Higher incidence of the SNP Met 788 Ile in the coding region of A20 in diffuse large B cell lymphomas

Wenzl, Kerstin; Hofer, Sybille; Troppan, Katharina; Lassnig, Markus; Steinbauer, Elisabeth; Wiltgen, Marco; Zulus, Barbara; Renner, Wilfried; Beham‐Schmid, Christine; Neumeister, Peter; Deutsch, Alexander

doi:10.1007/s13277-015-4322-1

Cited by 7 publications

(7 citation statements)

References 21 publications

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“…24 Some studies showed that TNFAIP3 could play an important role in immune and inflammatory responses mediated by cytokines. [24][25][26]…”

Section: Tnfaip3 Basic Characteristics Of Tnfaip3mentioning

confidence: 99%

“…In addition, TNFAIP3 reexpression can inhibit proliferation, decrease expression of target genes in NF-κB signaling pathway, increase cytotoxicity and induce apoptosis in cells lacking TNFAIP3. 25 At present, there are few studies on the mechanism of TNFAIP3. Wenzl et al found that TNFAIP3 rs143002189 polymorphism was the substitution of isoleucine (Met) by isoleucine (Ile) at 788 sites of ZnF7 amino acid chain, which altered the structure and appearance of protein leading to tumors.…”

Section: Physiological Functions and Mechanisms Of Tnfaip3mentioning

confidence: 99%

“…A study confirmed that inactivated TNFAIP3 could promote the activation of uncontrolled NF-κB signaling pathway, which improved cell viability and led to lymphoma. 25 Another study found that TNFAIP3, as a tumor suppressor gene, may be a key molecule in the transformation of chronic inflammation into cancer. 62 In multiple myeloma cells, TNFAIP3 was found to be inactivated mainly because of deletions, not body mutations or promoter methylation.…”

Section: Tnfaip3 and Malignant Tumorsmentioning

confidence: 99%

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<p>Tumor Necrosis Factor Alpha-Induced Proteins in Malignant Tumors: Progress and Prospects</p>

Guo¹,

Yuan²

2020

OTT

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Tumor necrosis factor (TNF) is the first cytokine used in tumor biotherapy, but TNFrelated drugs are limited by the lack of specific targets. Tumor necrosis factor alpha-induced proteins (TNFAIPs), derived from TNF, is a protein family and participates in proliferation, invasion and metastasis of tumor cells. In order to better understand biological functions and potential roles of TNFAIPs in malignant tumors, this paper in the form of "Gene-Protein-Tumor correlation" summarizes the biological characteristics, physiological functions and mechanisms of TNFAIPs by searching National Center of Biotechnology Information, GeneCards, UniProt and STRING databases. The relationship between TNFAIPs and malignant tumors is analyzed, and protein-protein interaction diagram in members of TNFAIPs is drawn based on TNF for the first time. We find that TNF as a key factor is related to TNFAIP1, TNFAIP3, TNFAIP5, TNFAIP6, TNFAIP8 and TNFAIP9, which can be directly involved in activating TNFAIP1, TNFAIP5, TNFAIP8 and TNFAIP9. We confirm that the mechanism of TNFAIP1, TNFAIP2 and TNFAIP3 inducing tumors may be related to NF-κB signaling pathway, but the mechanism of tumor induction by other members of TNFAIPs is not clear. In the future, translational studies are needed to explore the mechanisms of TNF-TNFAIPs-tumors.

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“…24 Some studies showed that TNFAIP3 could play an important role in immune and inflammatory responses mediated by cytokines. [24][25][26]…”

Section: Tnfaip3 Basic Characteristics Of Tnfaip3mentioning

confidence: 99%

Section: Physiological Functions and Mechanisms Of Tnfaip3mentioning

confidence: 99%

Section: Tnfaip3 and Malignant Tumorsmentioning

confidence: 99%

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<p>Tumor Necrosis Factor Alpha-Induced Proteins in Malignant Tumors: Progress and Prospects</p>

