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This Article Full Text Full Text (PDF) 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 Kuefer, M. U. Articles by Morris, S. W. Search for Related Content PubMed PubMed Citation Articles by Kuefer, M. U. Articles by Morris, S. W. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RAPID COMMUNICATION Retrovirus-Mediated Gene Transfer of NPM-ALK Causes Lymphoid Malignancy in Mice Martin U. Kuefer, A. Thomas Look, Karen Pulford, Frederick G. Behm, Paul K. Pattengale, David Y. Mason, and Stephan W. Morris From the Departments of Experimental Oncology, Hematology/Oncology, Pathology and Laboratory Medicine, St Jude Children's Research Hospital, Memphis, TN; the Department of Pediatrics, University of Tennessee College of Medicine, Memphis, TN; the Leukemia Research Fund Immunodiagnostics Unit, University Department of Cellular Science, John Radcliffe Hospital, Oxford, UK; and the Department of Pathology, Children's Hospital Los Angeles, Los Angeles, CA. Approximately 5% to 10% of all non-Hodgkin's lymphomas contain a t(2; 5)(p23; q35) chromosomal rearrangement, which we have previously shown results in the generation of the fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK). To assess the transforming potential of NPM-ALK in an animal model, we infected 5-fluorouracil-treated murine bone marrow using retroviral stocks and transplanted this infected marrow into lethally irradiated BALB/cByJ mice. Male mice were transplanted with bone marrow from female donors at 10 weeks of age, with 7 of the animals receiving marrow infected with a retroviral construct, pSRMSVtkneo-NPM-ALK, that contains the human NPM-ALK cDNA, and 4 serving as a control group, receiving "empty" pSRMSVtkneo-infected marrow. Whereas all mice in the control group were alive and well up to 11 months after transplantation, 4 of the 7 mice transplanted with marrow containing the NPM-ALK construct developed lymphoma within 4 to 6 months. Tumors arose in the mesenteric lymph nodes, with metastases to the lungs, kidneys, liver, spleen, and the paraspinal area. When cells from the tumors and bone marrow were transplanted into sublethally irradiated secondary recipients, 10 of these 13 mice developed tumors within 9 months. Immunoblot analysis of cell lysates using an ALK polyclonal antibody showed NPM-ALK expression in all tumors examined. Histologically, the tumors were composed of a uniform population of large immunoblastic cells with basophilic cytoplasm, centrally placed nuclei, and distinct nucleoli. Genotypic analysis showed that the tumors were B-lineage and clonal, with rearrangements of the Ig heavy- and  light-chain loci and no rearrangements of the T-cell receptor  locus. Immunocytochemical studies confirmed the presence of IgM heavy chains and  light chains within the tumor cells. Thus, in this retroviral gene transfer model, NPM-ALK expression in mice causes B-lineage large-cell lymphoma, suggesting a direct causative role for this activated fusion tyrosine kinase in human lymphoma. Blood, Vol. 90 No. 8 (July 15), 1997: pp. 2901-2910 © 1997 by The American Society of Hematology. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Marzec, Q. Zhang, A. Goradia, P. N. Raghunath, X. Liu, M. Paessler, H. Y. Wang, M. Wysocka, M. 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