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Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma
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ALK activation by the CLTC-ALK fusion is a recurrent event in large B-cell lymphoma

Pascale De Paepe1, Mathijs Baens, Han van Krieken

  • 1Department of Pathology, Center of Medical Genetics and Pediatric Oncology, Ghent University Hospital, Belgium.

Blood
|May 17, 2003
PubMed

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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