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Clonal Hematopoiesis and Evolution to Hematopoietic Malignancies
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Clonal hematopoiesis (CH) broadly describes the expansion of a clonal population of blood cells with one or more somatic mutations. Individuals with CH are at greater risk for hematological malignancies, cardiovascular disease, and increased mortality from non-hematological cancers. Understanding the causes of CH and how these mutant cells interact with cells of other tissues will provide critical insights into preleukemic development, stem cell biology, host-immune interactions, and cancer evolution. Here we discuss the clinical manifestations of CH, mechanisms contributing to its development, the role of CH in clonal evolution toward leukemia, and the contribution of CH to non-hematological disease states.
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“clonal hematopoiesis-associated mutations alter the behavior of hematopoietic stem cells (HSCs); some also confer a fitness advantage, leading to clonal expansion [27,28].”
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 [28]
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Cites
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
Arber, D. A., Orazi, A., Hasserjian, R., Thiele, J., Borowitz, M. J., Le Beau, M. M., Bloomfield, C. D., Cazzola, M., & Vardiman, J. W. (2016) · Blood · doi:10.1182/blood-2016-03-643544 · Cited by 10,119
Stem cells, cancer, and cancer stem cells
Reya, T., Morrison, S. J., Clarke, M. F., & Weissman, I. L. (2001) · Nature · doi:10.1038/35102167 · Cited by 9,738
Signatures of mutational processes in human cancer
Initiative, A. P. C. G., Alexandrov, L. B., ICGC Breast Cancer Consortium, ICGC MMML-Seq Consortium, PedBrain, I., Nik-Zainal, S., Wedge, D. C., Aparicio, S. A. J. R., Behjati, S., Biankin, A. V., et al. (2013) · Nature · doi:10.1038/nature12477 · Cited by 9,660
Bonnet, D. A., & Dick, J. E. (1997) · Nature Medicine · doi:10.1038/nm0797-730 · Cited by 7,197
Cancer Immunoediting: Integrating Immunity’s Roles in Cancer Suppression and Promotion
Schreiber, R. D., Old, L. J., & Smyth, M. J. (2011) · Science · doi:10.1126/science.1203486 · Cited by 6,474
Conversion of 5-Methylcytosine to 5-Hydroxymethylcytosine in Mammalian DNA by MLL Partner TET1
Tahiliani, M., Koh, K. P., Shen, Y., Pastor, W. A., Bandukwala, H., Brudno, Y., Agarwal, S., Iyer, L. M., Liu, D. R., Aravind, L., et al. (2009) · Science · doi:10.1126/science.1170116 · Cited by 5,836
Genomic and Epigenomic Landscapes of Adult De Novo Acute Myeloid Leukemia
The Cancer Genome Atlas Research Network (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1301689 · Cited by 5,078
Age-related clonal hematopoiesis associated with adverse outcomes
Jaiswal, S., Fontanillas, P., Flannick, J., Manning, A., Grauman, P. V., Mar, B. G., Lindsley, R. C., Mermel, C. H., Burtt, N., Chavez, A., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1408617 · Cited by 4,841
Genomic classification and prognosis in acute myeloid leukemia
Papaemmanuil, E., Gerstung, M., Bullinger, L., Gaidzik, V. I., Paschka, P., Roberts, N. D., Potter, N. E., Heuser, M., Thol, F., Bolli, N., et al. (2016) · New England Journal of Medicine · doi:10.1056/nejmoa1516192 · Cited by 4,350
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Vasan, N., Baselga, J., & Hyman, D. M. (2019) · Nature · doi:10.1038/s41586-019-1730-1 · Cited by 2,770
Clonal hematopoiesis in human aging and disease
Jaiswal, S., & Ebert, B. L. (2019) · Science · doi:10.1126/science.aan4673 · Cited by 1,156
“The role of CHIP-associated genes in hematopoiesis has been extensively reviewed elsewhere (41, 42).”
