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This Article Full Text Full Text (PDF) 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 El-Sabban, M. E. Articles by Bazarbachi, A. Search for Related Content PubMed PubMed Citation Articles by El-Sabban, M. E. Articles by Bazarbachi, A. Related Collections Neoplasia Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 October 2000, Vol. 96, No. 8, pp. 2849-2855 NEOPLASIA Arsenic-interferon--triggered apoptosis in HTLV-I transformed cells is associated with Tax down-regulation and reversal of NF-B activation Marwan E. El-Sabban, Rihab Nasr, Ghassan Dbaibo, Olivier Hermine, Nour Abboushi, Frédérique Quignon, Jean Claude Ameisen, Françoise Bex, Hugues de Thé, and Ali Bazarbachi From the Departments of Human Morphology, Internal Medicine, Biochemistry, and Pediatrics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; CNRS URA 1461 and Department of Hematology, Necker Hospital, Paris, France; UPR 9051 CNRS Laboratoire associé No. 11 du comité de Paris de la Ligue contre le Cancer, conventionné par l'Université Paris VII, Hôpital St Louis, Paris, France; INSERM CJF 9701, Hôpital Bichat, Paris, France; and Departement de Biologie Moléculaire, Université Libre de Bruxelles, Brussels, Belgium. Human T-cell lymphotropic virus type I (HTLV-I)-associated adult T-cell leukemia/lymphoma (ATL) is a malignancy of mature activated T cells resistant to conventional chemotherapy. The viral transactivator protein Tax plays a critical role in HTLV-I-induced transformation and apoptosis resistance by inducing IB- degradation, resulting in the activation of the NF-Bpathway. In these HTLV-I-transformed cells, arsenic trioxide (As) and interferon (IFN)- synergize to induce cell cycle arrest and apoptosis. We demonstrate that cell death induction is only partly dependent upon caspase activation and is not associated with modulation of bcl-2, bax, or p53 expression. However, combined As and IFN induce the degradation of Tax, associated with an up-regulation of IB- resulting in a sharp decrease in RelA DNA binding nuclear factor (NF)-B complexes because of the cytoplasmic retention of RelA. Taken the role of Tax in HTLV-I-induced transformation, its down-regulation probably accounts for cell death induction through inactivation of the NF-B pathway. Such specific targeting of the viral oncoprotein by As-IFN treatment, reminiscent of As targeting of promyelocytic leukemia/retinoic acid receptor- in acute promyelocytic leukemia, provides strong rational for combined As-IFN therapy in ATL patients. © 2000 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M.-O. Chandesris, D. Ghez, C. Besson, F. Suarez, R. Delarue, M.-T. Rubio, A. Bazarbachi, B. Varet, and O. Hermine Complete remission of a relapsing adult T cell leukaemia following treatment of a secondary acute promyelocytic leukaemia: towards a reappraisal of arsenic trioxide and all-transretinoic acid? BMJ Case Reports, August 10, 2009; 2009(aug10_1): bcr0120091449 - bcr0120091449. [Abstract] [Full Text] G. Kchour, M. Tarhini, M.-M. Kooshyar, H. El Hajj, E. Wattel, M. Mahmoudi, H. Hatoum, H. Rahimi, M. Maleki, H. Rafatpanah, et al. 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