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 Blood, 19 February 2009, Vol. 113, No. 8, pp. 1756-1758.
Prepublished online as a Blood First Edition Paper on December 24, 2008; DOI 10.1182/blood-2008-06-163287.

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Submitted June 16, 2008
Accepted December 3, 2008

A role for MEIS1 in MLL-fusion gene leukemia

Ashish R. Kumar, Quanzhi Li, Wendy A Hudson, Weili Chen, Thien Sam, Qing Yao, Erik A. Lund, Baolin Wu, Branden J Kowal, and John H. Kersey*

Masonic Cancer Center, University of Minnesota, Minneapolis, MN, United States
Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, United States
Department of Pediatrics, University of Minnesota, Minneapolis, MN, United States
Department of Laboratory Medicine & Pathology, University of Minnesota, Minneapolis, MN, United States

* Corresponding author; email: kerse001{at}umn.edu.

Leukemias with MLL-rearrangements are characterized by high expression of the homeo box gene MEIS1. In these studies, we knocked down Meis1 expression by shRNA lentivirus transduction in murine Mll-AF9 leukemia cells. Meis1 knockdown resulted in decreased proliferation and survival of murine Mll-AF9 leukemia cells. We also observed reduced clonogenic capacity and increased monocytic differentiation. The establishment of leukemia in transplant recipients was significantly delayed by Meis1 knockdown. Gene expression profiling of cells transduced with Meis1 shRNA showed reduced expression of genes associated with cell cycle entry and progression. shRNA mediated knockdown of MEIS1 in human MLL-fusion gene leukemia cell lines resulted in reduced cell growth. These results show that MEIS1 expression is important for MLL-rearranged leukemias and suggest that MEIS1 promotes cell cycle entry. Targeting MEIS1 may have therapeutic potential for treating leukemias expressing this transcription factor.


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