ArticleBlood cancer journal2022
Identification of novel STAT5B mutations and characterization of TCRβ signatures in CD4+ T-cell large granular lymphocyte leukemia.
Article in Blood cancer journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- A practical approach to risk stratification of incidental T-cell clonality.Blood advances · 2026Review
- TCR γδ cell-specific STAT5 gain of function induces a druggable chronic human immune dysregulation.Journal of human immunity · 2026Article
- Disease-associated mutations in the STAT5B SH2 domain reprogram hepatic cholesterol and lipid metabolism.Endocrinology · 2026Article
- Immunological features of acquired pure red cell aplasia: Specific human leucocyte antigen alleles, signal transducer and activator of transcription 3 mutations and a unique T-cell receptor beta motif.British journal of haematology · 2026Article
- [The value of T-cell receptor gene rearrangement in the auxiliary diagnosis of T-cell large granular lymphocytic leukemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- Disease-associated mutations in the STAT5B SH2 domain reprogram hepatic cholesterol and lipid metabolism.bioRxiv : the preprint server for biology · 2025Article
- Transcriptomic landscape of CD8+ and CD4 + T-LGL leukemia revealed the distinct impact of STAT3 and STAT5B activating mutations.Leukemia · 2025Article
- Y665F variant of mouse Stat5b protects against acute kidney injury through transcriptomic shifts in renal gene expression.Scientific reports · 2025Article
- STAT5B leukemic mutations, altering SH2 tyrosine 665, have opposing impacts on immune gene programs.Life science alliance · 2025Article
- NK-type large granular lymphocyte leukemia comes of age.HemaSphere · 2025Review
- Clinical features and outcomes in large granular lymphocyte leukemia - associated pure red cell aplasia with STAT3 mutation.Annals of hematology · 2025Article
- Disease-Associated Mutations of the STAT5B SH2 Domain Regulate Cytokine-Driven Enhancer Function and Mammary Development.Journal of mammary gland biology and neoplasia · 2025Article
- Classification of NK-large granular lymphocytic leukemia by CD56 expression.The oncologist · 2025Article
- Inborn Errors of Immunity Presenting with Early-Onset Severe Atopy.Medicina (Kaunas, Lithuania) · 2025Review
- T-cell clones of uncertain significance. When is the rogue clone dangerous?Haematologica · 2025Review
- Recurrent Missense Driver STAT5BAnti-cancer agents in medicinal chemistry · 2025Article
- The structural influence of the oncogenic driver mutation N642H in the STAT5B SH2 domain.Protein science : a publication of the Protein Society · 2025Article
- HSP and CD279 gene expression as candidate biomarkers in symptomatic LGLL patients.Discover oncology · 2024Article
- STAT5B SH2 variants disrupt mammary enhancers and the stability of genetic programs during pregnancy.bioRxiv : the preprint server for biology · 2024Article
- Diagnostic and prognostic molecular pathology of lymphoid malignancies.Virchows Archiv : an international journal of pathology · 2024Review
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD4+ T-cell large granular lymphocyte leukemia (T-LGLL) is a rare subtype of T-LGLL with unknown etiology. In this study, we molecularly characterized a cohort of patients (n = 35) by studying their T-cell receptor (TCR) repertoire and the presence of somatic STAT5B mutations. In addition to the previously described gain-of-function mutations (N642H, Y665F, Q706L, S715F), we discovered six novel STAT5B mutations (Q220H, E433K, T628S, P658R, P702A, and V712E). Multiple STAT5B mutations were present in 22% (5/23) of STAT5B mutated CD4+ T-LGLL cases, either coexisting in one clone or in distinct clones. Patients with STAT5B mutations had increased lymphocyte and LGL counts when compared to STAT5B wild-type patients. TCRβ sequencing showed that, in addition to large LGL expansions, non-leukemic T cell repertoires were more clonal in CD4+ T-LGLL compared to healthy. Interestingly, 25% (15/59) of CD4+ T-LGLL clonotypes were found, albeit in much lower frequencies, in the non-leukemic CD4+ T cell repertoires of the CD4+ T-LGLL patients. Additionally, we further confirmed the previously reported clonal dominance of TRBV6-expressing clones in CD4+ T-LGLL. In conclusion, CD4+ T-LGLL patients have a typical TCR and mutation profile suggestive of aberrant antigen response underlying the disease.
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