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Blood, 15 March 2007, Vol. 109, No. 6, pp. 2597-2603. Prepublished online as a Blood First Edition Paper on December 5, 2006; DOI 10.1182/blood-2006-05-020545. This Article Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2006-05-020545v1 109/6/2597    most recent Alert me when this article is cited Alert me if a correction is posted 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 Dutton, A. Articles by Murray, P. G Search for Related Content PubMed PubMed Citation Articles by Dutton, A. Articles by Murray, P. G Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 15, 2006 Accepted October 21, 2006 BMI-1 is induced by the Epstein-Barr virus oncogene LMP1, and regulates the expression of viral target genes in Hodgkin's lymphoma cells Amanda Dutton, Ciaran B Woodman, Marilyn B Chukwuma, James IK Last, Wenbin Wei, Martina Vockerodt, Karl RN Baumforth, Joanne R Flavell, Martin Rowe, A. Malcolm R Taylor, Lawrence S Young, and Paul G Murray* The Medical School, University of Birmingham, United Kingdom * Corresponding author; email: p.g.murray{at}bham.ac.uk. Polycomb Group (PcG) proteins are chromatin modifiers which are necessary for the maintenance and renewal of embryonic and adult stem cells. However, over-expression of the PcG protein, Bmi-1, causes lymphomas in transgenic mice. We show that Bmi-1 is upregulated in Hodgkin's lymphoma (HL) cells by the Epstein-Barr virus oncogene, latent membrane protein-1 (LMP1), and that this upregulation is mediated by NF-B signalling; we also show that Bmi-1 is upregulated by NF-B in EBV-negative HL cells. Downregulation of LMP1 and Bmi-1 decreased the survival of HL cells, suggesting that Bmi-1 may mediate the pro-survival effects of LMP1-induced NF-B signalling in HL cells. Transcriptional targets of Bmi-1 were identified following its knockdown in a HL cell line. We show here that both Bmi-1 and LMP1 downregulate the ataxia telangiectasia mutated (ATM) tumor suppressor. We conclude that Bmi-1 contributes to LMP1-induced oncogenesis in HL. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. Jiang, J. Li, and L. Song Bmi-1, stem cells and cancer Acta Biochim Biophys Sin, July 1, 2009; 41(7): 527 - 534. [Abstract] [Full Text] [PDF] A. Carbone, E. Cesarman, M. Spina, A. Gloghini, and T. F. Schulz HIV-associated lymphomas and gamma-herpesviruses Blood, February 5, 2009; 113(6): 1213 - 1224. [Abstract] [Full Text] [PDF] M. Janz and S. Mathas The pathogenesis of classical Hodgkin's lymphoma: what can we learn from analyses of genomic alterations in Hodgkin and Reed-Sternberg cells? Haematologica, September 1, 2008; 93(9): 1292 - 1295. [Full Text] [PDF] V. Stagni, M. G. di Bari, S. Cursi, I. Condo, M. T. Cencioni, R. Testi, Y. Lerenthal, E. Cundari, and D. Barila ATM kinase activity modulates Fas sensitivity through the regulation of FLIP in lymphoid cells Blood, January 15, 2008; 111(2): 829 - 837. [Abstract] [Full Text] [PDF]

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