 | lld:lifeskim |
pubmed-article:18973272 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
pubmed-article:18973272 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:18973272 | pubmed:dateCreated | 2008-11-27 | lld:pubmed |
pubmed-article:18973272 | pubmed:abstractText | Epstein-Barr Virus (EBV)-associated immunoblastic lymphoma occurs in immunocompromised patients such as those with AIDS or transplant recipients after primary EBV infection or reactivation of a preexisting latent EBV infection. In the present study, we evaluated the effect of ritonavir, an HIV protease inhibitor, on EBV-positive lymphoblastoid B cells in vitro and in mice model. We found that it induced cell-cycle arrest at G1-phase and apoptosis through down-regulation of cell-cycle gene cyclin D2 and antiapoptotic gene survivin. Furthermore, ritonavir suppressed transcriptional activation of NF-kappaB in these cells. Ritonavir efficiently prevented growth and infiltration of lymphoma cells in various organs of NOD/SCID/gammacnull mice at the same dose used for treatment of patients with AIDS. Our results indicate that ritonavir targets NF-kappaB activated in tumor cells and shows anti-tumor effects. These data also suggest that this compound may have promise for treatment or prevention of EBV-associated lymphoproliferative diseases that occur in immunocompromised patients. | lld:pubmed |
pubmed-article:18973272 | pubmed:language | eng | lld:pubmed |
pubmed-article:18973272 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18973272 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18973272 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18973272 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18973272 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18973272 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18973272 | pubmed:month | Feb | lld:pubmed |
pubmed-article:18973272 | pubmed:issn | 1097-0215 | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:SataTetsutaro... | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:YamamotoNorio... | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:YamamotoNaoki... | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:MoriNaokiN | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:YamamotoMichi... | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:KatanoHarutak... | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:TomitaMarikoM | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:DewanMd... | lld:pubmed |
pubmed-article:18973272 | pubmed:author | pubmed-author:AhmedSunjidaS | lld:pubmed |
pubmed-article:18973272 | pubmed:copyrightInfo | Copyright (c) 2008 Wiley-Liss, Inc. | lld:pubmed |
pubmed-article:18973272 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18973272 | pubmed:day | 1 | lld:pubmed |
pubmed-article:18973272 | pubmed:volume | 124 | lld:pubmed |
pubmed-article:18973272 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18973272 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18973272 | pubmed:pagination | 622-9 | lld:pubmed |
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pubmed-article:18973272 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:18973272 | pubmed:articleTitle | An HIV protease inhibitor, ritonavir targets the nuclear factor-kappaB and inhibits the tumor growth and infiltration of EBV-positive lymphoblastoid B cells. | lld:pubmed |
pubmed-article:18973272 | pubmed:affiliation | Department of Molecular Virology, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. | lld:pubmed |
pubmed-article:18973272 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18973272 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |