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Artículos de revistas sobre el tema "Clonal hematopoiesis of indeterminate potential"

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Publicado: 25 de enero de 2025
Última modificación: 31 de julio de 2025

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1

Papa, Veronica, Luisa Marracino, Francesca Fortini, et al. "Translating Evidence from Clonal Hematopoiesis to Cardiovascular Disease: A Systematic Review." Journal of Clinical Medicine 9, no. 8 (2020): 2480. http://dx.doi.org/10.3390/jcm9082480.

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Some random mutations can confer a selective advantage to a hematopoietic stem cell. As a result, mutated hematopoietic stem cells can give rise to a significant proportion of mutated clones of blood cells. This event is known as “clonal hematopoiesis.” Clonal hematopoiesis is closely associated with age, and carriers show an increased risk of developing blood cancers. Clonal hematopoiesis of indeterminate potential is defined by the presence of clones carrying a mutation associated with a blood neoplasm without obvious hematological malignancies. Unexpectedly, in recent years, it has emerged
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2

Steensma, David P. "Clinical consequences of clonal hematopoiesis of indeterminate potential." Blood Advances 2, no. 22 (2018): 3404–10. http://dx.doi.org/10.1182/bloodadvances.2018020222.

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Abstract Clonally restricted hematopoiesis is a common aging-associated biological state that predisposes to subsequent development of a hematological malignancy or cardiovascular death. Clonal expansion driven by leukemia-associated somatic mutations, such as DNMT3A, ASXL1, or TET2, is best characterized, but oligoclonality can also emerge without recognized leukemia-driver mutations, perhaps as a result of stochastic neutral drift. Murine models provide compelling evidence that a major mechanism of increased cardiovascular mortality in the context of clonal hematopoiesis is accelerated ather
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3

Steensma, David P. "Clinical consequences of clonal hematopoiesis of indeterminate potential." Hematology 2018, no. 1 (2018): 264–69. http://dx.doi.org/10.1182/asheducation-2018.1.264.

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Abstract Clonally restricted hematopoiesis is a common aging-associated biological state that predisposes to subsequent development of a hematological malignancy or cardiovascular death. Clonal expansion driven by leukemia-associated somatic mutations, such as DNMT3A, ASXL1, or TET2, is best characterized, but oligoclonality can also emerge without recognized leukemia-driver mutations, perhaps as a result of stochastic neutral drift. Murine models provide compelling evidence that a major mechanism of increased cardiovascular mortality in the context of clonal hematopoiesis is accelerated ather
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4

Boettcher, Steffen, and Benjamin L. Ebert. "Clonal Hematopoiesis of Indeterminate Potential." Journal of Clinical Oncology 37, no. 5 (2019): 419–22. http://dx.doi.org/10.1200/jco.2018.79.3588.

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5

Steensma, David P., Rafael Bejar, Siddhartha Jaiswal, et al. "Clonal hematopoiesis of indeterminate potential and its distinction from myelodysplastic syndromes." Blood 126, no. 1 (2015): 9–16. http://dx.doi.org/10.1182/blood-2015-03-631747.

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Abstract Recent genetic analyses of large populations have revealed that somatic mutations in hematopoietic cells leading to clonal expansion are commonly acquired during human aging. Clonally restricted hematopoiesis is associated with an increased risk of subsequent diagnosis of myeloid or lymphoid neoplasia and increased all-cause mortality. Although myelodysplastic syndromes (MDS) are defined by cytopenias, dysplastic morphology of blood and marrow cells, and clonal hematopoiesis, most individuals who acquire clonal hematopoiesis during aging will never develop MDS. Therefore, acquisition
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6

Ramdohr, Florian, Astrid Monecke, Madlen Jentzsch, et al. "Extramedullary Clonal Hematopoiesis with Indeterminate Potential." Clinical Lymphoma Myeloma and Leukemia 21, no. 9 (2021): e696-e698. http://dx.doi.org/10.1016/j.clml.2021.04.008.

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7

Libby, Peter, and Benjamin L. Ebert. "CHIP (Clonal Hematopoiesis of Indeterminate Potential)." Circulation 138, no. 7 (2018): 666–68. http://dx.doi.org/10.1161/circulationaha.118.034392.