p53: 800 million years of evolution and 40 years of discovery
Levine, A. J. (2020) · Nature reviews. Cancer · doi:10.1038/s41568-020-0262-1 · Cited by 876
High-intensity sequencing reveals the sources of plasma circulating cell-free DNA variants
Razavi, P., Li, B. T., Brown, D. N., Jung, B., Hubbell, E. A., Shen, R., Abida, W. M., Juluru, K., de Bruijn, I., Hou, C., et al. (2019) · Nature Medicine · doi:10.1038/s41591-019-0652-7 · Cited by 808
Heuser, M., Freeman, S. D., Ossenkoppele, G. J., Buccisano, F., Hourigan, C. S., Ngai, L. L., Tettero, J. M., Bachas, C., Baer, C. R., Béné, M. C., et al. (2021) · Blood · doi:10.1182/blood.2021013626 · Cited by 767
Pascual, J., Attard, G., Bidard, F.-C., Curigliano, G., De Mattos-Arruda, L., Diehn, M., Italiano, A., Lindberg, J., Merker, J. D., Montagut, C., et al. (2022) · Annals of Oncology · doi:10.1016/j.annonc.2022.05.520 · Cited by 783
“33,35 Genes mutated in CHIP partially overlap with solid tumour drivers.”
BackgroundInherited causes of clonal haematopoiesis in 97,691 whole genomes
Bick, A. G., Weinstock, J. S., Nandakumar, S. K., Fulco, C. P., Bao, E. L., Zekavat, S. M., Szeto, M. D., Liao, X., Leventhal, M. J., Nasser, J., et al. (2020) · Nature · doi:10.1038/s41586-020-2819-2 · Cited by 733
Somatic mutations precede acute myeloid leukemia years before diagnosis
Desai, P., Mencia-Trinchant, N., Savenkov, O., Simon, M. S., Cheang, G., Lee, S., Samuel, M., Ritchie, E. K., Guzman, M. L., Ballman, K. V., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0081-z · Cited by 619
Advances in acute myeloid leukemia
Newell, L. F., & Cook, R. J. (2021) · BMJ · doi:10.1136/bmj.n2026 · Cited by 461
PPM1D Mutations Drive Clonal Hematopoiesis in Response to Cytotoxic Chemotherapy
Hsu, J. I., Dayaram, T., Tovy, A., De Braekeleer, E., Jeong, M., Wang, F., Zhang, J., Heffernan, T. P., Gera, S., Kovacs, J. J., et al. (2018) · Cell stem cell · doi:10.1016/j.stem.2018.10.004 · Cited by 425
Microbial signals drive pre-leukaemic myeloproliferation in a Tet2-deficient host
Meisel, M., Hinterleitner, R., Pacis, A., Chen, L., Earley, Z. M., Mayassi, T., Pierre, J. F., Ernest, J. D., Galipeau, H. J., Thuille, N., et al. (2018) · Nature · doi:10.1038/s41586-018-0125-z · Cited by 406
Clonal haematopoiesis: connecting ageing and inflammation in cardiovascular disease
Jaiswal, S., & Libby, P. (2020) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0247-5 · Cited by 386
Cancer as a disease of old age: changing mutational and microenvironmental landscapes
Laconi, E., Marongiu, F., & DeGregori, J. (2020) · British Journal of Cancer · doi:10.1038/s41416-019-0721-1 · Cited by 348
Causes and Consequences of Hematopoietic Stem Cell Heterogeneity
Haas, S. F., Trumpp, A., & Milsom, M. D. (2018) · Cell stem cell · doi:10.1016/j.stem.2018.04.003 · Cited by 362
Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling
Hormaechea-Agulla, D., Matatall, K. A., Le, D. T., Kain, B., Long, X., Kus, P., Jaksik, R., Challen, G. A., Kimmel, M., & King, K. Y. (2021) · Cell Stem Cell · doi:10.1016/j.stem.2021.03.002 · Cited by 329
Ferrucci, L., Levine, M. E., Kuo, P.-L., & Simonsick, E. M. (2018) · Circulation Research · doi:10.1161/circresaha.118.312816 · Cited by 303
“even though there is little evidence that it is a risk factor for malignancy or acts as a causative driver of aging.(3) Of note,”
BackgroundMarnell, C. S., Bick, A. G., & Natarajan, P. (2021) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2021.07.004 · Cited by 313
Inflammation-Induced Tumorigenesis and Metastasis
Hibino, S., Kawazoe, T., Kasahara, H., Itoh, S., Ishimoto, T., Sakata‐Yanagimoto, M., & Taniguchi, K. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115421 · Cited by 319
Suppression of m6A reader Ythdf2 promotes hematopoietic stem cell expansion
Li, Z., Qian, P., Shao, W., Shi, H., He, X., Gogol, M., Yu, Z., Wang, Y., Qi, M., Zhu, Y., et al. (2018) · Cell Research · doi:10.1038/s41422-018-0072-0 · Cited by 263
Leukemic stem cells and therapy resistance in acute myeloid leukemia
Stelmach, P., & Trumpp, A. (2023) · Haematologica · doi:10.3324/haematol.2022.280800 · Cited by 273
mRNA vaccines in disease prevention and treatment
Zhang, G., Tang, T., Chen, Y., Huang, X., & Liang, T. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01579-1 · Cited by 273
