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Background  The  TNFAIP3  gene, which encodes a ubiquitin-modifying enzyme (A20) involved in the negative regulation of NF-κB signaling, is frequently inactivated by gene deletions/mutations in a variety of B-cell malignancies. However, the detection of this in primary Hodgkin lymphoma (HL) specimens is hampered by the scarcity of Hodgkin Reed-Sternberg (HR-S) cells even after enrichment by micro-dissection.    Methods  We used anti-CD30 immunofluorescence with fluorescence in-situ hybridization (FISH) to evaluate the relative number of TNFAIP3/CEP6 double-positive signals in CD30-positive cells.    Results  From a total of 47 primary classical Hodgkin lymphoma (cHL) specimens, 44 were evaluable. We found that the relative numbers of TNFAIP3/CD30 cells were distributed among three groups, corresponding to those having homozygous (11%), heterozygous (32%), and no (57%) deletions in  TNFAIP3 . This shows that  TNFAIP3  deletions could be sensitively detected using our chosen methods.    Conclusions  Comparing the results with mutation analysis,  TNFAIP3  inactivation was shown to have escaped detection in many samples with homozygous deletions. This suggests that  TNFAIP3  inactivation in primary cHL specimens might be more frequent than previously reported.

Deletion of the TNFAIP3/A20gene detected by FICTION analysis in classical Hodgkin lymphoma