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8

Testa, Ugo, Germana Castelli, and Elvira Pelosi. "CLONAL HEMATOPOIESIS: ROLE IN HEMATOLOGIC NON-HEMATOLOGIC." Mediterranean Journal of Hematology and Infectious Diseases 14, no. 1 (2022): e2022069. http://dx.doi.org/10.4084/mjhid.2022.069.

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Hematopoietic stem cells (HSCs) ensure the coordinated and balanced production of all hematopoietic cell types throughout life. Aging is associated with a gradual decline of the self-renewal and regenerative potential of HSCs and with the development of clonal hematopoiesis. Clonal hematopoiesis of indeterminate potential (CHIP) is a term defining the clonal expansion of genetically variant hematopoietic cells bearing one or more gene mutations and/or structural variants (such as copy number alterations). CHIP increases exponentially with age and is associated with cancers, including hematolog
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9

Nardi, Valentina, Frank C. Kuo, and Robert P. Hasserjian. "Premalignant Clonal Hematopoietic Proliferations." American Journal of Clinical Pathology 152, no. 3 (2019): 347–58. http://dx.doi.org/10.1093/ajcp/aqz079.

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AbstractObjectivesThe 2017 Workshop of the Society for Hematopathology/European Association for Hematopathology aimed to review premalignant clonal hematopoietic proliferations.MethodsThe workshop panel reviewed 27 cases of clonal proliferations of indeterminate significance or potential (18 myeloid, nine lymphoid) and rendered consensus diagnoses.ResultsImmunophenotyping and genetic studies on peripheral blood, bone marrow, and lymph node samples have led to the incidental detection of small clonal populations in asymptomatic individuals. These premalignant clonal myeloid and lymphoid prolife
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10

Sleptsov, A. A., M. S. Nazarenko, and V. Р. Puzyrev. "Common in atherogenesis and carcinogenesis: clonal hematopoiesis." Russian Journal of Cardiology 28, no. 10 (2023): 5511. http://dx.doi.org/10.15829/1560-4071-2023-5511.

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Clonal hematopoiesis is a common age-dependent state accompanied by the expansion of mutant hematopoietic stem cells as a result of somatic mutations and is associated with a high risk of hematopoietic neoplasms and cardiovascular diseases. Clonal hematopoiesis in human ontogenesis occurs asymptomatically, and the fraction of mutant clones can exceed more than 2% of the total pool of circulating nucleated blood cells by age 70. Due to the variability of the accumulation rate of mutant clones, signs of clonal hematopoiesis can be observed at a younger age. Clonal hematopoiesis may act as a beni
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11

Chen, Sisi, and Yan Liu. "p53 involvement in clonal hematopoiesis of indeterminate potential." Current Opinion in Hematology 26, no. 4 (2019): 235–40. http://dx.doi.org/10.1097/moh.0000000000000509.

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12

Lyasnikova, E. A., L. Yu Ivanchenko, S. N. Kozlova, M. Yu SITNIKOVA, A. A. Kostareva, and E. V. Shlyakhto. "Clonal hematopoiesis of indeterminate potential and heart failure." Russian Journal of Cardiology 29, no. 11S (2024): 6016. https://doi.org/10.15829/1560-4071-2024-6016.

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Modern studies demonstrate that clonal hematopoiesis of indeterminate potential (CHIP) is a risk factor for the development and prognosis of heart failure (HF) of various origin. The pathophysiology and consequences of CHIP are gene-specific. The mechanisms involved in this process are complex and indicate the central role of systemic and myocardial inflammation, including the immune response dependent on the inflammasome/interleukin-1β/interleukin-6 cascade. CHIP and associated inflammatory pathways represent a powerful potential target, which rationales the research in the area of various HF
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13

Aviv, Abraham, and Daniel Levy. "Hemothelium, Clonal Hematopoiesis of Indeterminate Potential, and Atherosclerosis." Circulation 139, no. 1 (2019): 7–9. http://dx.doi.org/10.1161/circulationaha.118.038434.

