Abstract
Rearrangements of the ALL-1/MLL1 gene underlie the majority of infant acute leukaemias, as well as of therapy-related leukaemias developing in cancer patients treated with inhibitors of topoisomerase II, such as VP16 and doxorubicin. The rearrangements fuse ALL-1 to any of >50 partner genes or to itself. Here, we describe the unique features of ALL-1-associated leukaemias, and recent progress in understanding molecular mechanisms involved in the activity of the ALL-1 protein and of its Drosophila homologue TRITHORAX.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Cell Transformation, Neoplastic
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Chromatin / metabolism*
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DNA-Binding Proteins / pharmacology*
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Disease Models, Animal
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Drosophila / genetics
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Drosophila Proteins / pharmacology*
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Gene Expression Regulation, Neoplastic*
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Histone-Lysine N-Methyltransferase / pharmacology*
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Humans
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Leukemia, Myeloid, Acute / genetics*
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Leukemia, Myeloid, Acute / physiopathology
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Mice
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Myeloid-Lymphoid Leukemia Protein
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology
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Proto-Oncogenes*
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Transcription Factors*
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Zinc Fingers
Substances
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Chromatin
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DNA-Binding Proteins
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Drosophila Proteins
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KMT2A protein, human
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Transcription Factors
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Myeloid-Lymphoid Leukemia Protein
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Histone-Lysine N-Methyltransferase
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Kmt2a protein, mouse
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TRR protein, Drosophila