Skip NavigationSkip to Content
Return Return to Search Results

Burkitt lymphoma in the mouse

  1. Author:
    Kovalchuk, A. L.
    Qi, C. F.
    Torrey, T. A.
    Taddesse-Heath, L.
    Feigenbaum, L.
    Park, S. S.
    Gerbitz, A.
    Klobeck, G.
    Hoertnagel, K.
    Polack, A.
    Bornkamm, G. W.
    Janz, S.
    Morse, H. C.

  2. Author Address

    NIAID, LIP, NIH, 7 Ctr Dr, Rm 7-304, MSC 0760, Bethesda, MD 20892 USA. NIAID, LIP, NIH, Bethesda, MD 20892 USA. NCI, Genet Lab, NIH, Bethesda, MD 20892 USA. NCI, Sci Applicat Int Corp, Frederick Canc Res Ctr, NIH, Frederick, MD 21702 USA. Inst Klin Mol Biol & Tumorgenet, D-81377 Munich, Germany. Univ Munich, Inst Physiol Chem, D-80336 Munich, Germany.
    1. Year: 2000
  2. Journal: Journal of Experimental Medicine
    1. 192
    2. 8
    3. Pages: 1183-1190
  4. Type of Article: Article
  1. Abstract:

    Chromosomal translocations juxtaposing the MYC protooncogene with regulatory sequences of immunoglobulin (Ig) H chain or kappa (Ig kappa) or lambda (Ig lambda) L chain genes and effecting deregulated expression of MYC are the hallmarks of human Burkitt lymphoma (BL). Here we report that lymphomas with striking similarities to BL develop in mice bearing a mutated human MYC gene controlled by a reconstructed Ig lambda locus encompassing all the elements required for establishment of locus control in vitro. Diffusely infiltrating lymphomas with a typical starry sky appearance occurred in multiple founders and an established line, indicating independence from positional effects. Monoclonal IgM(+)CD5(-)CD23(-) tumors developed from an initially polyclonal population of B cells. These results demonstrate chat the phenotype of B lineage lymphomas induced by MYC dysregulation is highly dependent on cooperativity among the regulatory elements that govern expression of the protooncogene and provide a new system for studying the pathogenesis of BL.

    See More

  1. Keywords:

External Sources

  1. No sources found.

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel