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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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

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.[1]


  1. ALK activation by the CLTC-ALK fusion is a recurrent event in large B-cell lymphoma. De Paepe, P., Baens, M., van Krieken, H., Verhasselt, B., Stul, M., Simons, A., Poppe, B., Laureys, G., Brons, P., Vandenberghe, P., Speleman, F., Praet, M., De Wolf-Peeters, C., Marynen, P., Wlodarska, I. Blood (2003) [Pubmed]
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