Abstract
The MLL gene at chromosome 11q23 is frequently rearranged in acute leukemia. Here we report the identification of a new MLL fusion partner in the case of an infant with AML-M4 and a t(11;17)(q23;q21) translocation. Fluorescence in situ hybridization (FISH) and RT-PCR analyses indicated a rearrangement of the MLL gene, but no fusion with previously identified MLL fusion partners at 17q, such as AF17 or MSF. Rapid amplification of cDNA ends (RACE) revealed an in-frame fusion of MLL to LASP1, a gene that is amplified and overexpressed in breast cancer. Retroviral transduction of myeloid progenitors demonstrated that MLL/LASP1 is the fourth known fusion of MLL with a cytoplasmic protein that has no in vitro transformation capability, thus establishing a potential subgroup among the MLL fusion proteins.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute Disease
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Adaptor Proteins, Signal Transducing
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Amino Acid Sequence
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Base Sequence
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Chromosomes, Human, Pair 11*
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Chromosomes, Human, Pair 17*
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Cytoskeletal Proteins
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DNA-Binding Proteins / genetics*
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Histone-Lysine N-Methyltransferase
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Homeodomain Proteins / genetics*
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Humans
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In Situ Hybridization
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LIM Domain Proteins
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Leukemia, Myeloid / genetics*
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Molecular Sequence Data
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Myeloid-Lymphoid Leukemia Protein
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Neoplasm Proteins*
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Proto-Oncogenes*
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Reverse Transcriptase Polymerase Chain Reaction
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Transcription Factors*
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Translocation, Genetic*
Substances
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Adaptor Proteins, Signal Transducing
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Cytoskeletal Proteins
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DNA-Binding Proteins
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Homeodomain Proteins
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KMT2A protein, human
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LASP1 protein, human
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LIM Domain Proteins
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Neoplasm Proteins
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Transcription Factors
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Myeloid-Lymphoid Leukemia Protein
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Histone-Lysine N-Methyltransferase