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14

Niño, Katia E., and Eric M. Pietras. "TNF Receptors Choose HSC Fate in Supporting Dnmt3a-Mutant Clonal Hematopoiesis." Cancer Discovery 12, no. 12 (2022): 2724–26. http://dx.doi.org/10.1158/2159-8290.cd-22-1022.

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Summary: TNFα receptor signaling distinctly promotes self-renewal and lymphoid differentiation in Dnmt3a-mutant hematopoietic stem cells, contributing to clonal hematopoiesis of indeterminate potential. See related article by SanMiguel et al., p. 2763 (3).
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15

Ganuza, Miguel, Trent Hall, David Finkelstein, et al. "The global clonal complexity of the murine blood system declines throughout life and after serial transplantation." Blood 133, no. 18 (2019): 1927–42. http://dx.doi.org/10.1182/blood-2018-09-873059.

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Abstract Although many recent studies describe the emergence and prevalence of “clonal hematopoiesis of indeterminate potential” in aged human populations, a systematic analysis of the numbers of clones supporting steady-state hematopoiesis throughout mammalian life is lacking. Previous efforts relied on transplantation of “barcoded” hematopoietic stem cells (HSCs) to track the contribution of HSC clones to reconstituted blood. However, ex vivo manipulation and transplantation alter HSC function and thus may not reflect the biology of steady-state hematopoiesis. Using a noninvasive in vivo col
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16

Bou Zerdan, Maroun, Lewis Nasr, Ludovic Saba, et al. "A Synopsis Clonal Hematopoiesis of Indeterminate Potential in Hematology." Cancers 14, no. 15 (2022): 3663. http://dx.doi.org/10.3390/cancers14153663.

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Clonal hematopoiesis of indeterminate potential can be defined as genetic mutations that correlate in hematologic neoplasia such as myelodysplastic syndrome. Patients with cytopenia increasingly undergo molecular genetic tests of peripheral blood or bone marrow for diagnostic purposes. Recently, a new entity has been demarcated to lessen the risk of incorrect diagnoses of hematologic malignancies. This new entity is a potential precursor of myeloid diseases, analogous to monoclonal gammopathy of undetermined significance as a potential precursor of multiple myeloma.
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17

Büttner, P., J. Böttner, K. Krohn, et al. "Clonal hematopoiesis of indeterminate potential in peripheral artery disease." Atherosclerosis 355 (August 2022): 2. http://dx.doi.org/10.1016/j.atherosclerosis.2022.06.093.

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18

Brogan, James, Ashwin Kishtagari, Robert W. Corty, et al. "Incidence of Cytopenia in Clonal Hematopoiesis of Indeterminate Potential." Blood 144, Supplement 1 (2024): 5637. https://doi.org/10.1182/blood-2024-205713.

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Background: Clonal hematopoiesis of indeterminate potential (CHIP) is a risk factor for myeloid neoplasms (MN) and multiple other diseases of aging. CHIP with concurrent cytopenia is a five-fold stronger risk factor for these diseases. However, the incidence of cytopenia in individuals with CHIP is not well-described. We quantify the incidence of cytopenia among 9,278 individuals with CHIP across three cohorts and identify risk factors for cytopenia among these individuals. Methods: Participants with genome sequencing from the All of Us Research Program (AoU) and Vanderbilt BioVU biorepository
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19

Lee, Man K. S., Dragana Dragoljevic, Camilla Bertuzzo Veiga, Nan Wang, Laurent Yvan-Charvet, and Andrew J. Murphy. "Interplay between Clonal Hematopoiesis of Indeterminate Potential and Metabolism." Trends in Endocrinology & Metabolism 31, no. 7 (2020): 525–35. http://dx.doi.org/10.1016/j.tem.2020.02.005.

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20

Khetarpal, Sumeet A., Arman Qamar, Alexander G. Bick, et al. "Clonal Hematopoiesis of Indeterminate Potential Reshapes Age-Related CVD." Journal of the American College of Cardiology 74, no. 4 (2019): 578–86. http://dx.doi.org/10.1016/j.jacc.2019.05.045.

