Age-related mutations associated with clonal hematopoietic expansion and malignancies
Open accessAbstract
Several genetic alterations characteristic of leukemia and lymphoma have been detected in the blood of individuals without apparent hematological malignancies. The Cancer Genome Atlas (TCGA) provides a unique resource for comprehensive discovery of mutations and genes in blood that may contribute to the clonal expansion of hematopoietic stem/progenitor cells. Here, we analyzed blood-derived sequence data from 2,728 individuals from TCGA and discovered 77 blood-specific mutations in cancer-associated genes, the majority being associated with advanced age. Remarkably, 83% of these mutations were from 19 leukemia and/or lymphoma-associated genes, and nine were recurrently mutated (DNMT3A, TET2, JAK2, ASXL1, TP53, GNAS, PPM1D, BCORL1 and SF3B1). We identified 14 additional mutations in a very small fraction of blood cells, possibly representing the earliest stages of clonal expansion in hematopoietic stem cells. Comparison of these findings to mutations in hematological malignancies identified several recurrently mutated genes that may be disease initiators. Our analyses show that the blood cells of more than 2% of individuals (5-6% of people older than 70 years) contain mutations that may represent premalignant events that cause clonal hematopoietic expansion.
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Mutations in DNMT3A and TET2 account for over 90% of CH cases.
“Mutations in DNMT3A and TET2 account for over 90% of CH cases2,6”
From TET2-mutant myeloid cells mitigate Alzheimer’s disease progression via CNS infiltration and enhanced phagocytosis in mice (2025) · cites this paper as [6]
The Results section (page unavailable) reports DNMT3A mutations in 18 cases and TET2 mutations in 9 among 58 cases with blood-specific mutations. Even if those cases did not overlap, the two genes would account for at most 27 of 58 cases—not over 90%. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredAging hematopoietic stem cells progressively accumulate mutations and molecular alterations that can impair cellular function, give rise to preleukemic stem cells, and initiate age-associated myeloid malignancies.
“Aging hematopoietic stem cells progressively accumulate mutations and molecular alterations, which can impair cellular function, give rise to preleukemic stem cells, and initiate age-associated myeloid malignancies45, 46.”
From Minimal PU.1 reduction induces a preleukemic state and promotes development of acute myeloid leukemia (2015) · cites this paper as [46]
The Introduction (page unavailable) says HSPCs accumulate mutations with age and that some mutations promote clonal expansion and can cooperate with later mutations to cause hematopoietic malignancies. The Discussion (page unavailable) describes some mutations as likely initiating events. The paper does not establish that these alterations impair cellular function or directly demonstrate the formation of preleukemic stem cells; it says accumulated mutations generally do not affect function. (LLM, conf=0.86)
Experimental — accuracy not yet measuredClonal hematopoiesis is associated with increased risk of cardiovascular events and blood cancers.
“This state of abnormal HSC expansion without overt hematologic disease is known as clonal hematopoiesis (CH), and is associated with increased risk of cardiovascular events and blood cancers (3)(4)(5).”
From <i>Txnip</i> Enhances Fitness of <i>Dnmt3a</i> -Mutant Hematopoietic Stem Cells via <i>p21</i> (2022) · cites this paper as [5]
The Discussion reports clonal expansion with leukemia-associated mutations in people without reported hematologic malignancies and suggests that this may contribute to the development of blood cancers. It says progression could not be determined in these participants, and our copy provides no evidence about cardiovascular events. (LLM, conf=0.86)
Experimental — accuracy not yet measuredLoss-of-function heterozygous mutations in TET2 account for about 10% to 30% of mutations found in CHIP carriers.
“Loss-of-function heterozygous mutations in epigenetic regulators DNMT3A (cytosine methyltransferase) and TET2 (methylcytosine dioxygenase) are the most frequently detected mutations in CHIP, accounting for about 50% to 60% and 10% to 30% of mutations found in CHIP carriers, respectively.1, 2, 3,7,8”
From Aging drives <i>Tet2</i> <i>+/−</i> clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [3]
The Results (page unavailable) report TET2 mutations in 9 of 58 cases with blood-specific mutations, a proportion within the claimed 10%–30% range, and give examples of TET2 frameshift and nonsense mutations. However, the paper does not establish that all TET2 mutations counted were heterozygous loss-of-function mutations, so it does not support that more specific percentage claim. (LLM, conf=0.83)
Experimental — accuracy not yet measuredLoss-of-function heterozygous mutations in DNMT3A account for about 50% to 60% of mutations found in CHIP carriers.
“Loss-of-function heterozygous mutations in epigenetic regulators DNMT3A (cytosine methyltransferase) and TET2 (methylcytosine dioxygenase) are the most frequently detected mutations in CHIP, accounting for about 50% to 60% and 10% to 30% of mutations found in CHIP carriers, respectively.1, 2, 3,7,8”
From Aging drives <i>Tet2</i> <i>+/−</i> clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [3]
The Results section, “Variants contributing to hematopoietic clonal expansion” (page unavailable), identifies DNMT3A as a recurrently mutated gene, with mutations in 18 cases. But it reports 64 blood-specific mutations in hematological-malignancy-associated genes, making the DNMT3A share about 28%, not 50%–60%. The passages also do not establish that the DNMT3A mutations were heterozygous loss-of-function mutations. (LLM, conf=0.88)
Experimental — accuracy not yet measured
CHIP carriers have about a 13-fold increased risk of developing myeloid hematological malignancies.
