Somatic Mutations and Clonal Hematopoiesis in Aplastic Anemia
Open accessAbstract
BACKGROUND: In patients with acquired aplastic anemia, destruction of hematopoietic cells by the immune system leads to pancytopenia. Patients have a response to immunosuppressive therapy, but myelodysplastic syndromes and acute myeloid leukemia develop in about 15% of the patients, usually many months to years after the diagnosis of aplastic anemia. METHODS: We performed next-generation sequencing and array-based karyotyping using 668 blood samples obtained from 439 patients with aplastic anemia. We analyzed serial samples obtained from 82 patients. RESULTS: Somatic mutations in myeloid cancer candidate genes were present in one third of the patients, in a limited number of genes and at low initial variant allele frequency. Clonal hematopoiesis was detected in 47% of the patients, most frequently as acquired mutations. The prevalence of the mutations increased with age, and mutations had an age-related signature. DNMT3A-mutated and ASXL1-mutated clones tended to increase in size over time; the size of BCOR- and BCORL1-mutated and PIGA-mutated clones decreased or remained stable. Mutations in PIGA and BCOR and BCORL1 correlated with a better response to immunosuppressive therapy and longer and a higher rate of overall and progression-free survival; mutations in a subgroup of genes that included DNMT3A and ASXL1 were associated with worse outcomes. However, clonal dynamics were highly variable and might not necessarily have predicted the response to therapy and long-term survival among individual patients. CONCLUSIONS: Clonal hematopoiesis was prevalent in aplastic anemia. Some mutations were related to clinical outcomes. A highly biased set of mutations is evidence of Darwinian selection in the failed bone marrow environment. The pattern of somatic clones in individual patients over time was variable and frequently unpredictable. (Funded by Grant-in-Aid for Scientific Research and others.).
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Immune signaling pathways contribute to DNMT3A-associated hematologic conditions including aplastic anemia, myeloproliferative neoplasms, myelodysplastic syndrome, and acute myelogenous leukemia.
“Immune signaling pathways are known to contribute to DNMT3A-associated hematologic conditions including aplastic anemia, myeloproliferative neoplasms, myelodysplastic syndrome, and acute myelogenous leukemia (Azrakhsh et al., 2019; Jacquelin et al., 2018; Yoshizato et al., 2015).”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Yoshizato et al., 2015
The Discussion (page unavailable) links DNMT3A-mutated clones in aplastic anemia to progression toward MDS/AML, and the paper describes aplastic anemia as immune-mediated. It does not establish that immune signaling pathways contribute to DNMT3A-associated disease across the listed conditions or address that mechanism in myeloproliferative neoplasms. The Discussion instead says it is unlikely that DNMT3A-mutated clones initiate a pathogenic immune response. (LLM, conf=0.86)
Experimental — accuracy not yet measuredClonal hematopoiesis is commonly found in aplastic anemia, a disorder caused by an autoimmune attack on bone marrow progenitor cells that results in severely depressed blood counts.
“Clonal hematopoiesis is also commonly found in aplastic anemia, a disorder caused by an autoimmune attack on bone marrow progenitor cells that results in severely depressed blood counts 59.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [59]
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“Clonal hematopoiesis is also commonly found in aplastic anemia, a disorder caused by an autoimmune attack on bone marrow progenitor cells that results in severely depressed blood counts (60).”
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- Authors
- Yoshizato, T., Dumitriu, B., Hosokawa, K., Makishima, H., Yoshida, K., Townsley, D., Sato-Otsubo, A., Sato, Y., Liu, D., Suzuki, H., Wu, C. O., Shiraishi, Y., Clemente, M. J., Kataoka, K., Shiozawa, Y., Okuno, Y., Chiba, K., Tanaka, H., Nagata, Y., Katagiri, T., Kon, A., Sanada, M., Scheinberg, P., Miyano, S., Maciejewski, J. P., Nakao, S., Young, N. S., & Ogawa, S.
- Affiliations
- Kanazawa University (JP)
- National Heart, Lung, and Blood Institute (US)
- Cleveland Clinic (US)
- Kyoto University (JP)
- Institute of Medical Science, The University of Tokyo (JP)
- Nagoya University (JP)
- ORCID
- Yoshizato, Tetsuichi
- Dumitriu, Bogdan
- Hosokawa, Kohei
- Makishima, Hideki
- Yoshida, Kenichi
- Sato, Yusuke
- Liu, Delong
- Suzuki, Hiromichi
- Wu, Colin O.
- Shiraishi, Yuichi
- Clemente, Michael J.
- Kataoka, Keisuke
- Okuno, Yusuke
- Chiba, Kenichi
- Tanaka, Hiroko
- Nagata, Yasunobu
- Katagiri, Takamasa
- Kon, Ayana
- Sanada, Masashi
- Scheinberg, Phillip
- Miyano, Satoru
- Maciejewski, Jaroslaw P.
- Nakao, Shinji
- Young, Neal S.
- Ogawa, Seishi
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2015-07-02
- Volume
- 373
- Issue
- 1
- Pages
- 35-47
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC7478337
- OpenAlex
- W783150221
- Cited by
- 646
- References
- 43
- Citations by year
- 2026: 49 · 2025: 48 · 2024: 44 · 2023: 51 · 2022: 55 · 2021: 61 · 2020: 60 · 2019: 70 · 2018: 79 · 2017: 68 · 2016: 51 · 2015: 9
- FWCI
- 54.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Kyoto University Research Information Repository (Kyoto University) (submittedVersion)
- Funders
- Aplastic Anemia and MDS International Foundation
- National Institutes of Health
- Japan Society for the Promotion of Science (26221308, 26253060, 23249052)
- National Heart, Lung, and Blood Institute (ZIAHL002315)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
- Health Sciences › Medicine › Emergency Medicine › Hematological disorders and diagnostics
- Keywords
- aplastic anemia, clonal hematopoiesis, somatic mutations, DNMT3A, ASXL1, BCOR, BCORL1, PIGA, immunosuppressive therapy response, progression-free survival, clonal dynamics, Darwinian selection, myelodysplastic syndrome, acute myeloid leukemia
- MeSH terms
- Age Factors, Aged, Anemia, Aplastic, Clone Cells, Female, Hematopoiesis, Humans, Karyotyping, Male, Middle Aged, Mutation, Myelodysplastic Syndromes, Risk Factors, Leukemia, Myeloid, Acute, Sequence Analysis, DNA, Polymorphism, Single Nucleotide
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