A20 is targeted by promoter methylation, deletion and inactivating mutation in MALT lymphoma

Chanudet, Estelle; Huang, Yuanxue; Ichimura, Koichi; Dong, Guangbin; Hamoudi, Rifat; Radford, John; Wotherspoon, Andrew; Isaacson, Peter G.; Ferry, Judith A.; Du, Ming‐Qing

doi:10.1038/leu.2009.234

Cited by 109 publications

(100 citation statements)

References 9 publications

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“…The incidence (28.6%) of A20 mutation in this series of OAML from Shanghai was higher than those from the UK and the USA (17%) 11 and from Japan (16%), 7 while the incidence of A20 deletion (8.6%) in this study was lower than those from the UK and the USA (17%) 3,11 and from Japan (21%). 7 Using pyrosequencing, we had previously demonstrated A20 promoter methylation in 7 of 27 (26%) cases from the UK and the USA, 11 but in only one of 105 (1%) cases in this study.…”

Section: A20 Genetic Abnormalities In Oamlcontrasting

confidence: 47%

A20 inactivation in ocular adnexal MALT lymphoma

Bi¹,

Zeng²,

Chanudet³

et al. 2011

Haematologica

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Section: A20 Genetic Abnormalities In Oamlcontrasting

confidence: 47%

A20 inactivation in ocular adnexal MALT lymphoma

Bi¹,

Zeng²,

Chanudet³

et al. 2011

Haematologica

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“…TNFAIP3 hypermethylation occurs in MALT lymphoma but not in chronic lymphocytic leukemia nor in multiple myeloma. 75 The tumor related DNA methylation occurs within 18 CpGs sites of the gene promoter in contrast to the intronic location that we identified.…”

Section: Novel Methylation Sites In Signaling Pathways: Maml2 Tagln3mentioning

confidence: 44%

The DNA methylation profile of activated human natural killer cells

et al. 2016

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Natural killer (NK) cells are now recognized to exhibit characteristics akin to cells of the adaptive immune system. The generation of adaptive memory is linked to epigenetic reprogramming including alterations in DNA methylation. The study herein found reproducible genome wide DNA methylation changes associated with human NK cell activation. Activation led predominately to CpG hypomethylation (81% of significant loci). Bioinformatics analysis confirmed that non-coding and gene-associated differentially methylated sites (DMS) are enriched for immune related functions (i.e., immune cell activation). Known DNA methylation-regulated immune loci were also identified in activated NK cells (e.g., TNFA, LTA, IL13, CSF2). Twenty-one loci were designated high priority and further investigated as potential markers of NK activation. BHLHE40 was identified as a viable candidate for which a droplet digital PCR assay for demethylation was developed. The assay revealed high demethylation in activated NK cells and low demethylation in na€ ıve NK, T-and B-cells. We conclude the NK cell methylome is plastic with potential for remodeling. The differentially methylated region signature of activated NKs revealed similarities with T cell activation, but also provided unique biomarker candidates of NK activation, which could be useful in epigenome-wide association studies to interrogate the role of NK subtypes in global methylation changes associated with exposures and/or disease states.

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“…77 By genomic profiling of so-called 'translocation negative' ocular adnexal EMZL, it was demonstrated that the A20 gene,-an essential global NK-kB inhibitor-, was found to be inactivated either by somatic deletion and/or mutation in ocular adnexal EMZL. 78,79 The A20 deletion is most commonly heterozygous, and is mutually exclusive from the above-described MALT1 and IGH translocations. Further, it was shown that the A20 mutation/deletion is significantly associated with an increased expression of NK-kB target genes.…”

Section: Extranodal Marginal Zone B-cell Lymphomamentioning

confidence: 99%

Molecular pathology of lymphoma

Coupland

2012

Eye

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Ocular lymphomas can be divided into intraocular lymphomas and ocular adnexal lymphomas. The vitreoretinal lymphomausually a diffuse large B-cell lymphoma (DLBCL) of high-grade malignancy-is the most common lymphoid malignancy arising in the eye, while the extranodal marginal zone B-cell lymphoma (EMZL), an indolent often recurrent tumour, occurs most frequently in the ocular adnexal tissue. The two lymphoma subtypes differ significantly in their clinical presentation, subsequent course and outcome as well as in their underlying morphological, immunophenotypical and genetic features. The molecular processes involved in DLBCL and EMZL development are complex, and include chromosomal translocations, mutations caused by aberrant somatic hypermutation, sporadic somatic mutations, and copy number alterations, characterized by deletions and amplifications. These lead to alterations in particular signalling pathways, which in turn activate transcription factors, such as nuclear factor NF-kB. This review provides an overview of the histological features of DLBCL and EMZL, and discusses the current insights into the molecular mechanisms underlying the development of these tumours, when they occur systemically and particularly when they arise in ocular tissues.

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A20 is targeted by promoter methylation, deletion and inactivating mutation in MALT lymphoma

Cited by 109 publications

References 9 publications

A20 inactivation in ocular adnexal MALT lymphoma

A20 inactivation in ocular adnexal MALT lymphoma

The DNA methylation profile of activated human natural killer cells

Molecular pathology of lymphoma

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