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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 Grote, D. Articles by Fielding, A. K. Search for Related Content PubMed PubMed Citation Articles by Grote, D. Articles by Fielding, A. K. Related Collections Immunobiology Neoplasia Gene Therapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 June 2001, Vol. 97, No. 12, pp. 3746-3754 GENE THERAPY Live attenuated measles virus induces regression of human lymphoma xenografts in immunodeficient mice Deanna Grote, Stephen J. Russell, Tatjana I. Cornu, Roberto Cattaneo, Richard Vile, Gregory A. Poland, and Adele K. Fielding From the Molecular Medicine Program, Clinical Pharmacology, and Division of Hematology, Mayo Clinic, Rochester, MN; and the Molecular Biology Institute, University of Zurich, Switzerland. Derivatives of the Edmonston-B strain of measles virus (MV-Ed) are safe, live attenuated measles virus (MV) vaccines that have been used worldwide for more than 30 years. The cytoreductive potential of MV-Ed has been investigated in murine models of both aggressive and indolent B-cell lymphoma in severe combined immunodeficient (SCID) mice. The rationale for these studies was generated by experience with viral fusogenic membrane glycoproteins as cytotoxic genes and the recognition of the potential of replicating viruses in the treatment of human malignancy. Intratumoral injection of both unmodified MV-Ed and a strain of MV-Ed genetically modified by the addition of a -galactosidase reporter gene (MVlacZ) induced regression of large established human lymphoma xenografts, in contrast to control therapy with UV-inactivated virus, in which all tumors progressed. The antitumor effect still occurred in the presence of passively transferred anti-MV antibody. Intravenous administration of MV also resulted in considerable slowing of tumor progression. Analysis of sections of residual tumor confirmed replication of MV within the tumors. Thus, the vaccine strain of MV mediates regression of large, established human B-cell lymphoma xenografts in SCID mice, and proof of principle is established that MV is oncolytic for lymphomas in vivo. Attenuated MVs may have value as a novel replicating-virus therapy for this group of disorders. © 2001 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: A. Gauvrit, S. Brandler, C. Sapede-Peroz, N. Boisgerault, F. Tangy, and M. Gregoire Measles Virus Induces Oncolysis of Mesothelioma Cells and Allows Dendritic Cells to Cross-Prime Tumor-Specific CD8 Response Cancer Res., June 15, 2008; 68(12): 4882 - 4892. [Abstract] [Full Text] [PDF] K. Hasegawa, C. Hu, T. Nakamura, J. D. Marks, S. J. Russell, and K.-W. Peng Affinity Thresholds for Membrane Fusion Triggering by Viral Glycoproteins J. Virol., December 1, 2007; 81(23): 13149 - 13157. [Abstract] [Full Text] [PDF] G. Ungerechts, C. Springfeld, M. E. Frenzke, J. Lampe, P. B. Johnston, W. B. Parker, E. J. Sorscher, and R. 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	Copyright © 2001 by American Society of Hematology         Online ISSN: 1528-0020