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Prepublished online as a Blood First Edition Paper on May 22, 2003; DOI 10.1182/blood-2003-03-0786.
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Blood, 1 October 2003, Vol. 102, No. 7, pp. 2568-2573
NEOPLASIA
ALK-positive diffuse large B-cell lymphoma is associated with Clathrin-ALK rearrangements: report of 6 cases
Randy D. Gascoyne,
Laurence Lamant,
Jose I. Martin-Subero,
Valia S. Lestou,
Nancy Lee Harris,
Hans-Konrad Müller-Hermelink,
John F. Seymour,
Lynda J. Campbell,
Douglas E. Horsman,
Isabelle Auvigne,
Estelle Espinos,
Reiner Siebert, and
Georges Delsol
From the Department of Oncogenesis and Signaling in Hematopoietic Cells, Institut National de la Santé et de la Recherche Médicale (INSERM) U-563, Centre de Physiopathologie de Toulouse-Purpan, Toulouse, France; the Department of Pathology and Laboratory Medicine, British Columbia Cancer Agency, Vancouver, BC, Canada; the Institute of Human Genetics, University Hospital Schleswig-Holstein Campus, Kiel, Germany; the Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA; the Institute of Pathology, Wurzburg, Germany; the Department of Medical Oncology, Peter MacCallum Cancer Institute, Melbourne, Australia; and the Victorian Cancer Cytogenetics Unit, St Vincent's Hospital, Victoria, Australia.
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 overexpress 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 6 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, multicolor karyotyping (M-FISH), and reverse transcriptase-polymerase chain reaction. These results clearly demonstrate that most 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. (Blood. 2003;102:2568-2573)
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