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Age-Related Clonal Hematopoiesis Associated with Adverse Outcomes
Open accessAbstract
BACKGROUND: The incidence of hematologic cancers increases with age. These cancers are associated with recurrent somatic mutations in specific genes. We hypothesized that such mutations would be detectable in the blood of some persons who are not known to have hematologic disorders. METHODS: We analyzed whole-exome sequencing data from DNA in the peripheral-blood cells of 17,182 persons who were unselected for hematologic phenotypes. We looked for somatic mutations by identifying previously characterized single-nucleotide variants and small insertions or deletions in 160 genes that are recurrently mutated in hematologic cancers. The presence of mutations was analyzed for an association with hematologic phenotypes, survival, and cardiovascular events. RESULTS: Detectable somatic mutations were rare in persons younger than 40 years of age but rose appreciably in frequency with age. Among persons 70 to 79 years of age, 80 to 89 years of age, and 90 to 108 years of age, these clonal mutations were observed in 9.5% (219 of 2300 persons), 11.7% (37 of 317), and 18.4% (19 of 103), respectively. The majority of the variants occurred in three genes: DNMT3A, TET2, and ASXL1. The presence of a somatic mutation was associated with an increase in the risk of hematologic cancer (hazard ratio, 11.1; 95% confidence interval [CI], 3.9 to 32.6), an increase in all-cause mortality (hazard ratio, 1.4; 95% CI, 1.1 to 1.8), and increases in the risks of incident coronary heart disease (hazard ratio, 2.0; 95% CI, 1.2 to 3.4) and ischemic stroke (hazard ratio, 2.6; 95% CI, 1.4 to 4.8). CONCLUSIONS: Age-related clonal hematopoiesis is a common condition that is associated with increases in the risk of hematologic cancer and in all-cause mortality, with the latter possibly due to an increased risk of cardiovascular disease. (Funded by the National Institutes of Health and others.).
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“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 [2]
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Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“CHIP has emerged as a clinically relevant state associated with increased all-cause mortality and a broad spectrum of non-malignant diseases, most prominently atherosclerotic cardiovascular disease and stroke [1,4,5].”
From Clonal Hematopoiesis of Indeterminate Potential as an Emerging Interdisciplinary Risk Factor in Alzheimer’s Disease: Current Evidence and Future Directions (2026) · cites this paper as [1]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [2]
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In the citing paper
“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 Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [2]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Furthermore, progression to hematological malignancies depends on the type and complexity of mutations in CHIP.2,5,6”
From Aging drives Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [2]
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“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 Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [2]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [2]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“More important, advanced age is the best predictor of CHIP, with a 5.6% or 18.4% prevalence in the sixth or ninth decade of life, respectively.2”
From Aging drives Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [2]
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In the citing paper
“are predicted to have high expansion rates (10% increase in mean VAF per year1, 2, 3,7)”
From Aging drives Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [2]
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“Clone size, which is approximated by the variant allele fraction (VAF), has previously been shown to be an important predictor of risk for blood cancer1,17 and cardiovascular outcomes8,9.”
From Clonal hematopoiesis is associated with protection from Alzheimer’s disease (2023) · cites this paper as [1]
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“Despite its hematologically silent nature, CH has been associated with increased mortality and morbidity [1,32].”
From Clonal hematopoiesis and inflammation – the perpetual cycle (2023) · cites this paper as [1]
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“although increased red cell distribution width (RDW) has been reported (Jaiswal et al., 2014).”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Jaiswal et al., 2014
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“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 Txnip Enhances Fitness of Dnmt3a -Mutant Hematopoietic Stem Cells via p21 (2022) · cites this paper as [3]
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“Instead, the discovery of widespread clonal expansions in ageing human tissues19,50–52 raises the possibility that some somatic mutations contribute to ageing by driving clonal expansions of functionally altered cells at a cost to the organism49,53,54.”
From Somatic mutation rates scale with lifespan across mammals (2022) · cites this paper as [50]
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“Methods adhered to published guidelines 77 .”
From Clonal hematopoiesis-associated motoric deficits caused by monocyte-derived microglia accumulating in aging mice (2025) · cites this paper as [77]
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“The isolated effects of individual inflammatory cytokines, including type 1 interferons (IFNa/b) 1-3 , type 2 IFN (IFNg) 4-6 , TNFa 7,8 , and IL-1 9-11 , have been well-documented in mouse hematopoietic development.”
From Type 1 interferon perturbates clonal competition by reshaping human blood development (2026) · cites this paper as [2]
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“Interestingly, while IFNa alters mouse HSC marker Sca-1 2 (rendering difficult the quantification of progenitor cell frequency changes by flow cytometric assessment in mice), IFNa did not alter CD90 expression after treatment in the HSPCs ( Fig. 2e, Supplementary Fig. 3c ).”
From Type 1 interferon perturbates clonal competition by reshaping human blood development (2026) · cites this paper as [2]
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In the citing paper
“Previously, induction of IFNa in mice have yielded mixed results demonstrating either an upregulation 2 or downregulation 53 of TNFa.”
From Type 1 interferon perturbates clonal competition by reshaping human blood development (2026) · cites this paper as [2]
Experimental — accuracy not yet measuredIn the citing paper
“clonal hematopoiesis is a frequent event in elderly people.”
From Aging of hematopoietic stem cells (2018) · cites this paper as [76]
In the citing paper
“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 [76]
In the citing paper
“The phenomenon also appears to be counterintuitively well tolerated, where HSCs containing oncogenic mutations can overtake most of the hematopoietic system without transforming into leukemia (Jaiswal et al., 2014).”
