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  • Oncogenomics
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The human LASP1 gene is fused to MLL in an acute myeloid leukemia with t(11;17)(q23;q21)

Oncogene volume 22, pages 157–160 (2003)Cite this article

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.

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Acknowledgements

This study was supported by the ‘Österreichische Kinderkrebshilfe’ and the German Cancer Foundation with a grant to AB (10-1658-Bo) and by DFG grants (SL27/4-1, SFB466/C7, SFB473/B10) to RS. This work resulted from a cooperation within the framework of the international BFM Study Group.

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Authors and Affiliations

  1. CCRI, Children's Cancer Research Institute, St. Anna Kinderspital, Kinderspitalgasse 6, Vienna, A–1090, Austria

    Sabine Strehl, Margit König & Oskar A Haas

  2. Department of Pediatric Hematology and Oncology, University of Giessen, Feulgenstraße 12, D-35392, Giessen, Germany

    Arndt Borkhardt & Uta E Fuchs

  3. Department of Genetics, University of Erlangen, Staudtstraße 5, D-91058, Erlangen, Germany

    Robert Slany

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  1. Sabine Strehl
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  2. Arndt Borkhardt
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  3. Robert Slany
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  4. Uta E Fuchs
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  5. Margit König
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  6. Oskar A Haas
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Correspondence to Oskar A Haas.

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Strehl, S., Borkhardt, A., Slany, R. et al. The human LASP1 gene is fused to MLL in an acute myeloid leukemia with t(11;17)(q23;q21). Oncogene 22, 157–160 (2003). https://doi.org/10.1038/sj.onc.1206042

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