ArticleCancer genetics2015
Emergence of clonal hematopoiesis in the majority of patients with acquired aplastic anemia.
Article in Cancer genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 110 citations in OpenAlex.
- Evidence- and opinion-based consensus from Delphi round 1 of the Asian aplastic anemia recommendation development.International journal of hematology · 2026Article
- Favorable Response to Immunosuppressive Therapy in Severe Aplastic Anemia With Trisomy 8 and BCOR Mutation: Sustained Hematologic Response Despite Evolving Mutational Profile-A Case Report.Clinical case reports · 2026Article
- Reconceptualizing Aplastic Anemia-Seed, Worm, Soil.Journal of clinical laboratory analysis · 2026Review
- Somatic mutations in CSK disrupt immune regulation in a Chinese aplastic anemia cohort.Communications biology · 2026Article
- High-resolution single-cell mapping of clonal hematopoiesis and structural variation in aplastic anemia.Nature genetics · 2026Article
- Metabolite-induced DNA damage drives stochastic stem cell loss and clonal hematopoiesis.Cell stem cell · 2026Article
- Clonal hematopoiesis may precede the diagnosis of aplastic anemia by several years.Blood advances · 2026Article
- Predicting secondary myeloid neoplasms in acquired aplastic anemia using machine learning models.Blood neoplasia · 2025Article
- Somatic mutations and the efficacy of immunosuppressive therapy in severe/very severe aplastic anemia and transfusion-dependent nonsevere aplastic anemia.Annals of hematology · 2025Article
- Origins of T-cell-mediated autoimmunity in acquired aplastic anaemia.British journal of haematology · 2025Review
- Recurrent Missense Driver STAT5BAnti-cancer agents in medicinal chemistry · 2025Article
- Hypomethylating agents are associated with high rates of hematologic toxicity in patients with secondary myeloid neoplasms developing after acquired aplastic anemia.Haematologica · 2024Article
- Clinical implications of myeloid malignancy‑related somatic mutations in aplastic anemia.Clinical and experimental medicine · 2023Article
- Paroxysmal Nocturnal Hemoglobinuria: Biology and Treatment.Medicina (Kaunas, Lithuania) · 2023Review
- Epigenetic regulation by ASXL1 in myeloid malignancies.International journal of hematology · 2023Review
- Mesenchymal Stem Cells in Acquired Aplastic Anemia: The Spectrum from Basic to Clinical Utility.International journal of molecular sciences · 2023Review
- Clinical and Molecular Determinants of Clonal Evolution in Aplastic Anemia and Paroxysmal Nocturnal Hemoglobinuria.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023Article
- Pathogenicity and impact of HLA class I alleles in aplastic anemia patients of different ethnicities.JCI insight · 2022Article
- Uncovering novel mutational signatures byCell genomics · 2022Article
- A multicentre trial of intensive immunosuppressive therapy combined with umbilical cord blood for the treatment of severe aplastic anaemia.Annals of hematology · 2022Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 3 institutions in 1 country.
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Abstract
Acquired aplastic anemia (aAA) is a nonmalignant disease caused by autoimmune destruction of early hematopoietic cells. Clonal hematopoiesis is a late complication, seen in 20-25% of older patients. We hypothesized that clonal hematopoiesis in aAA is a more general phenomenon, which can arise early in disease, even in younger patients. To evaluate clonal hematopoiesis in aAA, we used comparative whole exome sequencing of paired bone marrow and skin samples in 22 patients. We found somatic mutations in 16 patients (72.7%) with a median disease duration of 1 year; of these, 12 (66.7%) were patients with pediatric-onset aAA. Fifty-eight mutations in 51 unique genes were found primarily in pathways of immunity and transcriptional regulation. Most frequently mutated was PIGA, with seven mutations. Only two mutations were in genes recurrently mutated in myelodysplastic syndrome. Two patients had oligoclonal loss of the HLA alleles, linking immune escape to clone emergence. Two patients had activating mutations in key signaling pathways (STAT5B (p.N642H) and CAMK2G (p.T306M)). Our results suggest that clonal hematopoiesis in aAA is common, with two mechanisms emerging-immune escape and increased proliferation. Our findings expand conceptual understanding of this nonneoplastic blood disorder. Future prospective studies of clonal hematopoiesis in aAA will be critical for understanding outcomes and for designing personalized treatment strategies.
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