From Unraveling Hematopoiesis through the Lens of Genomics (2020) · cites this paper as Jaiswal et al., 2014
In the citing paper
“The size of these mutant clones was massive; in one study, a median of ~18% of blood cells carried the mutations 28.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“For example, CHIP has been reported to be more common in older men 28 and smokers 27 and less common in Hispanics 28, although these associations are all relatively modest.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“Indeed, in population-based cohorts that underwent exome sequencing, the presence of CHIP was associated with ~10-fold increased relative risk of these malignancies over several years of follow-up 27,28.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“CHIP itself does not denote a malignancy, nor is it associated with clinically significant alterations in blood counts 28,63.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“In an initial study, this risk could not be explained by cancer deaths but was instead related to increased cardiovascular mortality 28.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“In one study, 4% of CHIP carriers developed a blood cancer over the subsequent 8 years, corresponding to ~0.5% of CHIP cases converting to malignancy per year 28.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“Several studies have found that CHIP is associated with a 30–40% increased mortality risk 27,28,37.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“Myeloid malignancies were most common, although some people with CHIP did develop lymphoid cancers 27,28.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“Indeed, some individuals with clonal hematopoiesis have virtually all of their blood cells arising from a single mutated HSC 28.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“CHIP has been found to be associated with a 30% increase in the likelihood of having type 2 diabetes (T2D) 28.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“Studies of serial samples have shown that the trajectory of a clone can vary between people.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“Some people have clones that remain stagnant in size for many years, whereas other people have clones that show steady growth 28,33.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [28]
In the citing paper
“These findings are supported by recent findings demonstrating a causal link between mutations in HSPCs in the context of clonal hematopoiesis with indeterminate origin and altered transcriptional output of macrophages, which affect the vascular wall and contributes to atherosclerosis.83,84”
From Inflammatory bone marrow microenvironment (2019) · cites this paper as [84]
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Metadata
- Authors
- Jaiswal, S., Fontanillas, P., Flannick, J., Manning, A., Grauman, P. V., Mar, B. G., Lindsley, R. C., Mermel, C. H., Burtt, N., Chavez, A., Higgins, J. M., Moltchanov, V., Kuo, F. C., Kluk, M. J., Henderson, B., Kinnunen, L., Koistinen, H. A., Ladenvall, C., Getz, G., Correa, A., Banahan, B. F., Gabriel, S., Kathiresan, S., Stringham, H. M., McCarthy, M. I., Boehnke, M., Tuomilehto, J., Haiman, C., Groop, L., Atzmon, G., Wilson, J. G., Neuberg, D., Altshuler, D., & Ebert, B. L.
- Affiliations
- Brigham and Women's Hospital (US)
- Broad Institute (US)
- University of Helsinki (FI)
- University of Southern California (US)
- Helsinki University Hospital (FI)
- Lund University (SE)
- University of Mississippi Medical Center (US)
- University of Michigan (US)
- Centre for Human Genetics (GB)
- Universität für Weiterbildung Krems (AT)
- Albert Einstein College of Medicine (US)
- Harvard University (US)
- ORCID
- Jaiswal, Siddhartha
- Fontanillas, Pierre
- Flannick, Jason
- Manning, Alisa
- Mar, Brenton G.
- Lindsley, R. Coleman
- Mermel, Craig H.
- Chavez, Alejandro
- Higgins, John M.
- Kuo, Frank C.
- Kluk, Michael J.
- Kinnunen, Leena
- Koistinen, Heikki A.
- Ladenvall, Claes
- Getz, Gad
- Correa, Adolfo
- Banahan, Benjamin F.
- Gabriel, Stacey
- Kathiresan, Sekar
- Stringham, Heather M.
- McCarthy, Mark I.
- Boehnke, Michael
- Tuomilehto, Jaakko
- Groop, Leif
- Atzmon, Gil
- Wilson, James G.
- Neuberg, Donna
- Altshuler, David
- Ebert, Benjamin L.
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2014-12-25
- Volume
- 371
- Issue
- 26
- Pages
- 2488-2498
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC4306669
- OpenAlex
- W2149858388
- Cited by
- 4,841
- References
- 48
- Citations by year
- 2026: 423 · 2025: 446 · 2024: 494 · 2023: 521 · 2022: 536 · 2021: 520 · 2020: 454 · 2019: 387 · 2018: 356 · 2017: 301 · 2016: 237 · 2015: 151 · 2014: 6
- FWCI
- 164.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Lund University Publications (Lund University) (submittedVersion, other-oa)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- Funders
- Wellcome Trust (090367, 085475, 098381, 090532, 083948)
- National Institutes of Health (5rc2dk088389-02)
- National Institute on Aging (R01AG042188, P01AG021654, P30AG038072)
- National Heart, Lung, and Blood Institute (R01HL082945, T32HL066987)
- National Human Genome Research Institute (U54HG003067)
- National Cancer Institute (T32CA009216, T32CA009172, P01CA066996)
- National Institute of Diabetes and Digestive and Kidney Diseases (U01DK085526, U01DK085584, DP2DK098087, U01DK085501, U01DK085524, RC2-DK088389, U01DK085545, DK088389, P30DK020572)
- 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
- age-related clonal hematopoiesis, somatic mutations, all-cause mortality, coronary artery disease, ischemic stroke, cardiovascular disease, DNMT3A, TET2, ASXL1, peripheral blood, aging
- MeSH terms
- Adult, Age Factors, Aged, Aged, 80 and over, Blood, Cell Transformation, Neoplastic, Clone Cells, DNA Mutational Analysis, Hematopoiesis, Hematopoietic Stem Cells, Humans, Middle Aged, Mutation, Risk Factors, Hematologic Neoplasms, Young Adult, Exome
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