ArticleBlood2015
Activating STAT6 mutations in follicular lymphoma.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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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.
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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
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- Atopic dermatitis and lymphoma risk: a systematic review and meta-analysis.Frontiers in oncology · 2025Pooled it
- MS4A4A promotes macrophages M2 polarization via NF-κB /JAK-STAT6 axis, resulting GBM malignant progression.Oncogene · 2026Article
- Genomic heterogeneity in primary cutaneous follicular center lymphomas reveals different clinicopathological subgroups.HemaSphere · 2026Article
- STAT6: Multidimensional analysis from hematopoietic immune regulation to pathogenesis mechanisms and therapeutic targets in hematologic malignancies.Annals of hematology · 2026Review
- The CCL17-CCR4 Axis Is Critical for Mutant STAT6-Mediated Microenvironmental Remodeling and Therapeutic Resistance in Relapsed/Refractory Diffuse Large B-Cell Lymphoma.Cancer immunology research · 2026Article
- The Multifaceted Roles of STAT6: Implications for Precision Immunotherapeutics.ImmunoTargets and therapy · 2026Review
- Audit of B-cell cancer genes.Blood advances · 2025Review
- STAT6 mutations compensate for CREBBP mutations and hyperactivate IL4/STAT6/RRAGD/mTOR signaling in follicular lymphoma.Leukemia · 2025Article
- B Cell Differentiation and the Origin and Pathogenesis of Human B Cell Lymphomas.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Research progress on the mechanism of common inflammatory pathways in the pathogenesis and development of lymphoma.Annals of medicine · 2024Review
- STAT6 mutations enriched at diffuse large B-cell lymphoma relapse reshape the tumor microenvironment.International journal of hematology · 2024Article
- Article
- Autosomal Dominant STAT6 Gain of Function Causes Severe Atopy Associated with Lymphoma.Journal of clinical immunology · 2023Article
- The clinical and molecular taxonomy of t(14;18)-negative follicular lymphomas.Blood advances · 2023Article
- Mutations associated with progression in follicular lymphoma predict inferior outcomes at diagnosis: Alliance A151303.Blood advances · 2023Article
- JAKs and STATs from a Clinical Perspective: Loss-of-Function Mutations, Gain-of-Function Mutations, and Their Multidimensional Consequences.Journal of clinical immunology · 2023Review
- Severe allergic dysregulation due to a gain of function mutation in the transcription factor STAT6.The Journal of allergy and clinical immunology · 2023Article
- Human germline heterozygous gain-of-function STAT6 variants cause severe allergic disease.The Journal of experimental medicine · 2023Article
- Nuclear Export in Non-Hodgkin Lymphoma and Implications for Targeted XPO1 Inhibitors.Biomolecules · 2023Review
- Advances in the multi-omics landscape of follicular lymphoma.International journal of biological sciences · 2023Review
9 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Follicular lymphoma (FL) is the second most common non-Hodgkin lymphoma in the Western world. FL cell-intrinsic and cell-extrinsic factors influence FL biology and clinical outcome. To further our understanding of the genetic basis of FL, we performed whole-exome sequencing of 23 highly purified FL cases and 1 transformed FL case and expanded findings to a combined total of 114 FLs. We report recurrent mutations in the transcription factor STAT6 in 11% of FLs and identified the STAT6 amino acid residue 419 as a novel STAT6 mutation hotspot (p.419D/G, p.419D/A, and p.419D/H). FL-associated STAT6 mutations were activating, as evidenced by increased transactivation in HEK293T cell-based transfection/luciferase reporter assays, heightened interleukin-4 (IL-4) -induced activation of target genes in stable STAT6 transfected lymphoma cell lines, and elevated baseline expression levels of STAT6 target genes in primary FL B cells harboring mutant STAT6. Mechanistically, FL-associated STAT6 mutations facilitated nuclear residency of STAT6, independent of IL-4-induced STAT6-Y641 phosphorylation. Structural modeling of STAT6 based on the structure of the STAT1-DNA complex revealed that most FL-associated STAT6 mutants locate to the STAT6-DNA interface, potentially facilitating heightened interactions. The genetic and functional data combined strengthen the recognition of the IL-4/JAK/STAT6 axis as a driver of FL pathogenesis.
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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.