“mRNA vaccines against blood system cancer Hematological malignancies encompass a range of diseases involving the abnormal proliferation of hematopoietic stem cells, including leukemia, myeloma, and lymphoma.(176) Leukemia ranks as the first leading cause of cancer death among blood diseases and the tenth leading cause…”
BackgroundMeasuring Aging and Identifying Aging Phenotypes in Cancer Survivors
Guida, J. L., Ahles, T. A., Belsky, D., Campisi, J., Cohen, H. J., DeGregori, J., Fuldner, R., Ferrucci, L., Gallicchio, L., Gavrilov, L., et al. (2019) · JNCI: Journal of the National Cancer Institute · doi:10.1093/jnci/djz136 · Cited by 216
Mutated nucleophosmin 1 as immunotherapy target in acute myeloid leukemia
van der Lee, D. I., Reijmers, R. M., Honders, M. W., Hagedoorn, R. S., de Jong, R. C. M., Kester, M. G. D., van der Steen, D. M., de Ru, A. H., Kweekel, C., Bijen, H. M., et al. (2019) · Journal of Clinical Investigation · doi:10.1172/jci97482 · Cited by 207
Clinical consequences of clonal hematopoiesis of indeterminate potential
Steensma, D. P. (2018) · Blood Advances · doi:10.1182/bloodadvances.2018020222 · Cited by 194
“Investigators have focused on various MDS- and AML-associated phenomena that may aid and abet clonal evolution, which were recently cogently reviewed by Bowman et al.24 The primary driver of progression of CHIP to overt neoplasia has been assumed to be acquisition of new mutation in a clonal cell with self-renewal pro…”
BackgroundMethodInfluentialClinical consequences of clonal hematopoiesis of indeterminate potential
Steensma, D. P. (2018) · Hematology · doi:10.1182/asheducation-2018.1.264 · Cited by 189
“Investigators have focused on various MDS- and AML-associated phenomena that may aid and abet clonal evolution, which were recently cogently reviewed by Bowman et al.24 The primary driver of progression of CHIP to overt neoplasia has been assumed to be acquisition of new mutation in a clonal cell with self-renewal pro…”
BackgroundMethodInfluentialDysregulated haematopoietic stem cell behaviour in myeloid leukaemogenesis
Yamashita, M., Dellorusso, P. V., Olson, O. C., & Passegue, E. A. (2020) · Nature reviews. Cancer · doi:10.1038/s41568-020-0260-3 · Cited by 197
Cardiovascular Disease, Aging, and Clonal Hematopoiesis
Evans, M. A., Sano, S., & Walsh, K. X. (2019) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-012419-032544 · Cited by 169
“In particular, Tet2 deficiency in mice leads aberrant patterns of hematopoiesis, and Tet2deficient HSPCs display increased self-renewal and proliferative capacity in competition assays compared with their wild-type counterparts (62, 63).”
ResultInfluentialVelten, L., Story, B. A., Hernández-Malmierca, P., Raffel, S., Leonce, D. R., Milbank, J. H., Paulsen, M. S., Demir, A., Szu‐Tu, C., Frömel, R., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-21650-1 · Cited by 144
Loberg, M. A., Bell, R. K., Goodwin, L. O., Eudy, E., Miles, L. A., SanMiguel, J. M., Young, K. A., Bergstrom, D. E., Levine, R. L., Schneider, R. K., et al. (2019) · Leukemia · doi:10.1038/s41375-018-0368-6 · Cited by 134
Granulopoiesis and Neutrophil Homeostasis: A Metabolic, Daily Balancing Act
Yvan‐Charvet, L., & Ng, L. G. (2019) · Trends in Immunology · doi:10.1016/j.it.2019.05.004 · Cited by 137
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Challen, G., & Goodell, M. A. (2020) · Blood · doi:10.1182/blood.2020006510 · Cited by 131
Levine, A. J., Jenkins, N. A., & Copeland, N. G. (2019) · Cancer Cell · doi:10.1016/j.ccell.2018.11.009 · Cited by 121
Structure of nucleosome-bound DNA methyltransferases DNMT3A and DNMT3B
Xu, T.-H., Liu, M., Zhou, X. E., Liang, G., Zhao, G., Xu, H. E., Melcher, K., & Jones, P. A. (2020) · Nature · doi:10.1038/s41586-020-2747-1 · Cited by 131
Clonal hematopoiesis and inflammation: Partners in leukemogenesis and comorbidity
Cook, E. K., Luo, M., & Rauh, M. J. (2020) · Experimental Hematology · doi:10.1016/j.exphem.2020.01.011 · Cited by 124
Differences and similarities between cancer and somatic stem cells: therapeutic implications
Rossi, F., Noren, H., Jove, R., Beljanski, V., & Grinnemo, K. (2020) · Stem Cell Research & Therapy · doi:10.1186/s13287-020-02018-6 · Cited by 123
Reprogramming the epigenome with vitamin C
Lee Chong, T., Ahearn, E. L., & Cimmino, L. (2019) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00128 · Cited by 120
“TET proteins are important regulators of DNA methylation fidelity in HSCs, and loss of TET function occurs in a variety of hematologic malignancies (Guillamot et al., 2016; Bowman et al., 2018).”