Guo¹,

Yuan²

2020

OTT

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“…In general, members of this protein family differ more than 75% at the level of amino acid residues, indicating different biological function and their gene expression is induced by TNF-α [ 61 ]. The TNFAIP3 / A20 gene encodes a zinc finger protein acting as a ubiquitin modification enzyme, which plays a role as negative-feedback regulator of the NF-κB signaling pathway and as mediator of TNF apoptosis [ 61 , 62 ]. TNFAIP3 downregulates the activity of IRF-3, a key transcription factor for the induction of IFN-γ [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Dual RNA-Seq Enables Full-Genome Assembly of Measles Virus and Characterization of Host–Pathogen Interactions

et al. 2021

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Measles virus (MeV) has a negative-sense 15 kb long RNA genome, which is generally conserved. Recent advances in high-throughput sequencing (HTS) and Dual RNA-seq allow the analysis of viral RNA genomes and the discovery of viral infection biomarkers, via the simultaneous characterization of the host transcriptome. However, these host–pathogen interactions remain largely unexplored in MeV infections. We performed untargeted Dual RNA-seq in 6 pharyngeal and 6 peripheral blood mononuclear cell (PBMCs) specimens from patients with MeV infection, as confirmed via routine real-time PCR testing. Following optimised DNase treatment of total nucleic acids, we used the pharyngeal samples to build poly-A-enriched NGS libraries. We reconstructed the viral genomes using the pharyngeal datasets and we further conducted differential expression, gene-ontology and pathways enrichment analysis to compare both the pharyngeal and the peripheral blood transcriptomes of the MeV-infected patients vs. control groups of healthy individuals. We obtained 6 MeV genotype-B3 full-genome sequences. We minutely analyzed the transcriptome of the MeV-infected pharyngeal epithelium, detecting all known viral infection biomarkers, but also revealing a functional cluster of local antiviral and inflammatory immune responses, which differ substantially from those observed in the PBMCs transcriptome. The application of Dual RNA-seq technologies in MeV-infected patients can potentially provide valuable information on the virus genome structure and the cellular innate immune responses and drive the discovery of new targets for antiviral therapy.

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“…This mutation is sufficient to intrinsically activate survival signaling in the malignant B cells and obviates the need for upstream BCR signaling [103]. Loss of function mutations in the tumor suppressor A20 contributes to NF-κB pro-survival signaling have also been described in ABC DLBCL and CLL cases [105,106].…”

Section: Mutations In the Bcr Signaling Cascadementioning

confidence: 99%

The Antigen Receptor as a Driver of B-Cell Lymphoma Development and Evolution

Sepulveda¹,

Seija²,

Oppezzo³

et al. 2018

Hematology - Latest Research and Clinical Advances

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The expression of a functional antigen receptor is necessary for cell survival of normal B lymphocytes and most B-cell neoplasms alike. When the genetic modifications of the B-cell receptor locus fail to produce a functional antigen receptor or result in deleterious mutations of a previously expressed receptor, the affected B cell will undergo apoptosis. The three physiological mechanisms that generate the B-cell receptor, VDJ recombination, somatic hypermutation, and class switch recombination, can induce double-strand DNA breaks and can specifically contribute to lymphomagenesis. On the other hand, the B-cell receptor activation and signaling pathways, which provide strong survival and proliferation signals to normal B cells, can support the growth and evolution of malignant lymphocytes. As a result, an otherwise structurally normal B-cell receptor can behave, from the functional perspective, as a true oncogene. In this chapter, we provide an in-depth discussion of the most recently discovered recurrent mechanisms involving the B-cell receptor in lymphoma pathogenesis. The discussion is structured around two major topics: (1) the genetic mechanisms that create a functional antigen receptor and their errors leading to oncogenic events, and (2) the pathogenic activation of the B-cell receptor signaling cascade. Finally, we will briefly comment on novel emerging therapies targeting the B-cell receptor at different levels.

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Higher incidence of the SNP Met 788 Ile in the coding region of A20 in diffuse large B cell lymphomas

Cited by 7 publications

References 21 publications

<p>Tumor Necrosis Factor Alpha-Induced Proteins in Malignant Tumors: Progress and Prospects</p>

<p>Tumor Necrosis Factor Alpha-Induced Proteins in Malignant Tumors: Progress and Prospects</p>

Dual RNA-Seq Enables Full-Genome Assembly of Measles Virus and Characterization of Host–Pathogen Interactions

The Antigen Receptor as a Driver of B-Cell Lymphoma Development and Evolution

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