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21

Chen, Jianchun, Caitlyn Vlasschaert, Cassianne Robinson-Cohen, Bryan R. Kestenbaum, Ming-Zhi Zhang, and Raymond C. Harris. "Clonal Hematopoiesis of Indeterminate Potential Associates with Severe AKI." Journal of the American Society of Nephrology 34, no. 11S (2023): 772–73. http://dx.doi.org/10.1681/asn.20233411s1772d.

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22

Vlasschaert, Caitlyn, Bryan R. Kestenbaum, Samuel A. Silver, et al. "Clonal Hematopoiesis of Indeterminate Potential Is Associated with AKI." Journal of the American Society of Nephrology 34, no. 11S (2023): 432. http://dx.doi.org/10.1681/asn.20233411s1432a.

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23

Schenck, Ryan O., Niels A. Jakobsen, Virginia Turati, et al. "Abstract 634: Mutation agnostic diagnosis of clonal hematopoiesis of indeterminate potential using fluctuating methylation clocks." Cancer Research 82, no. 12_Supplement (2022): 634. http://dx.doi.org/10.1158/1538-7445.am2022-634.

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Abstract Clonal hematopoiesis (CH), such as clonal hematopoiesis of indeterminant potential (CHIP), is diagnosed based on somatic genomic alterations in the absence of hematologic malignancy. At present, CHIP is diagnosed using peripheral blood where putative driver point mutations and small insertions/deletions whose variant allele frequency is greater or equal to two percent. Generally, the prevalence of CH increases as an individual ages and conveys a risk for progression to a malignancy. Previously, we developed a method using fluctuating CpG (fCpG) sites to serve as a fluctuating methylat
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24

Olkhovskiy, I. A., J. G. Garber, A. S. Gorbenko, et al. "JAK2V617F-positive clonal hematopoiesis of indeterminate potential in pregnant women." Obstetrics, Gynecology and Reproduction 13, no. 3 (2019): 204–10. http://dx.doi.org/10.17749/2313-7347.2019.13.3.204-210.

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Aim: to assess the prevalence of V617F somatic mutation of the JAK2 gene in pregnant women.Materials and methods. This non-interventional study was performed in the framework of routine clinical practice and included 1532 samples of venous blood from pregnant women who applied for medical assistance at Krasnoyarsk Regional Clinical Center for Maternal and Child Welfare. We used blood samples left after all routine laboratory tests had been done. These leftovers were pooled in the way that ensured an equal ratio of nucleated cells. Each pool contained 7 separate blood samples. The unused sample
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25

Takahashi, Koichi, Feng Wang, Hagop Kantarjian, et al. "Copy number alterations detected as clonal hematopoiesis of indeterminate potential." Blood Advances 1, no. 15 (2017): 1031–36. http://dx.doi.org/10.1182/bloodadvances.2017007922.

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26

Saygin, Caner, and Lucy A. Godley. "Genetics of Myelodysplastic Syndromes." Cancers 13, no. 14 (2021): 3380. http://dx.doi.org/10.3390/cancers13143380.

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Myelodysplastic syndrome (MDS) describes a heterogeneous group of bone marrow diseases, now understood to reflect numerous germline and somatic drivers, characterized by recurrent cytogenetic abnormalities and gene mutations. Precursor conditions including clonal hematopoiesis of indeterminate potential and clonal cytopenia of undetermined significance confer risk for MDS as well as other hematopoietic malignancies and cardiovascular complications. The future is likely to bring an understanding of those individuals who are at the highest risk of progression to MDS and preventive strategies to
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27

Veiga, Camilla Bertuzzo, Erin M. Lawrence, Andrew J. Murphy, Marco J. Herold, and Dragana Dragoljevic. "Myelodysplasia Syndrome, Clonal Hematopoiesis and Cardiovascular Disease." Cancers 13, no. 8 (2021): 1968. http://dx.doi.org/10.3390/cancers13081968.

