ArticleThe Journal of clinical investigation2018
STAT5BN642H is a driver mutation for T cell neoplasia.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- The Prognostic Role of STAT5B Across Cancer Types and Comparative Analysis with STAT5A: A Systematic Review.Biomolecules · 2025Pooled it
- Disease-associated mutations in the STAT5B SH2 domain reprogram hepatic cholesterol and lipid metabolism.Endocrinology · 2026Article
- Preclinical models of hepatosplenic γδ T-cell lymphoma with an activating STAT5B mutation display sensitivity to JAK inhibitor upadacitinib.HemaSphere · 2026Article
- Impact of rare JAK/STAT germline mutations on vaccination-induced innate immune responses in a Tyrolian population.International journal of biological sciences · 2026Article
- Disease-associated mutations in the STAT5B SH2 domain reprogram hepatic cholesterol and lipid metabolism.bioRxiv : the preprint server for biology · 2025Article
- STAT5B leukemic mutations, altering SH2 tyrosine 665, have opposing impacts on immune gene programs.Life science alliance · 2025Article
- Allosteric Covalent Inhibitors of the STAT3 Transcription Factor from Virtual Screening.ACS medicinal chemistry letters · 2025Article
- Evolutionary Transcriptomics of Cancer Development.International journal of molecular sciences · 2025Article
- Models for T-large granular lymphocytic leukemia: how to mimic the cellular interplays in malignant autoimmunity.Leukemia · 2025Review
- Disease-Associated Mutations of the STAT5B SH2 Domain Regulate Cytokine-Driven Enhancer Function and Mammary Development.Journal of mammary gland biology and neoplasia · 2025Article
- Recurrent Missense Driver STAT5BAnti-cancer agents in medicinal chemistry · 2025Article
- PIM1 is a potential therapeutic target for the leukemogenic effects mediated by JAK/STAT pathway mutations in T-ALL/LBL.NPJ precision oncology · 2024Article
- Perinatal thymic-derived CD8αβ-expressing γδ T cells are innate IFN-γ producers that expand in IL-7R-STAT5B-driven neoplasms.Nature immunology · 2024Article
- Article
- Unveiling myeloid transformation: T-LGLL with eosinophilia masking myeloid-associated STAT5B mutation culminating in AML.British journal of haematology · 2024Article
- STAT5B SH2 variants disrupt mammary enhancers and the stability of genetic programs during pregnancy.bioRxiv : the preprint server for biology · 2024Article
- JAK-STAT signaling maintains homeostasis in T cells and macrophages.Nature immunology · 2024Article
- Hyperactive STAT5 hijacks T cell receptor signaling and drives immature T cell acute lymphoblastic leukemia.The Journal of clinical investigation · 2024Article
- Janus Kinase 3 (JAK3): A Critical Conserved Node in Immunity Disrupted in Immune Cell Cancer and Immunodeficiency.International journal of molecular sciences · 2024Review
- JAK/STAT in leukemia: a clinical update.Molecular cancer · 2024Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STAT5B is often mutated in hematopoietic malignancies. The most frequent STAT5B mutation, Asp642His (N642H), has been found in over 90 leukemia and lymphoma patients. Here, we used the Vav1 promoter to generate transgenic mouse models that expressed either human STAT5B or STAT5BN642H in the hematopoietic compartment. While STAT5B-expressing mice lacked a hematopoietic phenotype, the STAT5BN642H-expressing mice rapidly developed T cell neoplasms. Neoplasia manifested as transplantable CD8+ lymphoma or leukemia, indicating that the STAT5BN642H mutation drives cancer development. Persistent and enhanced levels of STAT5BN642H tyrosine phosphorylation in transformed CD8+ T cells led to profound changes in gene expression that were accompanied by alterations in DNA methylation at potential histone methyltransferase EZH2-binding sites. Aurora kinase genes were enriched in STAT5BN642H-expressing CD8+ T cells, which were exquisitely sensitive to JAK and Aurora kinase inhibitors. Together, our data suggest that JAK and Aurora kinase inhibitors should be further explored as potential therapeutics for lymphoma and leukemia patients with the STAT5BN642H mutation who respond poorly to conventional chemotherapy.
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