Methylation patterns in marginal zone lymphoma

Arribas, Alberto J.; Bertoni, Francesco

doi:10.1016/j.beha.2016.09.003

Cited by 9 publications

(12 citation statements)

References 75 publications

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“…In cases of MALT lymphoma, the frequency of methylated genes increases as throughout disease progression . Interestingly, hypomethylating agents have not been extensively studied within this clinical context.…”

Section: Discussionmentioning

confidence: 99%

“…27,28 In cases of MALT lymphoma, the frequency of methylated genes increases as throughout disease progression. 29 Interestingly, hypomethylating agents have not been extensively studied within this clinical context. Those with MALT lymphoma not responding to or not eligible for locally directed therapy have been effectively treated with the use of rituximab.…”

Section: Discussionmentioning

confidence: 99%

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Primary central nervous system marginal zone B‐cell lymphoma arising from the dural meninges: A case report and review of literature

Lopetegui‐Lia

Delasos

Asad

et al. 2020

Clinical Case Reports

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Primary central nervous system marginal zone B‐cell lymphoma arising from the dural meninges: A case report and review of literature

Lopetegui‐Lia

Delasos

Asad

et al. 2020

Clinical Case Reports

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“…In MALT lymphomas, promoter methylation seems to increase with a continuum from MALT lymphoma, to MALT lymphoma with large cell component, to DLBCL. Consistently, a series of tumor suppressor genes such as CDKN2A , DAPK1 , CDH1 , and TNFAIP3 are silenced via promoter methylation in MALT lymphoma progression 86 – 88 .…”

Section: Chromatin Remodeling and Epigenome Regulationmentioning

confidence: 99%

Recent advances in understanding the biology of marginal zone lymphoma

2018

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There are three different marginal zone lymphomas (MZLs): the extranodal MZL of mucosa-associated lymphoid tissue (MALT) type (MALT lymphoma), the splenic MZL, and the nodal MZL. The three MZLs share common lesions and deregulated pathways but also present specific alterations that can be used for their differential diagnosis. Although trisomies of chromosomes 3 and 18, deletions at 6q23, deregulation of nuclear factor kappa B, and chromatin remodeling genes are frequent events in all of them, the three MZLs differ in the presence of recurrent translocations, mutations affecting the NOTCH pathway, and the transcription factor Kruppel like factor 2 ( KLF2) or the receptor-type protein tyrosine phosphatase delta ( PTPRD). Since a better understanding of the molecular events underlying each subtype may have practical relevance, this review summarizes the most recent and main advances in our understanding of the genetics and biology of MZLs.

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“…We recognized that carcinogenesis‐ and arthritis‐associated DNA methylation profile changes are similar in a sense, as both are characterized by dominant genome‐wide hypomethylation affecting intergenic and intragenic regions, and infrequent promoter‐specific hypermethylation events . Accordingly, we hypothesized that a demethylating agent that proved to be effective in cancer treatment could also be effective in arthritis therapy.…”

Section: Resultsmentioning

confidence: 99%

Amelioration of Autoimmune Arthritis in Mice Treated With the DNA Methyltransferase Inhibitor 5′‐Azacytidine

Toth

Ocskó

Balog³

et al. 2019

Arthritis & Rheumatology

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Objective Disease‐associated, differentially hypermethylated regions have been reported in rheumatoid arthritis (RA), but no DNA methyltransferase inhibitors have been evaluated in either RA or any animal models of RA. The present study was conducted to evaluate the therapeutic potential of 5′‐azacytidine (5′‐azaC), a DNA methyltransferase inhibitor, and explore the cellular and gene regulatory networks involved in the context of autoimmune arthritis. Methods A disease‐associated genome‐wide DNA methylation profile was explored by methylated CpG island recovery assay–chromatin immunoprecipitation (ChIP) in arthritic B cells. Mice with proteoglycan‐induced arthritis (PGIA) were treated with 5′‐azaC. The effect of 5′‐azaC on the pathogenesis of PGIA was explored by measuring serum IgM and IgG1 antibody levels using enzyme‐linked immunosorbent assay, investigating the efficiency of class‐switch recombination (CSR) and Aicda gene expression using real‐time quantitative polymerase chain reaction, monitoring germinal center (GC) formation by immunohistochemistry, and determining alterations in B cell subpopulations by flow cytometry. The 5′‐azaC–induced regulation of the Aicda gene was explored using RNA interference, ChIP, and luciferase assays. Results We explored arthritis‐associated hypermethylated regions in mouse B cells and demonstrated that DNA demethylation had a beneficial effect on autoimmune arthritis. The 5′‐azaC–mediated demethylation of the epigenetically inactivated Ahr gene resulted in suppressed expression of the Aicda gene, reduced CSR, and compromised GC formation. Ultimately, this process led to diminished IgG1 antibody production and amelioration of autoimmune arthritis in mice. Conclusion DNA hypermethylation plays a leading role in the pathogenesis of autoimmune arthritis and its targeted inhibition has therapeutic potential in arthritis management.

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Methylation patterns in marginal zone lymphoma

Cited by 9 publications

References 75 publications

Primary central nervous system marginal zone B‐cell lymphoma arising from the dural meninges: A case report and review of literature

Primary central nervous system marginal zone B‐cell lymphoma arising from the dural meninges: A case report and review of literature

Recent advances in understanding the biology of marginal zone lymphoma

Amelioration of Autoimmune Arthritis in Mice Treated With the DNA Methyltransferase Inhibitor 5′‐Azacytidine

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