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Blood, 1 July 2007, Vol. 110, No. 1, pp. 107-115. Prepublished online as a Blood First Edition Paper on March 14, 2007; DOI 10.1182/blood-2006-08-039628. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-08-039628v1 110/1/107    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 Tanaka, Y. Articles by Kawamata, S. Search for Related Content PubMed PubMed Citation Articles by Tanaka, Y. Articles by Kawamata, S. Related Collections Hematopoiesis and Stem Cells Immunobiology Stem Cells in Hematology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Forced expression of Nanog in hematopoietic stem cells results in a T-cell disorder Yosuke Tanaka1, Takumi Era1, Shin-ichi Nishikawa1,2, and Shin Kawamata1,2 1 Riken Center for Developmental Biology, Kobe, Japan; 2 Foundation for Biomedical Research and Innovation, Kobe, Japan Nanog is a key molecule involved in the maintenance of the self-renewal of undifferentiated embryonic stem (ES) cells. In this work we investigate whether Nanog can enhance self-renewal in hematopoietic stem cells. Contrary to our expectation, no positive effect of Nanog transduction was detected in bone marrow reconstitution assays. However, recipients of Nanog-transduced (Nanog) hematopoietic stem cells (HSCs) invariantly develop a unique disorder typified by an atrophic thymus occupied by Nanog-expressing T-cell receptor–positive (TCR+) cells (Nanog T cells). All thymi are eventually occupied by Nanog T cells with CD25+CD44+ surface phenotype that home selectively to the thymus on transfer and suppress normal thymocyte development, which is partly ascribed to destruction of the microenvironment in the thymus cortex. Moreover, this initial disorder invariantly develops to a lymphoproliferative disorder, in which Nanog T cells undergo unlimited proliferation in the peripheral lymphoid tissues and eventually kill the host. This invariable end result suggests that Nanog is a candidate oncogene for T-cell malignancy. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. S. You, J. K. Kang, D.-W. Seo, J. H. Park, J. W. Park, J. C. Lee, Y. J. Jeon, E. J. Cho, and J.-W. Han Depletion of Embryonic Stem Cell Signature by Histone Deacetylase Inhibitor in NCCIT Cells: Involvement of Nanog Suppression Cancer Res., July 15, 2009; 69(14): 5716 - 5725. [Abstract] [Full Text] [PDF] X. Zhang, I. Neganova, S. Przyborski, C. Yang, M. Cooke, S. P. Atkinson, G. Anyfantis, S. Fenyk, W. N. Keith, S. F. Hoare, et al. A role for NANOG in G1 to S transition in human embryonic stem cells through direct binding of CDK6 and CDC25A J. Cell Biol., January 12, 2009; 184(1): 67 - 82. [Abstract] [Full Text] [PDF] N. Mise, T. Fuchikami, M. Sugimoto, S. Kobayakawa, F. Ike, T. Ogawa, T. Tada, S. Kanaya, T. Noce, and K. Abe Differences and similarities in the developmental status of embryo-derived stem cells and primordial germ cells revealed by global expression profiling. Genes Cells, August 1, 2008; 13(8): 863 - 877. [Abstract] [Full Text] [PDF]

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