ArticleScientific reports2023
Distinct mutational pattern of T-cell large granular lymphocyte leukemia combined with pure red cell aplasia: low mutational burden of STAT3.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Efficacy and influencing factors of immunosuppressive therapy for pure red cell aplasia: meta-analysis and systematic review.Annals of hematology · 2025Pooled it
- 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
- Favorable response to second-line sirolimus regardless ofTherapeutic advances in hematology · 2026Article
- Epidemiologic sequential analysis of pure red blood cell aplasia and T-cell large granular lymphocyte leukemia in Korea.Annals of hematology · 2025Article
- Clinical features and outcomes in large granular lymphocyte leukemia - associated pure red cell aplasia with STAT3 mutation.Annals of hematology · 2025Article
- Mutational heterogeneities in STAT3 and clonal hematopoiesis-related genes in acquired pure red cell aplasia.Annals of hematology · 2025Article
- Lenalidomide-induced pure red cell aplasia is associated with elevated expression of MHC-I molecules on erythrocytes.Nature communications · 2024Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cell large granular lymphocyte leukemia (T-LGL) is often accompanied by pure red cell aplasia (PRCA). A high depth of next generation sequencing (NGS) was used for detection of the mutational profiles in T-LGL alone (n = 25) and T-LGL combined with PRCA (n = 16). Beside STAT3 mutation (41.5%), the frequently mutated genes included KMT2D (17.1%), TERT (12.2%), SUZ12 (9.8%), BCOR (7.3%), DNMT3A (7.3%), and RUNX1 (7.3%). Mutations of the TERT promoter showed a good response to treatment. 3 of 41 (7.3%) T-LGL patients with diverse gene mutations were revealed as T-LGL combined with myelodysplastic syndrome (MDS) after review of bone marrow slide. T-LGL combined with PRCA showed unique features (low VAF level of STAT3 mutation, low lymphocyte count, old age). Low ANC was detected in a STAT3 mutant with a low level of VAF, suggesting that even the low mutational burden of STAT3 is sufficient for reduction of ANC. In retrospective analysis of 591 patients without T-LGL, one MDS patient with STAT3 mutation was revealed to have subclinical T-LGL. T-LGL combined with PRCA may be classified as unique subtype of T-LGL. High depth NGS can enable sensitive detection of concomitant MDS in T-LGL. Mutation of the TERT promoter may indicate good response to treatment of T-LGL, thus, its addition to an NGS panel may be recommended.
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