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Blood, 1 April 2004, Vol. 103, No. 7, pp. 2779-2786. Prepublished online as a Blood First Edition Paper on December 4, 2003; DOI 10.1182/blood-2003-10-3399. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-10-3399v1 103/7/2779    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 Linden, M. Articles by Van Ness, B. Search for Related Content PubMed PubMed Citation Articles by Linden, M. Articles by Van Ness, B. Related Collections Neoplasia Oncogenes and Tumor Suppressors Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Targeted overexpression of Bcl-XL in B-lymphoid cells results in lymphoproliferative disease and plasma cell malignancies Michael Linden, Nicole Kirchhof, Cathy Carlson, and Brian Van Ness From the Graduate Program in Microbiology, Immunology, and Cancer Biology, Univeristy of Minnesota; College of Veterinary Medicine, University of Minnesota; Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN; and University of Minnesota Cancer Center, Minneapolis, MN. Multiple myeloma is an incurable malignancy, and there is currently no mouse model that fully recapitulates the development and progression of the disease. We now describe a transgenic mouse that expresses a Bcl-XL transgene under the control of the 3' immunoglobulin light chain enhancer, which is most active in murine B cells in late developmental stages. These mice developed nonmalignant plasma cell foci in the bone marrow and soft tissues and hyaline tubular casts in the kidneys. Median survival of the 3'KE/Bcl-XL mice was similar to littermate controls. When the 3'KE/Bcl-XL mouse was crossed to an Eµ/c-Myc transgenic mouse, median survival of double transgenic progeny was 5.5 weeks. Peripheral blood and soft tissues were infiltrated with immature/mature B cells, and plasma cell lesions were identified in the bone marrow of all mice coexpressing Bcl-XL and c-Myc. These B- and plasma cell lesions demonstrated features consistent with malignancy. These results indicate that the 3' immunoglobulin light chain enhancer can effectively target expression of Bcl-XL to B cells in late developmental stages, and they provide direct evidence that Bcl-XL can contribute to plasmacytomagenesis. Furthermore, this murine model serves as an important step in developing a novel genetically induced mouse model of plasma cell malignancies exhibiting bone marrow involvement. (Blood. 2004;103:2779-2786) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: A new model of plasma cell proliferation Teru Hideshima and Kenneth C. Anderson Blood 2004 103: 2438-2439. [Full Text] [PDF] This article has been cited by other articles: K. L.M. Boylan, M. A. Gosse, S. E. Staggs, S. Janz, S. Grindle, G. S. Kansas, and B. G. Van Ness A Transgenic Mouse Model of Plasma Cell Malignancy Shows Phenotypic, Cytogenetic, and Gene Expression Heterogeneity Similar to Human Multiple Myeloma Cancer Res., May 1, 2007; 67(9): 4069 - 4078. [Abstract] [Full Text] [PDF] M. A. Linden, N. Kirchhof, and B. G. Van Ness Targeted Overexpression of Mutant Activated N-ras Leads to Aberrant Plasma Cell Biology. Blood (ASH Annual Meeting Abstracts), November 16, 2004; 104(11): 1416 - 1416. [Abstract]

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