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Blood, 1 July 2005, Vol. 106, No. 1, pp. 235-240. Prepublished online as a Blood First Edition Paper on March 24, 2005; DOI 10.1182/blood-2004-09-3748. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-09-3748v1 106/1/235    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kurokawa, M. Articles by Harrington, W. J. Search for Related Content PubMed PubMed Citation Articles by Kurokawa, M. Articles by Harrington, W. J., Jr Related Collections Neoplasia Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Azidothymidine inhibits NF-B and induces Epstein-Barr virus gene expression in Burkitt lymphoma Motoki Kurokawa, Subrata K. Ghosh, Juan Carlos Ramos, Abdul M. Mian, Ngoc L. Toomey, Lisa Cabral, Denise Whitby, Glen N. Barber, Dirk P. Dittmer, and William J. Harrington, Jr From the Department of Dermatology, Medical College, University of Miyazaki, Japan; Departments of Medicine and Microbiology and Immunology, University of Miami School of Medicine, FL: Viral Epidemiology Section, AIDS Vaccine Program, SAIC-Frederick, National Cancer Institute–Frederick, MD; and Department of Microbiology and Immunology, The University of North Carolina, Chapel Hill, NC. The antiviral compound azidothymidine (AZT), alone or in combination with other agents, induces apoptosis in early-passage, Epstein-Barr virus–positive Burkitt lymphoma (EBV+ BL) lines and has clinical activity in EBV+ BL. We report here a mechanism of AZT's antitumor activity. The nuclei of these cells contain activated nuclear factor-B (NF-B) subunits p50, c-Rel, RelB, and p52, but not p65. Treatment of primary EBV+ BL lines with AZT inhibited NF-B within 1 to 2 hours. This was followed by up-regulation of EBV gene expression including viral thymidine kinase (vTK) and apoptosis. Subclones of EBV+ BL cells that demonstrated activated p65 were resistant to AZT. In EBV+ BLs, AZT but not ganciclovir (GCV) was highly phosphorylated to its monophosphate form (AZT-MP). Phosphorylation, as well as apoptosis, was markedly enhanced in the presence of hydroxyurea. AZT inhibits NF-B and up-regulates EBV gene expression in primary EBV+ BLs. AZT with hydroxyurea may represent an inexpensive, targeted regimen for endemic BL. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F.-Z. Wang, D. Roy, E. Gershburg, C. B. Whitehurst, D. P. Dittmer, and J. S. Pagano Maribavir Inhibits Epstein-Barr Virus Transcription in Addition to Viral DNA Replication J. Virol., December 1, 2009; 83(23): 12108 - 12117. [Abstract] [Full Text] [PDF] Z. Han, D. Verma, C. Hilscher, D. P. Dittmer, and S. Swaminathan General and Target-Specific RNA Binding Properties of Epstein-Barr Virus SM Posttranscriptional Regulatory Protein J. Virol., November 15, 2009; 83(22): 11635 - 11644. [Abstract] [Full Text] [PDF] M. L. Gulley and W. Tang Laboratory Assays for Epstein-Barr Virus-Related Disease J. Mol. Diagn., July 1, 2008; 10(4): 279 - 292. [Abstract] [Full Text] [PDF] T. Xia, A. O'Hara, I. Araujo, J. Barreto, E. Carvalho, J. B. Sapucaia, J. C. Ramos, E. Luz, C. Pedroso, M. 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