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Of mice and MEN1: Insulinomas in a conditional mouse knockout

  1. Author:
    Crabtree, J. S.
    Scacheri, P. C.
    Ward, J. M.
    McNally, S. R.
    Swain, G. P.
    Montagna, C.
    Hager, J. H.
    Hanahan, D.
    Edlund, H.
    Magnuson, M. A.
    Garrett-Beal, L.
    Burns, A. L.
    Ried, T.
    Chandrasekharappa, S. C.
    Marx, S. J.
    Spiegel, A. M.
    Collins, F. S.

  2. Author Address

    NHGRI, NIH, Bldg 31,Rm 4B09, Bethesda, MD 20892 USA NHGRI, NIH, Bethesda, MD 20892 USA NCI, NIH, Bethesda, MD 20892 USA NIDDKD, NIH, Bethesda, MD 20892 USA NCI, NIH, Frederick, MD 21702 USA Univ Penn, Dept Med, Philadelphia, PA 19104 USA Univ Calif San Francisco, Dept Biochem, San Francisco, CA 94143 USA Umea Univ, Dept Microbiol, S-90187 Umea, Sweden Vanderbilt Univ, Med Ctr, Nashville, TN 37232 USA Collins FS NHGRI, NIH, Bldg 31,Rm 4B09, Bethesda, MD 20892 USA
    1. Year: 2003
  2. Journal: Molecular and Cellular Biology
    1. 23
    2. 17
    3. Pages: 6075-6085
  4. Type of Article: Article
  1. Abstract:

    Patients with multiple endocrine neoplasia type 1 (MEN1) develop multiple endocrine tumors, primarily affecting the parathyroid, pituitary, and endocrine pancreas, due to the inactivation of the MEN1 gene. A conditional mouse model was developed to evaluate the loss of the mouse homolog, Men1, in the pancreatic beta cell. Men1 in these mice contains exons 3 to 8 flanked by IoxP sites, such that, when the mice are crossed to transgenic mice expressing cre from the rat insulin promoter (RIP-cre), exons 3 to 8 are deleted in beta cells. By 60 weeks of age, >80% of mice homozygous for the floxed Men1 gene and expressing RIP-cre develop multiple pancreatic islet adenomas. The formation of adenomas results in elevated serum insulin levels and decreased blood glucose levels. The delay in tumor appearance, even with early loss of both copies of Men1, implies that additional somatic events are required for adenoma formation in beta cells. Comparative genomic hybridization of beta cell tumor DNA from these mice reveals duplication of chromosome 11, potentially revealing regions of interest with respect to tumorigenesis.

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