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    Deregulation of MUM1/IRF4 by chromosomal translocation in multiple myeloma

    Lida, Shinsuke and Rao, Pulivarthi H. and Butler, Marion P. and Corradini, Paolo and Boccadora, Mario and Klein, Bernard and Chaganti, R.S.K. and Dalla-Favera, Riccardo (1997) Deregulation of MUM1/IRF4 by chromosomal translocation in multiple myeloma. Nature Genetics, 17. pp. 226-230. ISSN 1061-4036

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    The pathogenesis of multiple myeloma (MM), an incurable tumour causing the deregulated proliferation of terminally differentiated 8 cells, is unknown 1• Chromosomal translocations (14q1) affecting band 14q32 and unidentified partner chromosomes are common in this tumour, suggesting that they may cause the activation of novel oncogenes2.3. By cloning the chromosomal breakpoints in an MM cell line, we show that the 14q+ translocation represents a t(6;14)(p2S;q32) and that this aberration is recurrent in MM, as it was found in two of eleven MM cell lines. The translocation juxtaposes the immunoglobulin heavy-chain (lgH) locus to MUM1 (mM:Itiple myeloma oncogene 1JIIRF4 gene, a member of the interferon regulatory factor (IRF) family known to be active in the control of 8-cell proliferation and differentiation. As a result, the MUM1RRF4 gene is overexpressed-an event that may contribute to tumorigenesis, as MUM11/RF4 has oncogenic activity in vitro. These findings identify a novel genetic alteration associated with MM, with implications for the pathogenesis and diagnostics of this tumour.

    Item Type: Article
    Keywords: Deregulation; MUM1/IRF4; chromosomal translocation; multiple myeloma;
    Academic Unit: Faculty of Science and Engineering > Biology
    Item ID: 12363
    Identification Number:
    Depositing User: Marion Butler
    Date Deposited: 04 Feb 2020 16:52
    Journal or Publication Title: Nature Genetics
    Publisher: Nature Research
    Refereed: Yes
    Use Licence: This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

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