“CHIP carriers have an about 13-fold increased risk of developing myeloid hematological malignancies and an increased risk of all-cause mortality, largely due to cardiovascular disease and stroke.1, 2, 3, 4”
From Aging drives <i>Tet2</i> <i>+/−</i> clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [3]
The Discussion (page not provided) says clonal hematopoietic changes may contribute to hematologic malignancies, but it does not report a 13-fold risk. It explicitly says the researchers could not determine whether participants with leukemia-associated mutations later developed a malignant hematologic disease. (LLM, conf=0.85)
Experimental — accuracy not yet measuredTET2 heterozygous loss-of-function mutations are predicted to have high expansion rates (10% increase in mean VAF per year).
“are predicted to have high expansion rates (10% increase in mean VAF per year1, 2, 3,7)”
From Aging drives <i>Tet2</i> <i>+/−</i> clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [3]
The Results (Variants contributing to hematopoietic clonal expansion; page unavailable) associate TET2 mutations with age, and the Discussion identifies TET2 among genes involved in clonal expansion. Neither passage predicts an expansion rate for heterozygous TET2 loss-of-function mutations or reports a 10% increase in mean VAF per year. (LLM, conf=0.87)
Experimental — accuracy not yet measuredCH-associated variants of Dnmt3a and Tet2 affect the HSPC methylome and have been shown to alter functions of monocyte-derived tissue macrophages and promote cardiovascular pathologies.
“CH-associated variants of the epigenetic writers and erasers Dnmt3a and Tet2, respectively, that affect the HSPC methylome have been shown to alter functions of monocyte-derived tissue M F and promote cardiovascular pathologies 31-34 .”
From Clonal hematopoiesis-associated motoric deficits caused by monocyte-derived microglia accumulating in aging mice (2025) · cites this paper as [32]
The Results (page unavailable) identify age-associated DNMT3A and TET2 mutations and suggest that they may initiate HSPC clonal expansion. Our copy does not show that these variants alter the HSPC methylome, change monocyte-derived tissue macrophage function, or promote cardiovascular pathology. (LLM, conf=0.88)
Experimental — accuracy not yet measuredCHIP carriers have increased risk of all-cause mortality, largely due to cardiovascular disease and stroke.
“CHIP carriers have an about 13-fold increased risk of developing myeloid hematological malignancies and an increased risk of all-cause mortality, largely due to cardiovascular disease and stroke.1, 2, 3, 4”
From Aging drives <i>Tet2</i> <i>+/−</i> clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [3]
The Results section on cancer types and sample characteristics notes that 22.1% of participants were deceased at sample procurement, but does not compare mortality in carriers and noncarriers. Searches for all-cause mortality, cardiovascular disease, stroke, and survival found no passage addressing the attributed risk or causes of death. (LLM, conf=0.76)
Experimental — accuracy not yet measuredClonal hematopoiesis is common in elderly people.
“clonal hematopoiesis is a frequent event in elderly people.”
From Aging of hematopoietic stem cells (2018) · cites this paper as [75]
The epigenetic genes most frequently affected in these conditions include DNMT3A, EZH2, TET2, and SETDB1.
“Epigenetic genes that are relatively frequently affected in these conditions include DNMT3A, EZH2, TET2, and SETDB1.”
From Aging of hematopoietic stem cells (2018) · cites this paper as [75]
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- Authors
- Xie, M., Lu, C., Wang, J., McLellan, M. D., Johnson, K. J., Wendl, M. C., McMichael, J. F., Schmidt, H. K., Yellapantula, V., Miller, C. A., Ozenberger, B. A., Welch, J. S., Link, D. C., Walter, M. J., Mardis, E. R., Dipersio, J. F., Chen, F., Wilson, R. K., Ley, T. J., & Ding, L.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Ding, Li
- ORCID
- Venue
- Nature Medicine
- Published
- 2014-10-19
- Volume
- 20
- Issue
- 12
- Pages
- 1472-1478
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4313872
- OpenAlex
- W1992826811
- Cited by
- 1,874
- References
- 44
- Citations by year
- 2026: 73 · 2025: 129 · 2024: 144 · 2023: 157 · 2022: 203 · 2021: 185 · 2020: 182 · 2019: 206 · 2018: 180 · 2017: 175 · 2016: 138 · 2015: 96 · 2014: 3 · 2012: 1
- FWCI
- 97.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Leukemia and Lymphoma Society
- National Heart, Lung, and Blood Institute (R00HL103975)
- National Human Genome Research Institute (U01HG006517, U54HG003079)
- National Cancer Institute (R01CA180006, P01CA101937)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Epidemiology › Multiple and Secondary Primary Cancers
- Keywords
- clonal hematopoiesis, hematopoietic stem and progenitor cells, DNMT3A, TET2, JAK2, ASXL1, TP53, GNAS, PPM1D, BCORL1, SF3B1, recurrent mutations
- MeSH terms
- Adult, Aged, Aged, 80 and over, Aging, Child, Female, Hematopoiesis, Hematopoietic Stem Cells, Humans, Male, Middle Aged, Mutation, Neoplasms, Young Adult
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