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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.

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NEOPLASIA

Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos

Kazuhiro Maki, Tetsuya Yamagata, Takashi Asai, Ieharu Yamazaki, Hideaki Oda, Hisamaru Hirai, and Kinuko Mitani

From the Department of Hematology, Dokkyo University School of Medicine, Tochigi, Japan; the Section on Immunology and Immunogenetics, Joslin Diabetes Center, Harvard Medical School, Boston, MA; the Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan; the Department of Clinical Laboratory and Pathology, Inoue Memorial Hospital, Chiba, Japan; and the Department of Pathology, Tokyo Women's Medical University, Tokyo, Japan.

The AML1/EVI1 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/EVI1 chimeric gene into mouse Aml1 genomic locus to explore its effect in developmental hematopoiesis in vivo. AML1/EVI1/+ embryo showed defective hematopoiesis in the fetal liver and died around embryonic day 13.5 (E13.5) as a result of hemorrhage in the central nervous system. The peripheral blood had yolk-sac-derived nucleated erythroblasts but lacked erythrocytes of the definitive origin. Although E12.5 fetal liver contained progenitors for macrophage only, E13.5 fetal liver contained multilineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte. No erythroid progenitor was detected in E12.5 or E13.5 fetal liver. Hematopoietic progenitors from E13.5 AML1/EVI1/+ fetal liver were highly capable of self-renewal compared with those 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/EVI1/+ fetal liver. (Blood. 2005;106:2147-2155)


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