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    The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2.

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    Authors
    Reiter, Andreas
    Walz, Christoph
    Watmore, Ann
    Schoch, Claudia
    Blau, Ilona
    Schlegelberger, Brigitte
    Berger, Ute
    Telford, Nicholas
    Aruliah, Shilani
    Yin, John A
    Vanstraelen, Danny
    Barker, Helen F
    Taylor, Peter C
    O'Driscoll, Aisling
    Benedetti, Fabio
    Rudolph, Cornelia
    Kolb, Hans-Jochem
    Hochhaus, Andreas
    Hehlmann, Rüdiger
    Chase, Andrew
    Cross, Nicholas C P
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    Affiliation
    III. Medizinische Universitätsklinik, Fakultät für Klinische Medizin Mannheim der Universität Heidelberg, Mannheim, Germany. andreas.reiter@med3.ma.uni-heidelberg.de
    Issue Date
    2005-04-01
    
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    Abstract
    We have identified a t(8;9)(p21-23;p23-24) in seven male patients (mean age 50, range 32-74) with diverse hematologic malignancies and clinical outcomes: atypical chronic myeloid leukemia/chronic eosinophilic leukemia (n = 5), secondary acute myeloid leukemia (n = 1), and pre-B-cell acute lymphoblastic leukemia (n = 1). Initial fluorescence in situ hybridization studies of one patient indicated that the nonreceptor tyrosine kinase Janus-activated kinase 2 (JAK2) at 9p24 was disrupted. Rapid amplification of cDNA ends-PCR identified the 8p22 partner gene as human autoantigen pericentriolar material (PCM1), a gene encoding a large centrosomal protein with multiple coiled-coil domains. Reverse transcription-PCR and fluorescence in situ hybridization confirmed the fusion in this case and also identified PCM1-JAK2 in the six other t(8;9) patients. The breakpoints were variable in both genes, but in all cases the chimeric mRNA is predicted to encode a protein that retains several of the predicted coiled-coil domains from PCM1 and the entire tyrosine kinase domain of JAK2. Reciprocal JAK2-PCM1 mRNA was not detected in any patient. We conclude that human autoantigen pericentriolar material (PCM1)-JAK2 is a novel, recurrent fusion gene in hematologic malignancies. Patients with PCM1-JAK2 disease are attractive candidates for targeted signal transduction therapy.
    Citation
    The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. 2005, 65 (7):2662-7 Cancer Res.
    Journal
    Cancer Research
    URI
    http://hdl.handle.net/10541/74917
    DOI
    10.1158/0008-5472.CAN-04-4263
    PubMed ID
    15805263
    Type
    Article
    Language
    en
    ISSN
    0008-5472
    ae974a485f413a2113503eed53cd6c53
    10.1158/0008-5472.CAN-04-4263
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