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Retroviral integration at the Epi1 locus cooperates with Nf1 gene loss in the progression to acute myeloid leukemia

  1. Author:
    Blaydes, S. M.
    Kogan, S. C.
    Truong, B. T. H.
    Gilbert, D. J.
    Jenkins, N. A.
    Copeland, N. G.
    Largaespada, D. A.
    Brannan, C. I.

  2. Author Address

    Univ Florida, Coll Med, Dept Mol Genet & Microbiol, Ctr Mammalian Genet, POB 100266, Gainesville, FL 32610 USA. Univ Florida, Coll Med, Dept Mol Genet & Microbiol, Ctr Mammalian Genet, Gainesville, FL 32610 USA. Univ Florida, Coll Med, Shands Canc Ctr, Gainesville, FL 32610 USA. Univ Calif San Francisco, Ctr Comprehens Canc, Dept Lab Med, San Francisco, CA 94143 USA. NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA. Univ Minnesota, Ctr Canc, Dept Genet Cell Biol & Dev, Minneapolis, MN 55455 USA. Brannan CI Univ Florida, Coll Med, Dept Mol Genet & Microbiol, Ctr Mammalian Genet, POB 100266, Gainesville, FL 32610 USA.
    1. Year: 2001
  2. Journal: Journal of Virology
    1. 75
    2. 19
    3. Pages: 9427-9434
  4. Type of Article: Article
  1. Abstract:

    Juvenile myelomonocytic leukemia (JMML) is a disease that occurs in young children and is associated with a high mortality rate. In most patients, JMML has a progressive course leading to death by virtue of infection, bleeding, or progression to acute myeloid leukemia (AML). As it is known that children with neurofibromatosis type 1 syndrome have a markedly increased risk of developing JMML, we have previously developed a mouse model of JMML through reconstitution of lethally irradiated mice with hematopoietic stem cells homozygous for a loss-of-function mutation in the Nf1 gene (D. L. Largaespada, C. I. Brannan, N. A. Jenkins, and N. G. Copeland, Nat. Genet. 12:137-143, 1996). In the course of these experiments, we found that all these genetically identical reconstituted mice developed a JMML-like disorder, but only a subset went on to develop more acute disease. This result strongly suggests that additional genetic lesions are responsible for disease progression to AML. Here, we describe the production of a unique tumor panel, created using the BXH-2 genetic background, for identification of these additional genetic lesions. Using this tumor panel, we have identified a locus, Epi1, which maps 30 to 40 kb downstream of the Myb gene and appears to be the most common site of somatic viral integration in BXH-2 mice. Our findings suggest that proviral integrations at Epi1 cooperate with loss of Nf1 to cause AML.

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