BackgroundThe role of TP53 in acute myeloid leukemia: Challenges and opportunities
Barbosa, K., Li, S., Adams, P. D., & Deshpande, A. J. (2019) · Genes Chromosomes and Cancer · doi:10.1002/gcc.22796 · Cited by 118
“offer a fitness advantage in the face of age-related and other genotoxic stresses.(32) This leads to the clonal outgrowth of a small pool of”
BackgroundInfluentialGenetic and epigenetic determinants of AML pathogenesis
Cai, S. F., & Levine, R. L. (2018) · Seminars in Hematology · doi:10.1053/j.seminhematol.2018.08.001 · Cited by 117
“This process of clonal evolution under selection pressure within the context of CH has been excellently reviewed by Bowman and colleagues [14].”
BackgroundClonal hematopoiesis in patients with rheumatoid arthritis
Savola, P., Lundgren, S., Keränen, M. A. I., Almusa, H., Ellonen, P., Leirisalo‐Repo, M., Kelkka, T., & Mustjoki, S. M. (2018) · Blood Cancer Journal · doi:10.1038/s41408-018-0107-2 · Cited by 112
Late relapse in acute myeloid leukemia (AML): clonal evolution or therapy-related leukemia?
Yilmaz, M. E., Wang, F., Loghavi, S., Bueso-Ramos, C., Gumbs, C. E., Little, L., Song, X., Zhang, J., Kadia, T. M., Borthakur, G. M., et al. (2019) · Blood Cancer Journal · doi:10.1038/s41408-019-0170-3 · Cited by 108
Epigenetic Regulation of Genomic Stability by Vitamin C
Brabson, J. P., Leesang, T. E., Mohammad, S., & Cimmino, L. (2021) · Frontiers in Genetics · doi:10.3389/fgene.2021.675780 · Cited by 111
Godsey, J. H., Silvestro, A., Barrett, J. C., Bramlett, K., Chudova, D., Deras, I., Dickey, J., Hicks, J., Johann, D. J., Leary, R., et al. (2020) · Clinical Chemistry · doi:10.1093/clinchem/hvaa164 · Cited by 104
“CHIP, which refers to the clonal expansion of white blood cells derived from a hematopoietic stem or progenitor cell that have acquired one or more somatic mutations (23), poses a unique challenge for NGSbased ctDNA assays since it can cause the apparent detection of tumor-associated somatic mutations in the plasma of…”
BackgroundFujino, T., Goyama, S., Sugiura, Y., Inoue, D., Asada, S., Yamasaki, S., Matsumoto, A., Yamaguchi, K., Isobe, Y., Tsuchiya, A., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-22053-y · Cited by 109
Silencing of LINE-1 retrotransposons is a selective dependency of myeloid leukemia
Gu, Z., Liu, Y., Zhang, Y., Cao, H., Lyu, J., Wang, X., Wylie, A., Newkirk, S. J., Jones, A. E., Lee, M., et al. (2021) · Nature Genetics · doi:10.1038/s41588-021-00829-8 · Cited by 111
Comprehensive diagnostics of acute myeloid leukemia by whole transcriptome RNA sequencing
Arindrarto, W., Borràs, D., de Groen, R. A. L., van den Berg, R. R., Locher, I. J., van Diessen, S. A. M. E., van der Holst, R., van der Meijden, E. D., Honders, M. W., de Leeuw, R. H., et al. (2020) · Leukemia · doi:10.1038/s41375-020-0762-8 · Cited by 105
CHIP Happens: Clonal Hematopoiesis of Indeterminate Potential and Its Relationship to Solid Tumors
Reed, S. C., Croessmann, S., & Park, B. H. (2022) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-22-2598 · Cited by 112
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Pich, O., Reyes-Salazar, I., González-Pérez, A., & López-Bigas, N. (2022) · Nature Communications · doi:10.1038/s41467-022-31878-0 · Cited by 100
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Khetarpal, S. A., Qamar, A., Bick, A. G., Fuster, J. J., Kathiresan, S., Jaiswal, S., & Natarajan, P. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.05.045 · Cited by 88
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Rodrigues, C. P., Shvedunova, M., & Akhtar, A. (2020) · Trends in Genetics · doi:10.1016/j.tig.2020.09.015 · Cited by 99
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BackgroundInfluentialGermline risk of clonal haematopoiesis
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Huang, Y., Chen, C.-W., Sundaramurthy, V., Slabicki, M. M., Hao, D., Watson, C. J., Tovy, A., Reyes, J. M., Dakhova, O., Crovetti, B. R., et al. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-0560 · Cited by 83
“Understanding the mechanisms through which HSC clones expand and associate with malignancy development is therefore of significant interest (6).”
