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DNMT3A and TET2 dominate clonal hematopoiesis and demonstrate benign phenotypes and different genetic predispositions
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had no impact on blood counts or indices. Mutational burden of both genes correlated with X-inactivation skewing but no significant association with age-adjusted telomere length reduction was documented. The discordance between the high prevalence of mutations in these 2 genes and their limited biological impact raise the question of the potential role of dysregulated epigenetic modifiers in normal aging hematopoiesis, which may include support to failing hematopoiesis.
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“Other studies have found links between CHIP and chronic obstructive pulmonary disease (COPD) 37,63.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [63]
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.
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“Various other systemic effects have been described in association with CH, including chronic obstructive pulmonary disease and other pulmonary disease [16,33,34]”
From Clonal hematopoiesis and inflammation – the perpetual cycle (2023) · cites this paper as [33]
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 [7]
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
“In the context of CHIP, TET2 mutations show highest clonal expansion rates over time (with an estimated 10% annual growth rate compared with 5% of DNMT3A mutations7,8,10).”
From Aging drives Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [7]
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 [7]
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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 [7]
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In the citing paper
“many have noted that DNMT3A mutations confer little phenotype on steady state hematopoiesis (Buscarlet et al., 2017)”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Buscarlet et al., 2017
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 [63]
In the citing paper
“However, CHIP was also strongly linked to smoking in these studies, so the result could be confounded by this association.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [63]
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Metadata
- Authors
- Buscarlet, M., Provost, S., Zada, Y. F., Barhdadi, A., Bourgoin, V., Lépine, G., Mollica, L., Szuber, N., Dubé, M.-P., & Busque, L.
- Affiliations
- Hôpital Maisonneuve-Rosemont (CA)
- Montreal Heart Institute (CA)
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2017-08-10
- Volume
- 130
- Issue
- 6
- Pages
- 753-762
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2728241634
- Cited by
- 383
- References
- 50
- Citations by year
- 2026: 22 · 2025: 34 · 2024: 37 · 2023: 47 · 2022: 59 · 2021: 55 · 2020: 46 · 2019: 40 · 2018: 34 · 2017: 6
- FWCI
- 26.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Concordia University
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- DNMT3A, TET2, clonal hematopoiesis, somatic mutations, X-inactivation skewing, telomere length, epigenetic regulators, genetic susceptibility, mutational burden
- MeSH terms
- DNA Methyltransferase 3A, Age Factors, Aged, Aged, 80 and over, Aging, Blood Cell Count, Clone Cells, DNA (Cytosine-5-)-Methyltransferases, DNA-Binding Proteins, Female, Hematopoiesis, Humans, Male, Middle Aged, Mutation, Proto-Oncogene Proteins, Cohort Studies, Hematologic Neoplasms, Genetic Predisposition to Disease, Dioxygenases, X Chromosome Inactivation, High-Throughput Nucleotide Sequencing, Telomere Homeostasis
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