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Blood, 15 October 2006, Vol. 108, No. 8, pp. 2726-2735. Prepublished online as a Blood First Edition Paper on June 8, 2006; DOI 10.1182/blood-2006-02-001594. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-02-001594v1 108/8/2726    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 Ma, Y. Articles by Chai, L. Search for Related Content PubMed PubMed Citation Articles by Ma, Y. Articles by Chai, L. Related Collections Neoplasia Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice Yupo Ma, Wei Cui, Jianchang Yang, Jun Qu, Chunhui Di, Hesham M. Amin, Raymond Lai, Jerome Ritz, Diane S. Krause, and Li Chai From the Division of Laboratory Medicine, Nevada Cancer Institute, Las Vegas; the Department of Pathology, Joint Program in Transfusion Medicine, Brigham and Women's Hospital/Children's Hospital Boston, Harvard Medical School, Boston, MA; the Department of Hematopathology, University of Texas M. D. Anderson Cancer Center, Houston; the Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Canada; the Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; and the Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT. SALL4, a human homolog to Drosophila spalt, is a novel zinc finger transcriptional factor essential for development. We cloned SALL4 and its isoforms (SALL4A and SALL4B). Through immunohistochemistry and real-time reverse-transcription-polymerase chain reaction (RT-PCR), we demonstrated that SALL4 was constitutively expressed in human primary acute myeloid leukemia (AML, n = 81), and directly tested the leukemogenic potential of constitutive expression of SALL4 in a murine model. SALL4B transgenic mice developed myelodysplastic syndrome (MDS)-like features and subsequently AML that was transplantable. Increased apoptosis associated with dysmyelopoiesis was evident in transgenic mouse marrow and colony-formation (CFU) assays. Both isoforms could bind to -catenin and synergistically enhanced the Wnt/-catenin signaling pathway. Our data suggest that the constitutive expression of SALL4 causes MDS/AML, most likely through the Wnt/-catenin pathway. Our murine model provides a useful platform to study human MDS/AML transformation, as well as the Wnt/-catenin pathway's role in the pathogenesis of leukemia stem cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Rizo, B. Dontje, E. Vellenga, G. de Haan, and J. J. Schuringa Long-term maintenance of human hematopoietic stem/progenitor cells by expression of BMI1 Blood, March 1, 2008; 111(5): 2621 - 2630. [Abstract] [Full Text] [PDF] J. Yang, L. Chai, F. Liu, L. M. Fink, P. Lin, L. E. Silberstein, H. M. Amin, D. C. Ward, and Y. Ma Bmi-1 is a target gene for SALL4 in hematopoietic and leukemic cells PNAS, June 19, 2007; 104(25): 10494 - 10499. [Abstract] [Full Text] [PDF]

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