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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.
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PLENARY PAPER
Abnormal microRNA-16 locus with synteny to human 13q14 linked to CLL in NZB mice
Elizabeth S. Raveche1,
Erica Salerno1,
Brian J. Scaglione1,
Vijaya Manohar2,
Fatima Abbasi3,
Yi-Chu Lin1,
Torgny Fredrickson4,
Pablo Landgraf7,
Sumant Ramachandra1,
Konrad Huppi5,
Jorge R. Toro6,
Vincent E. Zenger3,
Robert A. Metcalf3, and
Gerald E. Marti3
1 Department of Pathology and Lab Medicine, University of Medicine and Dentistry New Jersey/New Jersey Medical School, Newark, NJ;
2 Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, DC;
3 Center for Biologics Evaluation and Research/Food and Drug Administration, Bethesda, MD;
4 Laboratory of Immunopathology, National Institute of Allergy and Infectious Disease (NIAID), National Institutes of Health (NIH), Bethesda, MD;
5 Gene Silencing Section, Advanced Technology Center/National Cancer Institute (NCI), National Institutes of Health, Gaithersburg, MD;
6 Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD;
7 Laboratory of RNA Molecular Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY
New Zealand black (NZB) mice with autoimmune and B lymphoproliferative disease (B-LPD) are a model for human chronic lymphocytic leukemia (CLL). A genomewide 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+, B220dim, hyperdiploid LPD was linked to 3 loci on chromosomes 14, 18, and 19 that 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 mir-15a16-1. DNA sequencing of multiple NZB tissues identified a point mutation in the 3' flanking sequence of the identical microRNA, mir-16-1, 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 mir-15a/16-1 complex and the development of B-LPD in this spontaneous mouse model suggest that the altered expression of the mir-15a/16-1 is the molecular lesion in CLL.
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