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    Genomic characterization of the chromosomal breakpoints of t(4;14) of multiple myeloma suggests more than one possible aetiological mechanism.

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    Authors
    Fenton, James A L
    Pratt, Guy
    Rawstron, Andy C
    Sibley, Kathryn
    Rothwell, Dominic G
    Yates, Zoe
    Dring, Ann
    Richards, Steve J
    Ashcroft, A John
    Davies, Faith E
    Owen, Roger G
    Child, J Anthony
    Morgan, Gareth J
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    Affiliation
    Academic Unit of Haematology and Oncology, Algernon Firth Building, University of Leeds, LEEDS LS2 9JT, UK. jamesf@lrf.leeds.ac.uk
    Issue Date
    2003-02-20
    
    Metadata
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    Abstract
    Using FISH-based techniques, rearrangements of the immunoglobulin heavy-chain (IgH) locus at 14q32 have been found in the majority of cases of multiple myeloma (MM). Some of these IgH translocations are recurrent and we have characterized the genomic breakpoints of seven t(4;14) translocations from MM patients, using a combination of vectorette and conventional polymerase chain reaction methods, the aim being to understand the molecular mechanism leading to MM. Conventionally, the chromosome 14q32 breakpoints in these reciprocal translocations are believed to be located in the IgH mu switch (S) region and a further downstream S region with deletion of intervening DNA occurring as a result of aberrant class switch recombination (CSR); this was seen in five of the cases analysed. However, in two patients it was possible to demonstrate that the rearranged hybrid switch region sequence was joined to DNA from chromosome 4p16, suggesting that IgH translocations can occur in B cells that have already undergone legitimate CSR. The complex nature of these rearrangements leads us to speculate that primary IgH translocations may occur at different time points in the development in MM plasma cells, either at the time of physiological CSR or at a later stage, possibly involving a different mechanism.
    Citation
    Genomic characterization of the chromosomal breakpoints of t(4;14) of multiple myeloma suggests more than one possible aetiological mechanism. 2003, 22 (7):1103-13 Oncogene
    Journal
    Oncogene
    URI
    http://hdl.handle.net/10541/82375
    DOI
    10.1038/sj.onc.1206335
    PubMed ID
    12592397
    Type
    Article
    Language
    en
    ISSN
    0950-9232
    ae974a485f413a2113503eed53cd6c53
    10.1038/sj.onc.1206335
    Scopus Count
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