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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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MYELOID NEOPLASIA

Brief report

A role for MEIS1 in MLL-fusion gene leukemia

Ashish R. Kumar1,2,*, Quanzhi Li1,*, Wendy A. Hudson1, Weili Chen1, Thien Sam1, Qing Yao1, Erik A. Lund1, Baolin Wu3, Branden J. Kowal2, and John H. Kersey1,2,4

1 Masonic Cancer Center, 2 Department of Pediatrics, 3 Division of Biostatistics, School of Public Health, and 4 Department of Laboratory Medicine & Pathology, University of Minnesota, Minneapolis

Leukemias with MLL rearrangements are characterized by high expression of the homeobox 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 transplantation 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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Might as well face it: MLL's addicted to HOX
Blood, March 12, 2009; 113(11): 2372 - 2373.
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