SEARCH:   Advanced

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 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 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 Dutton, A. Articles by Murray, P. G. Search for Related Content PubMed PubMed Citation Articles by Dutton, A. Articles by Murray, P. G. Related Collections Neoplasia Oncogenes and Tumor Suppressors Free Research Articles Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Bmi-1 is induced by the Epstein-Barr virus oncogene LMP1 and regulates the expression of viral target genes in Hodgkin lymphoma cells Amanda Dutton1, Ciaran B. Woodman1, Marilyn B. Chukwuma1, James I. K. Last1, Wenbin Wei1, Martina Vockerodt1, Karl R. N. Baumforth1, Joanne R. Flavell1, Martin Rowe1, A. Malcolm R. Taylor1, Lawrence S. Young1, and Paul G. Murray1 1 Cancer Research UK Institute for Cancer Studies, The Medical School, University of Birmingham, Edgbaston, United Kingdom Polycomb group (PcG) proteins are chromatin modifiers that are necessary for the maintenance and renewal of embryonic and adult stem cells. However, overexpression of the PcG protein, Bmi-1, causes lymphoma in transgenic mice. We show that Bmi-1 is up-regulated in Hodgkin lymphoma (HL) cells by the Epstein-Barr virus (EBV) oncogene latent membrane protein-1 (LMP1) and that this up-regulation is mediated by NF-B signaling. We also show that Bmi-1 is up-regulated by NF-B in EBV-negative HL cells. Down-regulation of LMP1 and Bmi-1 decreased the survival of HL cells, suggesting that Bmi-1 may mediate the prosurvival effects of LMP1-induced NF-B signaling in HL cells. Transcriptional targets of Bmi-1 were identified after its knockdown in an HL cell line. We show here that Bmi-1 and LMP1 down-regulate the ataxia telangiectasia–mutated (ATM) tumor suppressor and 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] 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]

	Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020