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Blood, 15 June 2007, Vol. 109, No. 12, pp. 5079-5086. Prepublished online as a Blood First Edition Paper on March 9, 2007; DOI 10.1182/blood-2007-02-071225. This Article Full Text (PDF) All Versions of this Article: blood-2007-02-071225v1 109/12/5079    most recent Alert me when this article is cited Alert me if a correction is posted 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 Raveche, E. S Articles by Marti, G. E Search for Related Content PubMed PubMed Citation Articles by Raveche, E. S Articles by Marti, G. E Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 1, 2007 Accepted March 7, 2007 Abnormal microRNA-16 locus with synteny to human 13q14 linked to CLL in NZB mice Elizabeth S Raveche, Erica Salerno, Brian J Scaglione, Vijaya Manohar, Fatima Abbasi, Yi-Chu Lin, Torgny Fredrickson, Pablo Landgraf, Sumant Ramachandra, Konrad Huppi, Jorge R Toro, Vincent E Zenger, Robert A Metcalf, and Gerald E Marti* Department of Pathology & Laboratory Medicine, NJMS/UMDNJ, Newark, NJ, United States Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, DC, United States CBER, FDA/NIH, Bethesda, MD, United States Lab of Immunopathology, NIAID/NIH, Bethesda, MD, United States Lab of RNA Mol. Biol., Howard Hughes Med Inst, The Rockefeller University, New York, NY, United States Global Development, Schering-Plough Res Inst, Kenilworth, NJ, United States Gene Silencing Section, ATS/NCI/NIH, Gaithersburg, MD, United States Genetic Epidemology Branch, DCEG/NCIPS, Rockville, MD, United States * Corresponding author; email: gemarti{at}helix.nih.gov. NZB mice, with autoimmune and B lymphoproliferative disease (B-LPD), are a model for human chronic lymphocytic leukemia (CLL). A genome-wide linkage scan of the NZB loci associated with lymphoma was conducted in F1 backcrosses of NZB and a control strain, DBA/2. Of 202 mice phenotyped for the presence or absence of LPD, surface maker expression, DNA content and microsatellite polymorphisms, 74 had disease. The CD5+, IgM+, B220 dim, hyperdiploid LPD was linked to three loci on chromosomes 14, 18 and 19 which are distinct from previously identified autoimmunity-associated loci. The region of synteny with mouse D14mit160 is the human 13q14 region, associated with human CLL, containing microRNAs, mir15a/16-1. DNA sequencing of multiple NZB tissues identified a point mutation in the 3'flanking sequence of the identical micro RNA, mir16-1 and this mutation was not present in other strains, including the nearest neighbor, NZW. Levels of miR-16 were decreased in NZB lymphoid tissue. Exogenous miR-16 delivered to an NZB malignant B-1 cell line resulted in cell cycle alterations and increased apoptosis. Linkage of the mir15a/16-1 complex and the development of B-LPD in this spontaneous mouse model suggest that the altered expression of the miR15a/16-1 is the molecular lesion in CLL. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: MicroRNAs play a role in neoplasia Thomas J. Kipps Blood 2007 109: 5071-5072. [Full Text] [PDF] This article has been cited by other articles: M. V. Iorio and C. M. 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