BackgroundNormal Hematopoiesis Is a Balancing Act of Self-Renewal and RegenerationPreprint
Olson, O. C., Kang, Y.-A., & Passegue, E. A. (2020) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a035519 · Cited by 89
Technical and biological constraints on ctDNA-based genotyping
Herberts, C., & Wyatt, A. W. (2021) · Trends in cancer · doi:10.1016/j.trecan.2021.06.001 · Cited by 78
Loss of TET2 in human hematopoietic stem cells alters the development and function of neutrophils
Encabo, H. H., Aramburu, I. V., Albornoz, M. G., Piganeau, M., Wood, H. J., Song, A., Ferrelli, A., Sharma, A., Minutti, C. M., Domart, M., et al. (2023) · Cell stem cell · doi:10.1016/j.stem.2023.05.004 · Cited by 85
“The two most affected genes in CH are DNMT3A and TET2, two epigenetic factors involved in DNA methylation and demethylation, respectively.(9,10) Preleukemic mutations in HSC have been described to confer a repopulating advantage upon stress-induced hematopoiesis in mouse models, and recent works have aided our underst…”
Environmental influences on clonal hematopoiesis
King, K. Y., Huang, Y., Nakada, D., & Goodell, M. A. (2019) · Experimental Hematology · doi:10.1016/j.exphem.2019.12.005 · Cited by 75
“Thus, while CH is clearly associated with mortality, the interaction between environmental and genetic factors that drive its emergence remains unclear (Bowman et al., 2018; Steensma, 2018).”
BackgroundAnalysis of 153 115 patients with hematological malignancies refines the spectrum of familial risk
Sud, A., Chattopadhyay, S., Thomsen, H., Sundquist, K., Sundquist, J., Houlston, R. S., & Hemminki, K. (2019) · Blood · doi:10.1182/blood.2019001362 · Cited by 72
Rauch, P. J., Gopakumar, J., Silver, A. J., Nachun, D. C., Ahmad, H., McConkey, M. E., Nakao, T., Bosse, M. M., Rentz, T., Gonzalez, N. V., et al. (2023) · Nature Cardiovascular Research · doi:10.1038/s44161-023-00326-7 · Cited by 83
Wendorff, A. A., Quinn, S. A., Rashkovan, M., Madubata, C. J., Ambesi‐Impiombato, A., Litzow, M. R., Tallman, M. S., Paietta, E. M., Paganin, M., Basso, G., et al. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-18-1005 · Cited by 72
“Mutations that increase the self-renewal capacity of hematopoietic progenitors are postulated to play important roles in leukemia initiation and as potential drivers of leukemia-initiating cell activity (21, 34).”
