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Prepublished online as a Blood First Edition Paper on May 22, 2003; DOI 10.1182/blood-2003-03-0786. This Article Full Text (PDF) All Versions of this Article: 2003-03-0786v1 102/7/2568    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gascoyne, R. D Articles by Delsol, G. Search for Related Content PubMed PubMed Citation Articles by Gascoyne, R. D Articles by Delsol, G. Social Bookmarking                   What's this? Submitted March 14, 2003 Accepted May 12, 2003 ALK-positive diffuse large B-cell lymphoma is associated with Clathrin-ALK rearrangements: report of six cases Randy D Gascoyne*, Laurence Lamant, Jose I Martin-Subero, Valia S Lestou, Nancy L Harris, Hans K Muller-Hermelink, John F Seymour, Douglas E Horsman, Isabelle Auvigne, Estelle Espinos, Reiner Siebert, and Georges Delsol Pathology, British Columbia Cancer Agency, Vancouver, BC, Canada Pathology, CHU Purpan, Toulouse, France Genetics, Institute of Human Genetics, Kiel, Germany Pathology, Pathology Institute, Wurzburg, Wurzburg, Germany Pathology, Massachusetts General Hospital, Boston, MA, USA Medical Oncology, Peter MacCallum Cancer Institute, Melbourne, Australia * Corresponding author; email: rgascoyn{at}bccancer.bc.ca. Expression of ALK protein by lymphoid cells and the description of variant anaplastic lymphoma kinase (ALK) translocations have typically been restricted to cases of T cell and null anaplastic large cell lymphoma (ALCL). All such cases result from a novel fusion created by the ALK gene on chromosome 2p23 and NPM on 5q35 or other variant translocation partners. A rare variant of diffuse large B cell lymphoma (DLBCL), originally described in 1997, was thought to over-express full-length ALK in contrast to a chimeric protein characteristic of ALCL. However, full-length ALK protein lacks tyrosine kinase activity and thus the mechanism of oncogenesis has remained elusive. We describe six cases of ALK+ DLBCL characterized by a simple or complex t(2;17)(p23;q23) involving the clathrin gene (CLTC) at chromosome band 17q23 and the ALK gene at chromosome band 2p23. All cases were studied using fluorescence in-situ hybridization (FISH), complemented in one case with standard cytogenetic analysis, multi-color karyotyping (M-FISH) and RT-PCR. These results clearly demonstrate that the majority of cases of ALK+ DLBCL share the same mechanism of deregulated ALK expression. Moreover, these results demonstrate the presence of CLTC-ALK fusions in these tumors and extend the list of diseases associated with this genetic abnormality to include classical T cell or null ALCL, ALK+ DLBCL and inflammatory myofibroblastic tumors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Laurent, C. Do, R. D. Gascoyne, L. Lamant, L. Ysebaert, G. Laurent, G. Delsol, and P. Brousset Anaplastic Lymphoma Kinase-Positive Diffuse Large B-Cell Lymphoma: A Rare Clinicopathologic Entity With Poor Prognosis J. Clin. Oncol., September 1, 2009; 27(25): 4211 - 4216. [Abstract] [Full Text] [PDF] S. 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