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1 hape the genetic diversity of healthy blood (clonal hematopoiesis).
2 ion or chromosomal abnormality indicative of clonal hematopoiesis.
3 -forming unit colonies but not in those with clonal hematopoiesis.
4 eoplasms (MPN) characterized by multilineage clonal hematopoiesis.
5 polyclonal hematopoiesis and in 4 of 10 with clonal hematopoiesis.
6 identified in this subset with evidence for clonal hematopoiesis.
7 e myeloid skewing and mutations that lead to clonal hematopoiesis.
8 in myeloid malignancies and their precursor clonal hematopoiesis.
9 ts observed among genes also associated with clonal hematopoiesis.
10 most frequently mutated gene in age-related clonal hematopoiesis.
11 V600E mutation (P = .049) than those without clonal hematopoiesis.
12 were associated with DNMT3A and TET2 mutant clonal hematopoiesis.
13 sociation between cardiovascular disease and clonal hematopoiesis.
14 h identification of alterations arising from clonal hematopoiesis.
15 loid as well as lymphoid malignancies and in clonal hematopoiesis.
16 lls and demonstrate its utility for modeling clonal hematopoiesis.
17 lays an important role in the development of clonal hematopoiesis.
18 ions in genes not previously associated with clonal hematopoiesis.
19 y/mortality in individuals with age-related, clonal hematopoiesis.
20 genetic mechanism by which mutant p53 drives clonal hematopoiesis.
21 ts with cancer) had features consistent with clonal hematopoiesis.
22 2 gene in hematopoietic cell development and clonal hematopoiesis.
23 progenitor cells (HSPCs) and/or by promoting clonal hematopoiesis.
24 isorders in which recurrent mutations define clonal hematopoiesis.
25 ts with congenital neutropenia to assess for clonal hematopoiesis.
30 tion not only to MPN, but also to JAK2 V617F clonal hematopoiesis, a more common phenomenon that may
31 that define myelodysplastic syndromes (MDS): clonal hematopoiesis, aberrant differentiation, peripher
32 n review the role played by mutant DNMT3A in clonal hematopoiesis, accompanied by its effect on immun
33 odysplastic syndromes and are also common in clonal hematopoiesis, acute myeloid leukemia, chronic ly
36 imaging to investigate the interplay between clonal hematopoiesis and atherosclerosis in a longitudin
37 re subject to frequent missense mutations in clonal hematopoiesis and diverse neoplastic diseases.
39 (PMF) are chronic diseases characterized by clonal hematopoiesis and hyperproliferation of terminall
41 lore recent advances in the understanding of clonal hematopoiesis and its role in heart failure, emph
42 equencing data uncovers correlations between clonal hematopoiesis and lung cancer risk factors, ident
44 omising way to model the complex genetics of clonal hematopoiesis and myeloid disorders using CRISPR-
47 r disease-modifying drugs that can eradicate clonal hematopoiesis and/or prevent progression to more
48 re structural somatic variants indicative of clonal hematopoiesis, and are associated with aberrant l
50 identifies genetic variants correlated with clonal hematopoiesis, and highlights hundreds of potenti
52 ene are the most common cause of age-related clonal hematopoiesis (ARCH) in older individuals, and ar
56 increasing frequency with which people with clonal hematopoiesis are discovered and the need for cou
58 l hematopoiesis at the time of ABMT and that clonal hematopoiesis, as detected by the HUMARA assay, i
60 Indeed, several studies have now shown that clonal hematopoiesis associates with increased risk of a
61 at a significant proportion of patients have clonal hematopoiesis at the time of ABMT and that clonal
62 skewed XIP, and 10 of 78 (13.5%) either had clonal hematopoiesis at the time of ABMT or developed cl
65 ve resulted in highly sensitive detection of clonal hematopoiesis beyond these known driver genes.
