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The marked association of abnormalities of chromosome 11 long arm, band q23, with human leukaemia led to the identification of the 11q23 gene called MLL (or HTRX, HRX, TRX1, ALL-1). MLL can become fused with one of a remarkable panoply of genes from other chromosome locations in individual leukaemias, leading to either acute myeloid or lymphoid tumours (hence the name MLL for mixed lineage leukaemia). The unusual finding that a single protein could be involved in both myeloid and lymphoid malignancies and that the truncated protein could do so as a fusion with very disparate partners has prompted studies to define the molecular role of MLL-fusions in leukaemogenesis and to the development of MLL-controlled mouse models of leukaemogenesis. These studies have defined MLL-fusion proteins as regulators of gene expression, controlling such elements as HOX genes, and have indicated a variety of mechanisms by which MLL-fusion proteins contribute to leukaemogenesis.

Original publication

DOI

10.1016/j.semcancer.2005.01.007

Type

Journal article

Journal

Semin Cancer Biol

Publication Date

06/2005

Volume

15

Pages

175 - 188

Keywords

Animals, Bone Marrow, Cell Transformation, Neoplastic, Chromosomes, Humans, Leukemia, Myeloid-Lymphoid Leukemia Protein, Transcriptional Activation