The DOI matches its Crossref record; 74 of the 74 references it cites were found in a registry or an index.
What To Tell Your Patient With Clonal Hematopoiesis And Why: Insights From Two Specialized Clinics
Abstract
Acquired genetic mutations in hematopoietic stem or progenitor cells can lead to clonal expansion and imbalanced blood cell production. Clonal hematopoiesis is exceptionally common with human aging, confers a risk of evolution to overt hematologic malignancy, and also increases all-cause mortality and the risk of cardiovascular disease. The degree of risk depends on the specific mutation, number of mutations, mutant allele burden, and concomitant non-genetic risk factors (e.g., hypertension or cigarette smoking). People with clonal hematopoiesis may come to clinical attention in a variety of ways, including during the evaluation of a possible hematologic malignancy, as an incidental discovery during molecular analysis of a non-hematological neoplasm, after hematopoietic cell transplant, or as a result of germline testing for inherited variants. Even though the risk of clonal progression or a cardiovascular event in an individual patient may be low, the possibility of future clinical consequences may contribute to uncertainty and worry, since it is not yet known how to modify these risks. This review summarizes clinical considerations for patients with clonal hematopoiesis, including important points for hematologists to consider discussing with affected persons - individuals who may understandably be anxious about having a mutation in their blood that predisposes them to develop malignancy, but which is statistically more likely to result in a myocardial infarction or stroke. The increasing frequency with which people with clonal hematopoiesis are discovered and the need for counseling these patients is driving many institutions to create specialized clinics; we describe our own experience with forming such clinics.
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“Indeed, among patients with cardiovascular disease who received the IL-1β neutralizing antibody canakinumab, those with TET2 mutant CH showed a greater reduction in incident major adverse cardiovascular events compared with those with non-TET2 mutant CH and those without any CH 190 .”
From Clonal haematopoiesis and dysregulation of the immune system (2023) · cites this paper as [190]
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Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
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Age-related clonal hematopoiesis associated with adverse outcomes
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Clonal hematopoiesis and blood-cancer risk inferred from blood DNA sequence
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Efficacy and safety of low-dose colchicine after myocardial infarction
Tardif, J.-C., Kouz, S., Waters, D. D., Bertrand, O. F., Diaz, R., Maggioni, A. P., Pinto, F. J., Ibrahim, R., Gamra, H., Kiwan, G. S., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1912388 · Cited by 3,159
Clonal hematopoiesis and risk of atherosclerotic cardiovascular disease
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Clonal hematopoiesis of indeterminate potential and its distinction from myelodysplastic syndromes
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Self-citationAge-related mutations associated with clonal hematopoietic expansion and malignancies
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., et al. (2014) · Nature Medicine · doi:10.1038/nm.3733 · Cited by 1,874
The origin and evolution of mutations in acute myeloid leukemia
Welch, J. S., Ley, T. J., Link, D. C., Miller, C. A., Larson, D. E., Koboldt, D. C., Wartman, L. D., Lamprecht, T. L., Liu, F., Xia, J., et al. (2012) · Cell · doi:10.1016/j.cell.2012.06.023 · Cited by 1,575
Clonal hematopoiesis associated with TET2 deficiency accelerates atherosclerosis development in mice
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MYD88 L265P Somatic Mutation in Waldenström's Macroglobulinemia
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Cited by
Causes and consequences of clonal hematopoiesis
Weeks, L. D., & Ebert, B. L. (2023) · Blood · doi:10.1182/blood.2023022222 · Cited by 169
Clonal haematopoiesis and dysregulation of the immune system
Belizaire, R., Wong, W. J., Robinette, M. L., & Ebert, B. L. (2023) · Nature Reviews Immunology · doi:10.1038/s41577-023-00843-3 · Cited by 161
Clonal Hematopoiesis: Mechanisms Driving Dominance of Stem Cell Clones
Challen, G., & Goodell, M. A. (2020) · Blood · doi:10.1182/blood.2020006510 · Cited by 131
Mayerhofer, E., Strecker, C., Becker, H., Georgakis, M. K., Uddin, M. M., Hoffmann, M. M., Nadarajah, N., Meggendorfer, M., Haferlach, T., Rosand, J., et al. (2023) · Stroke · doi:10.1161/strokeaha.122.041416 · Cited by 41
Metadata
- Authors
- Steensma, D. P., & Bolton, K. L.
- Affiliations
- Dana-Farber Cancer Institute, Boston, Massachusetts, United States
- Memorial Sloan Kettering Cancer Center, New York, New York, United States
- ORCID
- Steensma, David P.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2020-07-31
- ISSN
- 0006-4971
- 1528-0020
- Cited by
- 14
- References
- 74
- Language
- en
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