BackgroundGuillamot, M., Ouazia, D., Dolgalev, I., Yeung, S. T., Kourtis, N., Dai, Y., Corrigan, K., Zea-Redondo, L., Saraf, A., Florens, L. A., et al. (2019) · Nature Immunology · doi:10.1038/s41590-019-0454-6 · Cited by 70
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Ferrari, S., Valeri, E., Conti, A., Scala, S., Aprile, A., Micco, R. D., Kajaste‐Rudnitski, A., Montini, E., Ferrari, G., Aiuti, A., et al. (2023) · Cell stem cell · doi:10.1016/j.stem.2023.04.014 · Cited by 75
41BB-based and CD28-based CD123-redirected T-cells ablate human normal hematopoiesis in vivo
Baroni, M. L., Sánchez‐Martínez, D., Gutiérrez‐Agüera, F., Roca-Ho, H., Castellà, M., Zanetti, S. R., Velasco-Hernández, T., de la Guardia, R. D., Castaño, J., Anguita, E., et al. (2020) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2020-000845 · Cited by 69
Trino, S., Lamorte, D., Caivano, A., Luca, L. D., Sgambato, A., & Laurenzana, I. (2020) · Leukemia · doi:10.1038/s41375-020-01104-1 · Cited by 73
Clonal hematopoiesis and non-hematologic disorders
Jaiswal, S. (2020) · Blood · doi:10.1182/blood.2019000989 · Cited by 182
Kolovos, P., Nishimura, K., Sankar, A., Sidoli, S., Cloos, P. A., Helin, K., & Christensen, J. F. (2020) · Genome Research · doi:10.1101/gr.261016.120 · Cited by 71
“5G).ASXL1 is frequently found mutated in clonal hematopoiesis, with high frequency in myelodysplastic syndromes (MDS), and various forms of myeloproliferative disease (MPD), including acute myeloid leukemia (AML) (Micol and Abdel-Wahab 2016; Bowman et al. 2018).”
BackgroundClonal hematopoiesis as a model for premalignant changes during aging
Steensma, D. P., & Ebert, B. L. (2019) · Experimental Hematology · doi:10.1016/j.exphem.2019.12.001 · Cited by 65
“Clonal hematopoiesis predisposes to overt cancer diagnosable using conventional World Health Organization (WHO) clinicopathological criteria [12], similar to somatic expansions in other tissues, but is also associated with increased all-cause mortality and a variety of clinical phenotypes [13].”
Clonal Hematopoiesis: Somatic Mutations in Blood Cells and Atherosclerosis
Natarajan, P., Jaiswal, S., & Kathiresan, S. (2018) · Circulation Genomic and Precision Medicine · doi:10.1161/circgen.118.001926 · Cited by 63
Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies
Zhao, Y., Huang, Z., & Peng, H. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.743006 · Cited by 62
“A single germline or somatic mutation in lymphatic hematopoietic stem cells may be prone to clonal expansion, depending on the acquired new mutation (88), which is commonly malignant and may result in an undesirable outcome, i.”
BackgroundArtemisinin-type drugs for the treatment of hematological malignancies
Mancuso, R. I., Foglio, M. A., & Saad, S. T. O. (2020) · Cancer Chemotherapy and Pharmacology · doi:10.1007/s00280-020-04170-5 · Cited by 61
Spontaneous and inherited TP53 genetic alterations
Levine, A. J. (2021) · Oncogene · doi:10.1038/s41388-021-01991-3 · Cited by 67
“Although these prevalence estimates are dynamically altered based on variable mutation classifications and highly impacted by some specific controvertible spontaneous TP53 mutations, the databases employed could introduce other possible biases, such as CHIP, or enrichment of mutations potentially associated with lower…”
BackgroundMuto, T., Guillamot, M., Yeung, J., Fang, J., Bennett, J. R., Nadorp, B., Lasry, A., Zea-Redondo, L., Choi, K., Gong, Y., et al. (2022) · Cell stem cell · doi:10.1016/j.stem.2021.12.007 · Cited by 60
“Tet2 is a common mutation in pre-leukemic HSCs, however, secondary events are required for malignant transformation(Bowman et al., 2018; Steensma et al., 2015).”
Hsu, J., Reilly, A., Hayes, B. J., Clough, C. A., Konnick, E. Q., Torok‐Storb, B., Gülsüner, S., Wu, D., Becker, P. S., Keel, S., et al. (2019) · Blood · doi:10.1182/blood.2018884338 · Cited by 63
The evolution of hematopoietic cells under cancer therapy
Pich, O., Cortés‐Bullich, A., Muiños, F., Pratcorona, M., González-Pérez, A., & López-Bigas, N. (2021) · Nature Communications · doi:10.1038/s41467-021-24858-3 · Cited by 60
Current and Developing Liquid Biopsy Techniques for Breast Cancer
Wu, H., & Chu, P. (2022) · Cancers · doi:10.3390/cancers14092052 · Cited by 66
Clonal Hematopoiesis: From Mechanisms to Clinical Intervention
Köhnke, T., & Majeti, R. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-0901 · Cited by 63
Cardiovascular Disease Among Patients With AML and CHIP-Related Mutations
Arguelles, O. C., Schöffel, A. C., Capo‐Chichi, J., Abdel-Qadir, H. M., Schuh, A. C., Estrada, M. C., Liu, S., Gupta, V. K., Schimmer, A. D., Yee, K. W. L., et al. (2022) · JACC CardioOncology · doi:10.1016/j.jaccao.2021.11.008 · Cited by 60
“The clonal hematopoiesis spectrum extends from CH of indeterminate potential (CHIP) and clonal cytopenias of undetermined significance to myelodysplastic syndrome and acute myeloid leukemia (AML).(3,4) It is estimated that about 10% of individuals >70 years of age have CHIP.”
