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BCL6 locus is hypermethylated in angioimmunoblastic T-cell lymphoma
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BCL6 locus is hypermethylated in angioimmunoblastic T-cell lymphoma
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Journal Article
BCL6 locus is hypermethylated in angioimmunoblastic T-cell lymphoma
2017
Overview
BCL6, a master transcription factor for differentiation of follicular helper T (TFH) cells, is highly expressed in angioimmunoblastic T-cell lymphoma (AITL) and peripheral T-cell lymphomas (PTCL) containing tumor cells with TFH features.
TET2
, encoding an epigenetic regulator, is frequently mutated in AITL/PTCL. We previously reported that
Tet2
knockdown mice developed T-cell lymphomas with TFH features. Hypermethylation of the
Bcl6
locus followed by BCL6 upregulation was thought to be the key event for lymphoma development in mice. The mechanisms by which BCL6 expression is upregulated in human AITL/PTCL, however, have not been elucidated. Here, we investigated the impact of
TET2
mutations on methylation of
BCL6
locus in human AITL/PTCL samples. Hypermethylation of the
BCL6
locus was more frequent in PTCL samples than B-cell lymphoma samples (PTCL vs B-cell lymphomas: 9/42 vs 0/35). PTCL samples with
TET2
mutations were more frequently hypermethylated than those without
TET2
mutations (PTCL with
TET2
mutations vs without mutations: 6/22 vs 0/17). BCL6 expression in hypermethylated samples was higher than that in low methylated samples. Deregulated BCL6 expression caused by hypermethylation and
TET2
mutations may result in skewed TFH differentiation and eventually contribute to AITL/PTCL development in patients, as well as lymphoma development in
Tet2
knockdown mice.
Publisher
Springer Japan,Springer Nature B.V
