ArticleAnnals of hematology2025
Mutational heterogeneities in STAT3 and clonal hematopoiesis-related genes in acquired pure red cell aplasia.
Article in Annals of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
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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.
The trial behind it
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
3 citing papers in PubMed.
- 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
- Comprehensive analysis of the clinical feature, myeloid neoplasm-related gene mutation profiles and T cell diversity acquired pure red cell aplasia.Annals of hematology · 2025Article
- Clinical features and influencing factors analysis of T-cell large granular lymphocytic leukemia complicated with pure red cell aplasia.Frontiers in immunology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors.
Funding
Abstract
Dysregulation of T cell-mediated immunity is considered a major pathophysiological mechanism in acquired pure red cell aplasia (PRCA), including idiopathic PRCA, large granular lymphocytic leukemia-associated PRCA, and thymoma-associated PRCA. Although STAT3 mutations are frequently detected in PRCA patients, the roles of other mutational profiles and their impact on clinical characteristics remain unclear. In this study, whole-exome sequencing and targeted sequencing using a custom-designed panel were performed on 53 PRCA patients. The most frequently mutated genes were STAT3 (36%), PCLO (9%), TET2 (9%), NEB (6%), DNMT3A (6%), and POT1 (6%). Based on genetic profiles, patients were classified into three groups: those with STAT3 variants (group S), those without STAT3 variants but with variants in clonal hematopoiesis (CH)-related genes (group C), and those without variants in either STAT3 or CH-related genes (group O). Patients in group O had a higher median age compared to group S, while group S exhibited milder anemia severity than group C. Additionally, POT1 variants were associated with the idiopathic subtype of PRCA in females, often co-occurring with STAT3 variants. Variants in CH-related genes and other genes, including STAT3 and POT1, may play crucial roles in the pathophysiology of PRCA.
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