SEARCH:   Advanced

Blood, 1 July 2007, Vol. 110, No. 1, pp. 388-392. Prepublished online as a Blood First Edition Paper on March 14, 2007; DOI 10.1182/blood-2006-12-064816. This Article Full Text Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2006-12-064816v1 110/1/388    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 Dik, W. A. Articles by Langerak, A. W. Search for Related Content PubMed PubMed Citation Articles by Dik, W. A. Articles by Langerak, A. W. Related Collections Neoplasia Oncogenes and Tumor Suppressors Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief Report Different chromosomal breakpoints impact the level of LMO2 expression in T-ALL Willem A. Dik1, Bertrand Nadel2, Grzegorz K. Przybylski3,4, Vahid Asnafi5, Piotr Grabarczyk4, Jean Marc Navarro2, Brenda Verhaaf1, Christian A. Schmidt4, Elizabeth A. Macintyre5, Jacques J. M. van Dongen1, and Anton W. Langerak1 1 Department of Immunology, Erasmus Medical Center, Rotterdam, The Netherlands; 2 Centre d'Immunologie de Marseille-Luminy (CIML), Institute Nationale de Santé et Recherche Médicale-Centre Nationale de Recherche Scientifique (INSERM-CNRS)-Université de la Méditerranée, Marseille, France; 3 Institute of Human Genetics, Polish Academy of Sciences, Poznan, Poland; 4 Klinik für Innere Medizin C, Universität Greifswald, Germany; 5 Department of Hematology, Université Paris-Descartes, Faculté de Médecine, Hôpital Necker-Enfants-Malades, Paris, France The t(11;14)(p13;q11) is presumed to arise from an erroneous T-cell receptor delta TCRD V(D)J recombination and to result in LMO2 activation. However, the mechanisms underlying this translocation and the resulting LMO2 activation are poorly defined. We performed combined in vivo, ex vivo, and in silico analyses on 9 new t(11;14)(p13;q11)-positive T-cell acute lymphoblastic leukemia (T-ALL) as well as normal thymocytes. Our data support the involvement of 2 distinct t(11;14)(p13;q11) V(D)J-related translocation mechanisms. We provide compelling evidence that removal of a negative regulatory element from the LMO2 locus, rather than juxtaposition to the TCRD enhancer, is the main determinant for LMO2 activation in the majority of t(11;14)(p13;q11) translocations. Furthermore, the position of the LMO2 breakpoints in T-ALL in the light of the occurrence of TCRD-LMO2 translocations in normal thymocytes points to a critical role for the exact breakpoint location in determining LMO2 activation levels and the consequent pressure for T-ALL development. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. van Steensel, D. Paridaens, B. Schrijver, G. M. Dingjan, P. L. A. van Daele, P. M. van Hagen, W. A. van den Bosch, H. A. Drexhage, H. Hooijkaas, and W. A. Dik Imatinib Mesylate and AMN107 Inhibit PDGF-Signaling in Orbital Fibroblasts: A Potential Treatment for Graves' Ophthalmopathy Invest. Ophthalmol. Vis. Sci., July 1, 2009; 50(7): 3091 - 3098. [Abstract] [Full Text] [PDF]

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