ArticleProceedings of the National Academy of Sciences of the United States of America2015
Lymphomagenic CARD11/BCL10/MALT1 signaling drives malignant B-cell proliferation via cooperative NF-κB and JNK activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 76 citations in OpenAlex.
- A DLBCL Prognostic model superior to the IPI score: Mechanistic study and clinical validation based on RFC2- and RFC4-mediated DNA damage repair.Clinical and experimental medicine · 2026Article
- Therapeutic targeting of MALT1 in oncology: Mechanism, inhibitor development, and clinical prospects.Journal of cell communication and signaling · 2026Review
- Potentiation of noncanonical NF-κB signaling and marginal zone B cell expansion by CARD11-mediated regulation of p100 processing.Cell reports · 2025Article
- Update on the pathogenesis and clinical management ofWorld journal of gastrointestinal pathophysiology · 2025Review
- Screening and analysis of plasma differential lncRNA/mRNA in early pregnancy of preeclampsia.Malawi medical journal : the journal of Medical Association of Malawi · 2025Article
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Enforced CARD11/MALT1 signaling in dendritic cells triggers hemophagocytic lymphohistiocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Virus-driven dysregulation of the BCR pathway: a potential mechanism for the high prevalence of HIV related B-cell lymphoma.Annals of hematology · 2024Review
- Essential role of Card11 in airway hyperresponsiveness in high-fat diet-induced obese mice.Experimental & molecular medicine · 2024Article
- A new-disease-causing dominant-negative variant in CARD11 gene in a Chinese case with recurrent fever.Scientific reports · 2024Article
- Article
- Review
- Role of non-World journal of gastroenterology · 2023Review
- MALT1 accelerates proatherogenic vascular smooth muscle cell growth, invasion and synthetic phenotype switching via nuclear factor‑κB signaling‑dependent way.Experimental and therapeutic medicine · 2023Article
- NF-κB mediated regulation of tumor cell proliferation in hypoxic microenvironment.Frontiers in pharmacology · 2023Review
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- CARD11 mutation and HBZ expression induce lymphoproliferative disease and adult T-cell leukemia/lymphoma.Communications biology · 2022Article
- An Isolated Mesenteric Presentation of a Nodal Peripheral T Cell Lymphoma with T Follicular Helper Cell Phenotype.Hematology reports · 2022Article
- Targeting a Novel G-Quadruplex in theGenes · 2022Article
- USP12 promotes CD4Cell death and differentiation · 2021Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
The aggressive activated B cell-like subtype of diffuse large B-cell lymphoma is characterized by aberrant B-cell receptor (BCR) signaling and constitutive nuclear factor kappa-B (NF-κB) activation, which is required for tumor cell survival. BCR-induced NF-κB activation requires caspase recruitment domain-containing protein 11 (CARD11), and CARD11 gain-of-function mutations are recurrently detected in human diffuse large B-cell lymphoma (DLBCL). To investigate the consequences of dysregulated CARD11 signaling in vivo, we generated mice that conditionally express the human DLBCL-derived CARD11(L225LI) mutant. Surprisingly, CARD11(L225LI) was sufficient to trigger aggressive B-cell lymphoproliferation, leading to early postnatal lethality. CARD11(L225LI) constitutively associated with B-cell CLL/lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma translocation gene 1 (MALT1) to simultaneously activate the NF-κB and c-Jun N-terminal kinase (JNK) signaling cascades. Genetic deficiencies of either BCL10 or MALT1 completely rescued the phenotype, and pharmacological inhibition of JNK was, similar to NF-κB blockage, toxic to autonomously proliferating CARD11(L225LI)-expressing B cells. Moreover, constitutive JNK activity was observed in primary human activated B cell-like (ABC)-DLBCL specimens, and human ABC-DLBCL cells were also sensitive to JNK inhibitors. Thus, our results demonstrate that enforced activation of CARD11/BCL10/MALT1 signaling is sufficient to drive transformed B-cell expansion in vivo and identify the JNK pathway as a therapeutic target for ABC-DLBCL.
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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.