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Blood, 15 May 2004, Vol. 103, No. 10, pp. 3890-3896. Prepublished online as a Blood First Edition Paper on January 15, 2004; DOI 10.1182/blood-2003-10-3695. This Article Full Text (PDF) Supplemental Table All Versions of this Article: 2003-10-3695v1 103/10/3890    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 Morrow, M. Articles by Williams, O. Search for Related Content PubMed PubMed Citation Articles by Morrow, M. Articles by Williams, O. Related Collections Related Article in Blood Online Social Bookmarking                   What's this? Submitted October 29, 2003 Accepted January 10, 2004 TEL-AML1 promotes development of specific hematopoietic lineages consistent with pre-leukemic activity Michelle Morrow, Sarah Horton, Dimitris Kioussis, Hugh J Brady, and Owen Williams* Molecular Haematology and Cancer Biology Unit, Institute of Child Health, University College London, London, United Kingdom Division of Molecular Immunology, National Institute for Medical Research, London, United Kingdom * Corresponding author; email: Owen.Williams{at}ich.ucl.ac.uk. The t(12;21)(p13;q22) translocation is the most common chromosomal abnormality yet identified in any pediatric leukemia and gives rise to the TEL-AML1 fusion product. In order to investigate the effects of TEL-AML1 on hematopoiesis, fetal liver hematopoietic progenitor cells (HPC) were transduced with retroviral vectors expressing this fusion protein. We show that TEL-AML1 dramatically alters differentiation of HPC in vitro, preferentially promoting B lymphocyte development, enhancing self-renewal of B cell precursors and leading to the establishment of long-term growth factor dependent pre-B cell lines. However, it had no effect on myeloid development in vitro. Further experiments were performed to determine whether TEL-AML1 also demonstrates lineage-specific activity in vivo. TEL-AML1 expressing HPC displayed a competitive advantage in reconstituting both B cell and myeloid lineages in vivo but had no effect on reconstitution of the T cell lineage. Despite promoting these alterations in hematopoiesis, TEL-AML1 did not induce leukemia in transplanted mice. Our study provides a unique insight into the role of TEL-AML1 in leukemia predisposition and a potential model to study the mechanism of leukemogenesis associated with this fusion. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: TEL-AML1 and BCR-ABL: different leukemias, similar questions Linda Stork Blood 2004 103: 3611-3612. [Full Text] [PDF] This article has been cited by other articles: S. J. Horton, V. Walf-Vorderwulbecke, S. J. Chatters, N. J. Sebire, J. de Boer, and O. Williams Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities Blood, May 14, 2009; 113(20): 4922 - 4929. [Abstract] [Full Text] [PDF] L. Roudaia, M. D. Cheney, E. Manuylova, W. Chen, M. Morrow, S. Park, C.-T. Lee, P. Kaur, O. Williams, J. H. Bushweller, et al. CBF{beta} is critical for AML1-ETO and TEL-AML1 activity Blood, March 26, 2009; 113(13): 3070 - 3079. [Abstract] [Full Text] [PDF] K. Schmidt, K. Seeger, C. Scheibenbogen, R. Bender, M. Abdulla, S. Sussmilch, A. Salama, and A. 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CpG Island Methylator Phenotype Redefines the Prognostic Effect of t(12;21) in Childhood Acute Lymphoblastic Leukemia. Clin. Cancer Res., August 15, 2006; 12(16): 4845 - 4850. [Abstract] [Full Text] [PDF] S. J. Horton, D. G. Grier, G. J. McGonigle, A. Thompson, M. Morrow, I. De Silva, D. A. Moulding, D. Kioussis, T. R.J. Lappin, H. J.M. Brady, et al. Continuous MLL-ENL Expression Is Necessary to Establish a "Hox Code" and Maintain Immortalization of Hematopoietic Progenitor Cells Cancer Res., October 15, 2005; 65(20): 9245 - 9252. [Abstract] [Full Text] [PDF]

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