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Azidothymidine inhibits NF-kappa B and induces Epstein-Barr virus gene expression in Burkitt lymphoma

  1. Author:
    Kurokawa, M.
    Ghosh, S. K.
    Ramos, J. C.
    Mian, A. M.
    Toomey, N. L.
    Cabral, L.
    Whitby, D.
    Barber, G. N.
    Dittmer, D. P.
    Harrington, W. J.

  2. Author Address

    Univ Miami, Sch Med, Sylvester Comprehens Canc Ctr, Dept Med, Miami, FL 33136 USA. Univ Miami, Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA. Miyazaki Univ, Coll Med, Dept Dermatol, Miyazaki, Japan. NCI, Viral Epidemiol Sect, AIDS Vaccine Program, SAIC Frederick, Frederick, MD 21701 USA. Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC USA Harrington, WJ, Univ Miami, Sch Med, Sylvester Comprehens Canc Ctr, Dept Med, Room 3400,1475 NW 12th Ave D8-4, Miami, FL 33136 USA
    1. Year: 2005
    2. Date: JUL 1
  2. Journal: Blood
    1. 106
    2. 1
    3. Pages: 235-240
  4. Type of Article: Article
  1. Abstract:

    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-kappa B (NF-kappa B) sub-units p50, c-Rel, RelB, and p52, but not p65. Treatment of primary EBV+ BL lines with AZT inhibited NF-kappa 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-MID). Phosphorylation, as well as apoptosis, was markedly enhanced in the presence of hydroxyurea. AZT inhibits NF-kappa B and up-regulates EBV gene expression in primary EBV+ BLs. AZT with hydroxyurea may represent an inexpensive, targeted regimen for endemic BL

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External Sources

  1. View record in Web of Science®
  2. WOS: 000230156500040

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