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Title: ALK activation by the CLTC-ALK fusion is a recurrent event in large B-cell lymphoma.
Author(s): Paepe, P. de; Baens, M; Krieken, J.H.J.M. van ; Verhasselt, B.; Stul, M.; Simons, A. ; Poppe, B.; Laureys, G.; Brons, P.P.T. ; Vandenberghe, P.; Speleman, F.; Praet, M.; Wolf-Peeters, C. de; Marynen, P.; Wlodarska, I.
Publication year: 2003
Source: Blood, vol. 102, iss. 7, (2003), pp. 2638-2641
ISSN: 0006-4971
DOI: https://doi.org/10.1182/blood-2003-04-1050
Publication type: Article / Letter to editor

Please use this identifier to cite or link to this item : http://hdl.handle.net/2066/144450   http://hdl.handle.net/2066/144450

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Subject: UMCN 1.2: Molecular diagnosis, prognosis and monitoring
UMCN 1.3: Tumor microenvironment
UMCN 1.4: Immunotherapy, gene therapy and transplantation
Organization: Pathology
Human Genetics
Paediatrics
Journal title:
Blood
Volume: vol. 102
Issue: iss. 7
Page start: p. 2638
Page end: p. 2641
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.

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