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Prepublished online as a Blood First Edition Paper on May 15, 2003; DOI 10.1182/blood-2003-04-1050.
Blood, 1 October 2003, Vol. 102, No. 7, pp. 2638-2641 ALK activation by the CLTC-ALK fusion is a recurrent event in large B-cell lymphomaFrom 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.
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)
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