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The development of myelodysplasia syndromes (MDS) is multiphasic and can be driven by a plethora of genetic mutations and/or abnormalities. MDS is characterized by a hematopoietic differentiation block, evidenced by increased immature hematopoietic cells, termed blast cells and decreased mature circulating leukocytes in at least one lineage (i.e., cytopenia). Clonal hematopoiesis of indeterminate potential (CHIP) is a recently described phenomenon preceding MDS development that is driven by somatic mutations in hemopoietic stem cells (HSCs). These mutant HSCs have a competitive advantage over
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28

Gaulin, Charles, Katalin Kelemen, and Cecilia Arana Yi. "Molecular Pathways in Clonal Hematopoiesis: From the Acquisition of Somatic Mutations to Transformation into Hematologic Neoplasm." Life 12, no. 8 (2022): 1135. http://dx.doi.org/10.3390/life12081135.

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Hematopoietic stem cell aging, through the acquisition of somatic mutations, gives rise to clonal hematopoiesis (CH). While a high prevalence of CH has been described in otherwise healthy older adults, CH confers an increased risk of both hematologic and non-hematologic diseases. Classification of CH into clonal hematopoiesis of indeterminate potential (CHIP) and clonal cytopenia of undetermined significance (CCUS) further describes this neoplastic myeloid precursor state and stratifies individuals at risk of developing clinically significant complications. The sequential acquisition of driver
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29

Hoermann, Gregor, Georg Greiner, Andrea Griesmacher, and Peter Valent. "Clonal Hematopoiesis of Indeterminate Potential: A Multidisciplinary Challenge in Personalized Hematology." Journal of Personalized Medicine 10, no. 3 (2020): 94. http://dx.doi.org/10.3390/jpm10030094.

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Clonal hematopoiesis of indeterminate potential (CHIP) is a common age-related condition that represents a potential pre-phase of hematologic neoplasm. Next-generation sequencing (NGS) is used to detect and monitor clonal hematopoiesis, and the spectrum of mutations substantially overlaps with that of myeloid neoplasms with DNMT3A, TET2, ASXL1, and JAK2 being the most frequently mutated. While, in general, the risk of progression to an overt myeloid neoplasm is only modest, the progression risk increases in patients with unexplained cytopenia or multiple mutations. In addition, CHIP represents
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30

Sorscher, Steven. "Letter to the Editor: Significance of Clonal Hematopoiesis of Indeterminate Potential." Journal of the National Comprehensive Cancer Network 16, no. 9 (2018): 1032–33. http://dx.doi.org/10.6004/jnccn.2018.7075.

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31

Dufossée, Mélody, Séverine Marti, Sami Fawaz, et al. "Clonal hematopoiesis of indeterminate potential: A cardiovascular risk factor among others." Archives of Cardiovascular Diseases Supplements 14, no. 2 (2022): 147. http://dx.doi.org/10.1016/j.acvdsp.2022.04.008.

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32

Sebastian, Kimberley N., Hatice Gülçin Özer, Cory Howard, et al. "Abstract 1620: Clonal hematopoiesis of indeterminate potential in the companion dog." Cancer Research 82, no. 12_Supplement (2022): 1620. http://dx.doi.org/10.1158/1538-7445.am2022-1620.

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Abstract Background: Clonal hematopoiesis of indeterminate potential (CHIP) is a clinical entity of aging humans that is characterized by cancer-associated mutations in white blood cells, without evidence of overt neoplasia. CHIP has been associated with an increased risk of hematologic cancers, cardiovascular disease, and all-cause mortality. We hypothesized that somatic mutations in specific genes associated with human CHIP would be detectable in the blood of aged dogs not known to have hematologic disorders. Methods: DNA from paired germline and whole blood samples from 93 geriatric canine
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33

Sella, Tal, Geoffrey Fell, Peter Grant Miller, et al. "Testing for clonal hematopoiesis of indeterminate potential in breast cancer survivors." Journal of Clinical Oncology 39, no. 15_suppl (2021): e24108-e24108. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e24108.