BackgroundThomas, M. E., Abdelhamed, S., Hiltenbrand, R., Schwartz, J. R., Sakurada, S. M., Walsh, M. F., Song, G., Ma, J., Pruett‐Miller, S. M., & Klco, J. M. (2021) · Leukemia · doi:10.1038/s41375-021-01212-6 · Cited by 59
Calcium regulation of stem cells
Snoeck, H. (2020) · EMBO Reports · doi:10.15252/embr.202050028 · Cited by 59
“Heterozygous TET2 mutations are drivers in a large fraction of myeloid malignancies [142–145] and are frequently encountered in clonal hematopoiesis of undermined significance, a condition where the contribution of one HSC clone to the blood increases with age and that is associated with elevated incidence of hematolo…”
Hand in hand: intrinsic and extrinsic drivers of aging and clonal hematopoiesis
SanMiguel, J. M., Young, K. A., & Trowbridge, J. J. (2020) · Experimental Hematology · doi:10.1016/j.exphem.2020.09.197 · Cited by 59
Inflammatory Cytokines Shape an Altered Immune Response During Myeloid Malignancies
Camacho, V., Kuznetsova, V., & Welner, R. S. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.772408 · Cited by 60
“Mutations in epigenetic regulators, specifically enzymes regulating the modification and methylation of DNA such as DNMT3A, ASXL1, TET2, represent the majority of CHIP mutations (24).”
BackgroundHiga, K. C., Goodspeed, A., Chavez, J. S., De Dominici, M., Danis, E., Zaberezhnyy, V., Rabe, J. L., Tenen, D. G., Pietras, E. M., & DeGregori, J. (2021) · Journal of Experimental Medicine · doi:10.1084/jem.20200560 · Cited by 57
“Risk factors associated with hematologic disorders include age and prior exposure to radiation or chemotherapy, conditions characterized by underlying inflammation (Bowman et al., 2018).”
BackgroundClonal hematopoiesis in sickle cell disease
Liggett, L. A., Cato, L. D., Weinstock, J. S., Zhang, Y., Nouraie, M. S., Gladwin, M. T., Garrett, M. E., Ashley‐Koch, A. E., Telen, M. J., Custer, B., et al. (2022) · Journal of Clinical Investigation · doi:10.1172/jci156060 · Cited by 61
“However, the clinical implications of small clones in predisposing to myeloid malignancies is unknown and existing literature suggests that only larger clones with VAFs > 10% have prognostic impact [8, 9, 11, 10, 11].”
Huang, Y., Chen, C.-W. D., Sundaramurthy, V., Slabicki, M. M., Hao, D., Watson, C. J., Tovy, A., Reyes, J. M., Dakhova, O., Crovetti, B. R., et al. (2021) · Apollo (University of Cambridge) · doi:10.17863/cam.74923 · Cited by 56
Burden of AML, 1990-2019: Estimates From the Global Burden of Disease Study
Jani, C., Ahmed, A., Singh, H., Mouchati, C., Omari, O. A., Bhatt, P. S., Sharma, R., Farooq, M., Liu, W., Shalhoub, J., et al. (2023) · JCO Global Oncology · doi:10.1200/go.23.00229 · Cited by 56
Wong, W., Bhatt, S. T., Trinkaus, K. M., Pusic, I., Elliott, K., Mahajan, N., Wan, F., Switzer, G. E., Confer, D. L., DiPersio, J. F., et al. (2020) · Science Translational Medicine · doi:10.1126/scitranslmed.aax6249 · Cited by 52
“Despite not having CHIP, it has been hypothesized that the AYA population harbors hematopoietic somatic mutations of low VAF, undetectable via standard NGS (18), and these mutations could serve as a reservoir for future disease development when relevant selective pressure is present (19).”
