ALK activation by the CLTC-ALK fusion is a recurrent event in large B-cell lymphoma.
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SourceBlood, 102, 7, (2003), pp. 2638-2641
Article / Letter to editor
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SubjectUMCN 1.2: Molecular diagnosis, prognosis and monitoring; UMCN 1.3: Tumor microenvironment; UMCN 1.4: Immunotherapy, gene therapy and transplantation
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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