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e24108 Background: Clonal hematopoiesis of Indeterminate Potential (CHIP) is associated with adverse clinical outcomes including increased risk of hematologic malignancies and heart disease. Limited data suggest an increased prevalence of CHIP in patients treated for solid tumors, particularly after exposure to radiation and chemotherapy. CHIP testing may inform risk-reduction strategies for cancer survivors. Little is known about patient knowledge, attitudes, and preferences regarding CHIP testing. Methods: We surveyed survivors without history of recurrence participating in an ongoing prospe
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34

Huang, Yi-Chun, and Chao-Yung Wang. "Telomere Attrition and Clonal Hematopoiesis of Indeterminate Potential in Cardiovascular Disease." International Journal of Molecular Sciences 22, no. 18 (2021): 9867. http://dx.doi.org/10.3390/ijms22189867.

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Clinical evidence suggests that conventional cardiovascular disease (CVD) risk factors cannot explain all CVD incidences. Recent studies have shown that telomere attrition, clonal hematopoiesis of indeterminate potential (CHIP), and atherosclerosis (telomere–CHIP–atherosclerosis, TCA) evolve to play a crucial role in CVD. Telomere dynamics and telomerase have an important relationship with age-related CVD. Telomere attrition is associated with CHIP. CHIP is commonly observed in elderly patients. It is characterized by an increase in blood cell clones with somatic mutations, resulting in an inc
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35

Patel, Jay L. "The Clinical and Laboratory Features of Clonal Hematopoiesis of Indeterminate Potential." Advances in Molecular Pathology 1, no. 1 (2018): 37–42. http://dx.doi.org/10.1016/j.yamp.2018.06.005.

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36

Durrani, Jibran, Hassan Awada, Ashwin Kishtagari, et al. "Large Granular Lymphocytic Leukemia Coexists with Clonal Hematopoiesis of Indeterminate Potential." Blood 134, Supplement_1 (2019): 3743. http://dx.doi.org/10.1182/blood-2019-129330.

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Large granular lymphocytic leukemia (LGL) is a lymphoproliferative cytotoxic T cell (CTL) that typically presents in elderly population. The spectrum of the disease ranges from semi-reactive oligoclonal to clonal CTL expansion, and from silent to a chronic leukemia with para-neoplastic manifestation. However the description of the disease still preceded the new genetic landscape mapping techniques. In lieu of this, we analyzed the genetic landscape of LGL using a set of 33 genes. Interestingly, not only did the deeper analysis help with a better understanding of the complex CTL proliferative p
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37

Conces, Madison, Ying Ni, Peter Bazeley, Bhumika Patel, Pauline Funchain, and Hetty E. Carraway. "Clonal hematopoiesis of indeterminate potential (CHIP) mutations in solid tumor malignancies." Journal of Clinical Oncology 37, no. 15_suppl (2019): 1507. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.1507.

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1507 Background: CHIP predisposes to a higher risk of developing hematological malignancies and cardiac events. Multiple germline mutations have been recognized as contributing to CHIP, most notably ASXL1, DNMT3A, and TET2. The frequency of CHIP mutations in solid tumor malignancies (STM) is unknown. We report the frequency and incidence of CHIP mutations in adult patients (pts) with STM. Methods: Data from 880 pts with STM who underwent next generation sequencing (NGS) at Foundation One from 2013-2017 was collected. This excluded two pts with known primary hematological malignancies who were
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38

Soyfer, Eli M., and Angela G. Fleischman. "Inflammation in Myeloid Malignancies: From Bench to Bedside." Journal of Immunotherapy and Precision Oncology 4, no. 3 (2021): 160–67. http://dx.doi.org/10.36401/jipo-21-3.

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ABSTRACT Myeloid malignancies, stemming from a somatically mutated hematopoietic clone, can cause a wide variety of clinical consequences, including pancytopenia in myelodysplastic syndrome, overproduction of three myeloid lineages in myeloproliferative neoplasm, and the rapid growth of immature hematopoietic cells in acute myeloid leukemia (AML). It is becoming clear that inflammation is a hallmark feature of clonal myeloid conditions, ranging from clonal hematopoiesis of indeterminate potential to AML. Fundamental findings from laboratory research on inflammation in myeloid malignancies has
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39

Malcovati, Luca, and Mario Cazzola. "The shadowlands of MDS: idiopathic cytopenias of undetermined significance (ICUS) and clonal hematopoiesis of indeterminate potential (CHIP)." Hematology 2015, no. 1 (2015): 299–307. http://dx.doi.org/10.1182/asheducation-2015.1.299.

