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Blood, 15 September 2005, Vol. 106, No. 6, pp. 2147-2155. Prepublished online as a Blood First Edition Paper on May 24, 2005; DOI 10.1182/blood-2004-11-4330. This Article Full Text (PDF) All Versions of this Article: 2004-11-4330v1 106/6/2147    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Maki, K. Articles by Mitani, K. Search for Related Content PubMed PubMed Citation Articles by Maki, K. Articles by Mitani, K. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 12, 2004 Accepted May 16, 2005 Dysplastic definitive hematopoiesis in AML1/Evi-1 knock-in embryos Kazuhiro Maki, Tetsuya Yamagata, Takashi Asai, Ieharu Yamazaki, Hideaki Oda, Hisamaru Hirai, and Kinuko Mitani* Department of Hematology, Dokkyo University School of Medicine, Tochigi, Japan Section on Immunology and Immunogenetics, Joslin Diabetes Center, Harvard Medical School, Boston, USA Department of Hematology & Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan Department of Clinical Laboratory and Pathology, Inoue Memorial Hospital, Chiba, Japan Department of Pathology, Tokyo Women's Medical University, Tokyo, Japan * Corresponding author; email: kinukom-tky{at}umin.ac.jp. The AML1/Evi-1 chimeric gene is created by the t(3;21)(q26;q22) chromosomal translocation seen in patients with leukemic transformation of myelodysplastic syndrome or blastic crisis of chronic myelogenous leukemia. We knocked-in the AML1/Evi-1 chimeric gene into mouse AML1 genomic locus to explore its effect in developmental hematopoiesis in vivo. AML1/Evi-1/+ embryo showed defective hematopoiesis in the fetal liver, and died around E13.5 due to hemorrhage in the central nervous system. The peripheral blood had yolk sac-derived nucleated erythroblasts but lacked erythrocytes of the definitive origin. While E12.5 fetal liver contained progenitors for macrophage only, E13.5 fetal liver contained multi-lineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte. No erythroid progenitor was detected in E12.5 or E13.5 fetal liver. Hematopoietic progenitor from E13.5 AML1/Evi-1/+ fetal liver was highly self-renewal compared to that from wild-type liver. Maintained expression of PU.1 gene and decreased expression of LMO2 and SCL genes may explain the aberrant hematopoiesis in AML1/Evi-1/+ fetal liver. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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