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M506855200v1
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Papers In Press, published online ahead of print September 30, 2005
J. Biol. Chem, 10.1074/jbc.M506855200
Submitted on June 23, 2005
Accepted on September 30, 2005

The INV(16) cooperates with ARF haploinsuffiency to induce acute myeloid leukemia

Isabel Moreno-Miralles, Ling Pan, Jennifer Keates-Baleeiro, Kristie Durst-Goodwin, Chunying Yang, Hyung-Gyoon Kim, Mary Ann Thompson, Christopher A. Klug, John L. Cleveland, and Scott W. Hiebert

Biochemistry Dept., Vanderbilt Univ. School of Medicine, Nashville, TN 37232

Corresponding Author: scott.hiebert{at}vanderbilt.edu

The inv(16) is one of the most frequent chromosomal translocations associated with acute myeloid leukemia and creates a chimeric fusion protein consisting of most of the RUNX1 co-factor core binding factor beta (CBFß) fused to the smooth muscle myosin heavy chain MYH11. Expression of the ARF tumor suppressor is regulated by RUNX1, suggesting that the inv(16) fusion protein (IFP) may repress ARF expression. We established a murine bone marrow transplant model of the inv(16) in which wild type, Arf +/- and Arf -/- bone marrow were engineered to express the IFP. IFP expression was sufficient to induce a myelomonocytic AML even when expressed in wild type bone marrow, yet removal of only a single allele of Arf greatly accelerated the disease, indicating that Arf is haploinsufficent for the induction of AML in the presence of the inv(16).


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