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AbstractThe WHO classification provides the best diagnostic approach to myelodysplastic syndromes (MDS). However, biologic and analytic limitations have emerged in the criteria currently adopted to establish the diagnosis and to classify MDS. The provisional category of idiopathic cytopenia of undetermined significance (ICUS) has been proposed to describe patients in whom MDS is possible but not proven. To formulate a diagnosis of ICUS, a thorough diagnostic work-up is required and repeated tests should be performed to reach a conclusive diagnosis. Recent studies provided consistent evidence o
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40

Lin, Amy E., Philipp J. Rauch, Siddhartha Jaiswal, and Benjamin L. Ebert. "Clonal Hematopoiesis: Confluence of Malignant and Nonmalignant Diseases." Annual Review of Cancer Biology 6, no. 1 (2022): 187–200. http://dx.doi.org/10.1146/annurev-cancerbio-060121-120026.

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Clonal hematopoiesis of indeterminate potential (CHIP) is a state in which somatic mutations in hematopoietic stem cells lead to clonal expansion of blood cells in individuals without hematologic malignancy. The mutated genes, including TET2, DNMT3A, ASXL1, TP53, JAK2, and SF3B1, are also recurrently mutated in myeloid malignancies. Individuals with CHIP have an increased risk of developing a hematologic cancer. Moreover, individuals with CHIP have an elevated risk of all-cause mortality that is significantly attributable to cardiovascular disease, independent of traditional risk factors. The
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41

Busque, Lambert, Maxine Sun, Manuel Buscarlet, et al. "High-sensitivity C-reactive protein is associated with clonal hematopoiesis of indeterminate potential." Blood Advances 4, no. 11 (2020): 2430–38. http://dx.doi.org/10.1182/bloodadvances.2019000770.

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Abstract Clonal hematopoiesis of indeterminate potential (CHIP) is predictive of hematological cancers and cardiovascular diseases, but the etiology of CHIP initiation and clonal expansion is unknown. Several lines of evidence suggest that proinflammatory cytokines may favor mutated hematopoietic stem cell expansion. To investigate the potential link between inflammation and CHIP, we performed targeted deep sequencing of 11 genes previously implicated in CHIP in 1887 subjects aged >70 years from the Montreal Heart Institute Biobank, of which 1359 had prior coronary artery disease (CAD),
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Zhang, Qi, Rita Yim, Paul Lee, Lynn Chin, Vivian Li, and Harinder Gill. "Implications of Clonal Hematopoiesis in Hematological and Non-Hematological Disorders." Cancers 16, no. 23 (2024): 4118. https://doi.org/10.3390/cancers16234118.

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Clonal hematopoiesis (CH) is associated with an increased risk of developing myeloid neoplasms (MNs) such as myelodysplastic neoplasm (MDS) and acute myeloid leukemia (AML). In general, CH comprises clonal hematopoiesis of indeterminate potential (CHIP) and clonal cytopenia of undetermined significance (CCUS). It is an age-related phenomenon characterized by the presence of somatic mutations in hematopoietic stem cells (HSCs) and hematopoietic stem and progenitor cells (HSPCs) that acquire a fitness advantage under selection pressure. Individuals with CHIP have an absolute risk of 0.5–1.0% per
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43

Chavakis, Triantafyllos, Ben Wielockx, and George Hajishengallis. "Inflammatory Modulation of Hematopoiesis: Linking Trained Immunity and Clonal Hematopoiesis with Chronic Disorders." Annual Review of Physiology 84, no. 1 (2022): 183–207. http://dx.doi.org/10.1146/annurev-physiol-052521-013627.

