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Rearrangements of the mixed lineage leukemia gene MLL are associated with aggressive lymphoid and myeloid leukemias. The resulting MLL fusion proteins enforce high-level expression of HOX genes and the HOX cofactor MEIS1, which is pivotal for leukemogenesis. Both wild-type MLL and MLL fusion proteins interact with the tumor suppressor menin and with the Hoxa9 locus in vivo. Here, we show that MLL sequences between amino acids 5 and 44 are required for interaction with menin and for the transformation of hematopoietic progenitors. Blocking the MLL-menin interaction by the expression of a dominant negative inhibitor composed of amino terminal MLL sequences down-regulates Meis1 expression and inhibits cell proliferation, suggesting that targeting this interaction may be an effective therapeutic strategy for leukemias with MLL rearrangements.

Original publication

DOI

10.1158/0008-5472.CAN-06-2369

Type

Journal article

Journal

Cancer Res

Publication Date

01/08/2007

Volume

67

Pages

7275 - 7283

Keywords

Cell Proliferation, Cell Transformation, Neoplastic, Cells, Cultured, Chromatin Immunoprecipitation, Down-Regulation, Gene Expression, Histone-Lysine N-Methyltransferase, Homeodomain Proteins, Humans, Immunoprecipitation, Kidney, Leukemia, Myeloid, Myeloid Ecotropic Viral Integration Site 1 Protein, Myeloid-Lymphoid Leukemia Protein, Neoplasm Proteins, Polymerase Chain Reaction, Proto-Oncogene Proteins