ArticleThe Journal of experimental medicine2012
The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 4 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
197 citing papers in PubMed, 4 syntheses or guidelines pooled it, 378 citations in OpenAlex.
- Genetic alterations and their prognostic impact in marginal zone lymphoma: a meta-analysis.Annals of hematology · 2025Pooled it
- Guideline
- Mutational landscape of marginal zone B-cell lymphomas of various origin: organotypic alterations and diagnostic potential for assignment of organ origin.Virchows Archiv : an international journal of pathology · 2022Pooled it
- Systematic Review of Somatic Mutations in Splenic Marginal Zone Lymphoma.Scientific reports · 2019Pooled it
- Venetoclax and ibrutinib induces durable clinical responses in marginal zone lymphoma.Blood advances · 2026Trial
- Trial
- Trial
- Relapsed diffuse large B-cell lymphoma present different genomic profiles between early and late relapses.Oncotarget · 2016Trial
- Germline and somatic genetic variations of TNFAIP3 in lymphoma complicating primary Sjogren's syndrome.Blood · 2013Trial
- Whole exome sequencing identifies novel recurrently mutated genes in patients with splenic marginal zone lymphoma.PloS one · 2013Trial
- Integrated multiomic profiling reveals 2 distinct splenic marginal zone lymphoma subgroups with prognostic relevance.Blood advances · 2026Article
- The expanding landscape of Deltex: signaling crosstalk and clinical implications.Cellular and molecular life sciences : CMLS · 2026Review
- Genomic and transcriptomic evaluation of primary and recurrent luminal B-like breast cancer.ESMO open · 2026Article
- The role of notch signaling in tumor angiogenesis in hematological malignancies.Frontiers in oncology · 2026Review
- Correlated Expression of Notch2 and ADAM17 in Primary Sjögren's Syndrome Salivary Glands.Journal of clinical medicine · 2025Article
- Potentiation of noncanonical NF-κB signaling and marginal zone B cell expansion by CARD11-mediated regulation of p100 processing.Cell reports · 2025Article
- Nodal Marginal Zone Lymphoma with Prominent Expansion of PD-1+ T-Follicular Helper Cells: A Persistent Diagnostic Challenge with a Heterogeneous Mutational Architecture.International journal of molecular sciences · 2025Article
- Integrated genomics with refined cell-of-origin subtyping distinguishes subtype-specific mechanisms of treatment resistance and relapse in diffuse large B-cell lymphoma.Blood cancer journal · 2025Article
- Male Sex, B Symptoms, Bone Marrow Involvement, and Genetic Alterations as Predictive Factors in Diffuse Large B-Cell Lymphoma.International journal of molecular sciences · 2025Article
- Significance of Notch Signaling in Salivary Gland Development and Diseases.Journal of clinical medicine · 2025Review
137 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
40 authors at 15 institutions in 3 countries.
Funding
Abstract
Splenic marginal zone lymphoma (SMZL) is a B cell malignancy of unknown pathogenesis, and thus an orphan of targeted therapies. By integrating whole-exome sequencing and copy-number analysis, we show that the SMZL exome carries at least 30 nonsilent gene alterations. Mutations in NOTCH2, a gene required for marginal-zone (MZ) B cell development, represent the most frequent lesion in SMZL, accounting for ∼20% of cases. All NOTCH2 mutations are predicted to cause impaired degradation of the NOTCH2 protein by eliminating the C-terminal PEST domain, which is required for proteasomal recruitment. Among indolent B cell lymphoproliferative disorders, NOTCH2 mutations are restricted to SMZL, thus representing a potential diagnostic marker for this lymphoma type. In addition to NOTCH2, other modulators or members of the NOTCH pathway are recurrently targeted by genetic lesions in SMZL; these include NOTCH1, SPEN, and DTX1. We also noted mutations in other signaling pathways normally involved in MZ B cell development, suggesting that deregulation of MZ B cell development pathways plays a role in the pathogenesis of ∼60% SMZL. These findings have direct implications for the treatment of SMZL patients, given the availability of drugs that can target NOTCH, NF-κB, and other pathways deregulated in this disease.
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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.