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Inflammation-adapted hematopoietic stem and progenitor cells (HSPCs) have long been appreciated as key drivers of emergency myelopoiesis, thereby enabling the bone marrow to meet the elevated demand for myeloid cell generation under various stress conditions, such as systemic infection, inflammation, or myelosuppressive insults. In recent years, HSPC adaptations were associated with potential involvement in the induction of long-lived trained immunity and the emergence of clonal hematopoiesis of indeterminate potential (CHIP). Whereas trained immunity has context-dependent effects, protective
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44

Babushok, Daria V. "A brief, but comprehensive, guide to clonal evolution in aplastic anemia." Hematology 2018, no. 1 (2018): 457–66. http://dx.doi.org/10.1182/asheducation-2018.1.457.

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Abstract Acquired aplastic anemia (AA) is an immune-mediated bone marrow aplasia that is strongly associated with clonal hematopoiesis upon marrow recovery. More than 70% of AA patients develop somatic mutations in their hematopoietic cells. In contrast to other conditions linked to clonal hematopoiesis, such as myelodysplastic syndrome (MDS) or clonal hematopoiesis of indeterminate potential in the elderly, the top alterations in AA are closely related to its immune pathogenesis. Nearly 40% of AA patients carry somatic mutations in the PIGA gene manifested as clonal populations of cells with
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45

Schenck, Ryan O., Niels Asger Jakobsen, Virginia Turati, et al. "Abstract A019: Mutation agnostic diagnosis of clonal hematopoiesis of indeterminate potential (CHIP) using fluctuating methylation clocks." Cancer Research 82, no. 10_Supplement (2022): A019. http://dx.doi.org/10.1158/1538-7445.evodyn22-a019.

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Abstract Clonal hematopoiesis (CH), such as clonal hematopoiesis of indeterminant potential (CHIP), is diagnosed based on somatic genomic alterations in the absence of hematologic malignancy. At present, CHIP is diagnosed using peripheral blood, where putative driver point mutations and small insertions/deletions whose variant allele frequency is greater or equal to two percent. Generally, the prevalence of CH increases as an individual ages and conveys a risk for progression to a malignancy. CH is thought to be driven by the underlying hematopoietic stem cells of an unknown quantity, with est
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46

DeZern, Amy E., Luca Malcovati, and Benjamin L. Ebert. "CHIP, CCUS, and Other Acronyms: Definition, Implications, and Impact on Practice." American Society of Clinical Oncology Educational Book, no. 39 (May 2019): 400–410. http://dx.doi.org/10.1200/edbk_239083.

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Unexplained blood cytopenias can be a clinical challenge for patients and clinicians alike. The relationship between these cytopenias and myeloid neoplasms like myelodysplastic syndromes (MDS) is currently an area of active research. There have been marked developments in our understanding of clonal hematopoiesis based on findings of somatic mutations in genes known to be associated with MDS. This has led to newer terms to describe precursor states to MDS, such as clonal hematopoiesis of indeterminate potential (CHIP) and clonal cytopenia of undetermined significance (CCUS). These conditions m
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47

Marnell, Christopher S., Alexander Bick, and Pradeep Natarajan. "Clonal hematopoiesis of indeterminate potential (CHIP): Linking somatic mutations, hematopoiesis, chronic inflammation and cardiovascular disease." Journal of Molecular and Cellular Cardiology 161 (December 2021): 98–105. http://dx.doi.org/10.1016/j.yjmcc.2021.07.004.

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48

Godfrey, Sarah, Hannah Rosenblum, Jianhua Zhao, et al. "CLONAL HEMATOPOIESIS OF INDETERMINATE POTENTIAL (CHIP) IN WILD-TYPE TRANSTHYRETIN CARDIAC AMYLOIDOSIS." Journal of the American College of Cardiology 77, no. 18 (2021): 3305. http://dx.doi.org/10.1016/s0735-1097(21)04659-3.

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49

Hirano, Teruyuki, and Scott E. Kasner. "Stranger Than Fiction, Clonal Hematopoiesis of Indeterminate Potential, and Small Vessel Pathology." Stroke 53, no. 3 (2022): 798–99. http://dx.doi.org/10.1161/strokeaha.121.037678.

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50

Heuser, Michael, Felicitas Thol, and Arnold Ganser. "Clonal Hematopoiesis of Indeterminate Potential." Deutsches Aerzteblatt Online, May 6, 2016. http://dx.doi.org/10.3238/arztebl.2016.0317.

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