ArticleOncogene2017
Molecular impact of selective NFKB1 and NFKB2 signaling on DLBCL phenotype.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- TRAF3 loss-of-function reveals the noncanonical NF-κB pathway as a therapeutic target in diffuse large B cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- SAMHD1 expression contributes to doxorubicin resistance and predicts survival outcomes in diffuse large B-cell lymphoma patients.NAR cancer · 2024Article
- Chitin Extracted from the Shell of Blue Swimming Crabs (Marine drugs · 2023Article
- ADAR1-mediated RNA editing promotes B cell lymphomagenesis.iScience · 2023Article
- The NF-κB multidimer system model: A knowledge base to explore diverse biological contexts.Science signaling · 2023Review
- Altered mRNA Expression of NFKB1 and NFKB2 Genes in Penile Lichen Sclerosus, Penile Cancer and Zoon Balanitis.Journal of clinical medicine · 2022Article
- Genome-wide CRISPR screens reveal synthetic lethal interaction between CREBBP and EP300 in diffuse large B-cell lymphoma.Cell death & disease · 2021Article
- Identification of Hub Genes and Key Pathways Associated with Peripheral T-cell Lymphoma.Current medical science · 2020Article
- Integrating clinical, molecular, proteomic and histopathological data within the tissue context: tissunomics.Histopathology · 2019Review
- Oncogenic MYD88 mutations in lymphoma: novel insights and therapeutic possibilities.Cancer immunology, immunotherapy : CII · 2018Review
- Novel phosphorylated TAK1 species with functional impact on NF-κB and β-catenin signaling in human Cutaneous T-cell lymphoma.Leukemia · 2018Article
- NFKB1 and Cancer: Friend or Foe?Cells · 2018Review
- NF-κB Activation in Lymphoid Malignancies: Genetics, Signaling, and Targeted Therapy.Biomedicines · 2018Review
- Gene regulation and suppression of type I interferon signaling by STAT3 in diffuse large B cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
Corrections and comments
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diffuse large B-cell lymphoma (DLBCL) has been categorized into two molecular subtypes that have prognostic significance, namely germinal center B-cell like (GCB) and activated B-cell like (ABC). Although ABC-DLBCL has been associated with NF-κB activation, the relationships between activation of specific NF-κB signals and DLBCL phenotype remain unclear. Application of novel gene expression classifiers identified two new DLBCL categories characterized by selective p100 (NF-κB2) and p105 (NF-κB1) signaling. Interestingly, our molecular studies showed that p105 signaling is predominantly associated with GCB subtype and histone mutations. Conversely, most tumors with p100 signaling displayed ABC phenotype and harbored ABC-associated mutations in genes such as MYD88 and PIM1. In vitro, MYD88 L265P mutation promoted p100 signaling through TAK1/IKKα and GSK3/Fbxw7a pathways, suggesting a novel role for this protein as an upstream regulator of p100. p100 signaling was engaged during activation of normal B cells, suggesting p100's role in ABC phenotype development. Additionally, silencing p100 in ABC-DLBCL cells resulted in a GCB-like phenotype, with suppression of Blimp, IRF4 and XBP1 and upregulation of BCL6, whereas introduction of p52 or p100 into GC cells resulted in differentiation toward an ABC-like phenotype. Together, these findings identify specific roles for p100 and p105 signaling in defining DLBCL molecular subtypes and posit MYD88/p100 signaling as a regulator for B-cell activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.