ArticleNature communications2015
Activating mutations of STAT5B and STAT3 in lymphomas derived from γδ-T or NK cells.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers.
What it found
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The trial behind it
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Who cites it
242 citing papers in PubMed, 382 citations in OpenAlex.
- Phase 2 multicenter maintenance study of golidocitinib, A JAK1 selective inhibitor, in patients with peripheral T cell lymphomas after first-line systemic therapy (JACKPOT26).Blood cancer journal · 2026Trial
- Trial
- Combination of anti-PD-1 antibody with P-GEMOX as a potentially effective immunochemotherapy for advanced natural killer/T cell lymphoma.Signal transduction and targeted therapy · 2020Trial
- CNS involvement by EBV-positive extranodal T-cell lymphoma harboring STAT3 Y640F mutation following allogeneic hematopoietic stem cell transplantation: A case report.Radiology case reports · 2026Article
- Review
- T cell lymphomas: cancers of aberrant immune synapse signalling.Nature reviews. Immunology · 2026Review
- Primary Extranodal Natural Killer/T-Cell Lymphoma of the Central Nervous System: A Rare Case Report with Diagnostic and Management ChallengesTurkish journal of haematology : official journal of Turkish Society of Haematology · 2026Article
- Putative Clonal Evolution in aEJHaem · 2026Article
- Integrated Evolutionary and Multi-Omic Analysis of STAT Family Activation Across Solid Tumors.Genes · 2026Article
- Clinical relevance of mosaic variants detected by exome sequencing.The Journal of allergy and clinical immunology · 2026Article
- Discovery of SD-965 as a Potent, Selective, and Efficacious STAT3 PROTAC Degrader.Journal of medicinal chemistry · 2026Article
- Preclinical models of hepatosplenic γδ T-cell lymphoma with an activating STAT5B mutation display sensitivity to JAK inhibitor upadacitinib.HemaSphere · 2026Article
- Primary gastric EBV-positive cytotoxic-molecule-negative T-cell lymphoma with TET2 multihit mutations: a case report.Journal of clinical and experimental hematopathology : JCEH · 2026Article
- JAK Inhibitors in the Treatment of T-Cell Lymphomas: Current Evidence and Future Directions.Cancers · 2026Review
- T-cell lymphoma-associated STAT3 variants impose a type 1 regulatory-like phenotype.Frontiers in immunology · 2026Article
- γδ T cells: bridging innate and adaptive immunity in development, tissue residency, and disease.Frontiers in immunology · 2026Review
- Case report and literature review: Golidocitinib as a potential treatment for monomorphic epitheliotropic intestinal T-cell lymphoma.Frontiers in oncology · 2026Article
- Aggressive Natural Killer Cell Leukemia: A Rare and Rapidly Progressive Hematologic Malignancy-Case Report and Literature Review.Case reports in hematology · 2026Article
- Mature NK-cell lymphoma presenting with chylothorax and delirium: a rare emergency case.International journal of emergency medicine · 2025Article
- The Significance of the Microenvironment in T/Nk-Cell Neoplasms.International journal of molecular sciences · 2025Review
182 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors at 7 institutions in 3 countries.
Funding
Abstract
Lymphomas arising from NK or γδ-T cells are very aggressive diseases and little is known regarding their pathogenesis. Here we report frequent activating mutations of STAT3 and STAT5B in NK/T-cell lymphomas (n=51), γδ-T-cell lymphomas (n=43) and their cell lines (n=9) through next generation and/or Sanger sequencing. STAT5B N642H is particularly frequent in all forms of γδ-T-cell lymphomas. STAT3 and STAT5B mutations are associated with increased phosphorylated protein and a growth advantage to transduced cell lines or normal NK cells. Growth-promoting activity of the mutants can be partially inhibited by a JAK1/2 inhibitor. Molecular modelling and surface plasmon resonance measurements of the N642H mutant indicate a marked increase in binding affinity of the phosphotyrosine-Y699 with the mutant histidine. This is associated with the prolonged persistence of the mutant phosphoSTAT5B and marked increase of binding to target sites. Our findings suggest that JAK-STAT pathway inhibition may represent a therapeutic strategy.
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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.