ALK activation by the CLTC-ALK fusion is a recurrent event in large B-cell lymphoma

Author:

De Paepe Pascale1,Baens Mathijs1,van Krieken Han1,Verhasselt Bruno1,Stul Michel1,Simons Annet1,Poppe Bruce1,Laureys Geneviève1,Brons Paul1,Vandenberghe Peter1,Speleman Frank1,Praet Marleen1,De Wolf-Peeters Chris1,Marynen Peter1,Wlodarska Iwona1

Affiliation:

1. From the Departments of Pathology, Clinical Chemistry, Microbiology and Immunology, and Molecular Diagnostics, Center of Medical Genetics and Pediatric Oncology, Ghent University Hospital, Belgium; the Department of Human Genetics and Flanders Interuniversity Institute for Biotechnology, Division for Morphology and Molecular Pathology, Catholic University of Leuven, Belgium; and the Departments of Pathology, Human Genetics, and Pediatric Oncology, University Medical Center Nijmegen, the Netherlands.

Abstract

Abstract We present 3 cases of large B-cell lymphoma (LBCL) with a granular cytoplasmic staining for anaplastic lymphoma kinase (ALK). All of the cases showed striking similarities in morphology and immunohistochemical profile characterized by a massive monomorphic proliferation of CD20-/CD138+ plasmablast-like cells. In one of the cases, initially diagnosed as a null-type anaplastic large cell lymphoma (ALCL), the B-cell phenotype became evident only at recurrence. Fluorescent in situ hybridization (FISH) and molecular studies led to the detection of a CLTC-ALK rearrangement in all 3 cases, without any evidence of full-length ALK receptor expression. The associated t(2;17)(p23;q23) was demonstrated in the karyotype of 2 cases. Although a similar CLTC-ALK aberration was previously identified in ALK-positive T-/null cell ALCL and inflammatory myofibroblastic tumor, its association with ALK-positive LBCL seems to be specific and intriguing. (Blood. 2003;102:2638-2641)

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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