BackgroundImmunosenescence and lymphomagenesis
Mancuso, S., Carlisi, M., Santoro, M., Napolitano, M., Raso, S., & Siragusa, S. M. (2018) · Immunity & Ageing · doi:10.1186/s12979-018-0130-y · Cited by 54
The Source and Dynamics of Adult Hematopoiesis: Insights from Lineage Tracing
Pucella, J. N., Upadhaya, S., & Reizis, B. (2020) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-020520-114601 · Cited by 53
ASXL1/2 mutations and myeloid malignancies
Medina, E. A., Delma, C. R., & Yang, F. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01336-x · Cited by 55
“CHIP portends an increased risk of developing a hematologic malignancy [14] and underscores the concept that myeloid malignancies develop initially from a pre-leukemic stem cell that accumulates additional genetic alterations to become a malignant/leukemic stem cell with dysregulated self-renewal, enhanced proliferati…”
BackgroundTP53 in Acute Myeloid Leukemia: Molecular Aspects and Patterns of Mutation
George, B., Kantarjian, H. M., Baran, N., Krocker, J. D., & Rios, A. A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221910782 · Cited by 53
“These findings support the perceived fitness advantage conferred by TP53 through enhancement of HSC selfrenewal in light of genotoxic stresses [47].”
BackgroundInternational stem cell tourism: a critical literature review and evidence-based recommendations
Lyons, S., Salgaonkar, S., & Flaherty, G. T. (2021) · International Health · doi:10.1093/inthealth/ihab050 · Cited by 48
Clonal hematopoiesis, aging, and cardiovascular diseases
Pardali, E., Dimmeler, S., Zeiher, A. M., & Rieger, M. A. (2019) · Experimental Hematology · doi:10.1016/j.exphem.2019.12.006 · Cited by 50
Clonal Hematopoiesis and Its Impact on Cardiovascular Disease
Sano, S., Wang, Y., & Walsh, K. X. (2018) · Circulation Journal · doi:10.1253/circj.cj-18-0871 · Cited by 50
Delineating the evolutionary dynamics of cancer from theory to reality
Božić, I., & Wu, C. J. (2020) · Nature Cancer · doi:10.1038/s43018-020-0079-6 · Cited by 46
Bone Marrow Immune Microenvironment in Myelodysplastic Syndromes
Kouroukli, O., Symeonidis, A. S., Foukas, P. G., Maragkou, M., & Kourea, E. P. (2022) · Cancers · doi:10.3390/cancers14225656 · Cited by 52
Choi, J., Bogenberger, J. M., & Tibes, R. (2020) · Targeted Oncology · doi:10.1007/s11523-020-00711-3 · Cited by 45
Functional and epigenetic phenotypes of humans and mice with DNMT3A Overgrowth Syndrome
Smith, A. M., LaValle, T. A., Shinawi, M. S., Ramakrishnan, S. M., Abel, H., Hill, C. A., Kirkland, N. M., Rettig, M. P., Helton, N., Heath, S. E., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-24800-7 · Cited by 50
Yu, K., Deuitch, N. T., Merguerian, M., Cunningham, L., Davis, J., Bresciani, E., Diemer, J. L., Andrews, E. T., Young, A., Donovan, F. X., et al. (2023) · Blood Advances · doi:10.1182/bloodadvances.2023011165 · Cited by 42
“Large population studies showed that CH increases the risks of atherosclerotic cardiovascular diseases, 12,13 hematologic neoplasms, 11,14 and other nonmalignant diseases.”
Background
Metadata
- Authors
- Bowman, R. L., Busque, L., & Levine, R. L.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Hôpital Maisonneuve-Rosemont (CA)
- Corresponding author
- Levine, Ross L.
- Venue
- Cell stem cell
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 22
- Issue
- 2
- Pages
- 157-170
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- PMC
- PMC5804896
- OpenAlex
- W2786854070
- Cited by
- 448
- References
- 112
- Citations by year
- 2026: 29 · 2025: 38 · 2024: 37 · 2023: 56 · 2022: 54 · 2021: 69 · 2020: 67 · 2019: 71 · 2018: 25
- FWCI
- 9.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Damon Runyon Cancer Research Foundation
- National Cancer Institute (P30 CA008748)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- clonal hematopoiesis, somatic mutations, hematologic malignancies, leukemia, clonal evolution, hematopoietic stem cells, cardiovascular disease, tumor evolution
- MeSH terms
- Hematopoiesis, Humans, Mutation, Stochastic Processes, Hematologic Neoplasms, Epigenesis, Genetic, Clonal Evolution
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