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Int J Cancer. 2016 Jan 1;138(1):121-4. doi: 10.1002/ijc.29697. Epub 2015 Jul 30.

Recurrent alterations of TNFAIP3 (A20) in T-cell large granular lymphocytic leukemia.

Author information

1
Department of Haematology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
2
Institute of Cell Biology (Cancer Research), Medical Faculty, University of Duisburg-Essen, Essen, Germany.
3
Institute of Human Genetics, Christian-Albrechts-University Kiel and University Hospital Schleswig-Holstein, Kiel, Germany.
4
Genome Informatics, Institute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
5
Laboratory for Molecular Biology and Tumor Cytogenetics, Department of Haematology and Oncology, Linz, Austria.
6
Division of Haematology and Haemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.

Abstract

The pathogenesis of T-cell large granular lymphocytic leukemia (T-LGL) is poorly understood, as STAT3 mutations are the only known frequent genetic lesions. Here, we identified non-synonymous alterations in the TNFAIP3 tumor suppressor gene in 3 of 39 T-LGL. In two cases these were somatic mutations, in one case the somatic origin was likely. A further case harbored a SNP that is a known risk allele for autoimmune diseases and B cell lymphomas. Thus, TNFAIP3 mutations represent recurrent genetic lesions in T-LGL that affect about 8% of cases, likely contributing to deregulated NF-κB activity in this leukemia.

KEYWORDS:

NF-κB; STAT3; T-LGL; TNFAIP3; tumor suppressor gene

PMID:
26199174
DOI:
10.1002/ijc.29697
[Indexed for MEDLINE]
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