67 his context, somatic alterations can promote clonal hematopoiesis by improving the competitive fitnes
69 e we study this phenomenon in the context of clonal hematopoiesis (CH) and the development of therapy
82 studies have reported an association between clonal hematopoiesis (CH) in the infused PBSC product an
102 asured within the hematopoietic compartment, clonal hematopoiesis (CH) is now recognized as a common
104 at acquired hematologic mutations leading to clonal hematopoiesis (CH) may further increase vulnerabi
108 t that many treated patients have persistent clonal hematopoiesis (CH) that may not reflect residual
112 etic stem cell (HSC) mutations can result in clonal hematopoiesis (CH) with heterogeneous clinical ou
115 most frequently mutated genes in age-related clonal hematopoiesis (CH), alongside DNA methyltransfera
128 This cfDNA sequencing approach revealed that clonal hematopoiesis constitutes a pervasive biological
134 phenomenon marked by expansion of cells with clonal hematopoiesis driver mutations, has been associat
136 zed in n=6 patients with HF harboring DNMT3A clonal hematopoiesis-driver mutations and n=4 patients w
137 es and T cells of patients with HF harboring clonal hematopoiesis-driver mutations in DNMT3A exhibit
138 ugh experimental studies suggest that DNMT3A clonal hematopoiesis-driver mutations may enhance inflam
141 hematopoiesis, most individuals who acquire clonal hematopoiesis during aging will never develop MDS
143 , establishing the causal role of smoking in clonal hematopoiesis has been limited by observational s
145 lly heterogeneous disorders characterized by clonal hematopoiesis, impaired differentiation, peripher
146 splastic lineages) from 67 patients revealed clonal hematopoiesis in 13 (50%) of 26 cases with MDS-PA
148 f TCA established the presence or absence of clonal hematopoiesis in about 90% of female subjects.
150 HUMARA alleles, was reported as evidence of clonal hematopoiesis in approximately 30% of elderly wom
153 mosome genes (qTCA) and found no evidence of clonal hematopoiesis in healthy nonanemic elderly person
155 understanding of the processes that promote clonal hematopoiesis in IBMFSs may inform clinical surve
161 issue of Blood, Eskelund et al characterize clonal hematopoiesis in serial samples from persons with
162 been observed in AML and in individuals with clonal hematopoiesis in the absence of leukemic transfor
165 second most commonly mutated gene linked to clonal hematopoiesis, in the hematopoietic cells of athe
166 es clinical considerations for patients with clonal hematopoiesis, including important points for hem
167 rdiovascular disease and are associated with clonal hematopoiesis, inflammation, and adverse vascular
169 expected consequence of mutation-associated clonal hematopoiesis is an increased risk of hematologic
174 al (CHIP), also referred to as aging-related clonal hematopoiesis, is defined as an asymptomatic clon
176 discuss recent advances in our knowledge of clonal hematopoiesis, its relationship to malignancies,
177 emorial Sloan Kettering (MSK) and the Korean Clonal Hematopoiesis (KoCH) consortia, we show that CH i
178 vascular event in an individual patient with clonal hematopoiesis may be low, the possibility of futu
180 e germline variants of genes associated with clonal hematopoiesis may increase the likelihood that an
181 ic morphology of blood and marrow cells, and clonal hematopoiesis, most individuals who acquire clona
185 ns in TET2 occur frequently in patients with clonal hematopoiesis, myelodysplastic syndrome (MDS), an
191 mutations in the peripheral blood is termed clonal hematopoiesis of indeterminate potential (CHIP) a
199 of somatic mutations in blood cell lineages, clonal hematopoiesis of indeterminate potential (CHIP) i
227 lthough the cause of these t-MNs is unknown, clonal hematopoiesis of indeterminate potential (CHIP) v
230 d dysplastic hematopoiesis can be considered clonal hematopoiesis of indeterminate potential (CHIP),
232 logous process happens in a condition called clonal hematopoiesis of indeterminate potential (CHIP),
233 ns in hematopoietic cells, frequently called clonal hematopoiesis of indeterminate potential (CHIP),
247 ith increased inflammatory responsiveness is clonal hematopoiesis of indeterminate potential (CHIP).
248 -lived trained immunity and the emergence of clonal hematopoiesis of indeterminate potential (CHIP).
249 iovascular risk factor has recently emerged: clonal hematopoiesis of indeterminate potential (CHIP).
250 tion sequencing (NGS) discovered age-related clonal hematopoiesis of indeterminate potential (CHIP).
251 critical as underscored by the incidence of clonal hematopoiesis of indeterminate potential associat
252 unotherapy outcomes to account for potential clonal hematopoiesis of indeterminate potential contamin
253 with a focus on the prevalence and impact of clonal hematopoiesis of indeterminate potential in patie
256 In an adenine-induced CKD mouse model, Tet2-clonal hematopoiesis of indeterminate potential was link
257 es describe the emergence and prevalence of "clonal hematopoiesis of indeterminate potential" in aged
258 associated with hyperinflammatory responses (clonal hematopoiesis of indeterminate potential, CHIP),
259 stic boundaries between MDS, MDS/MPNs, sAML, clonal hematopoiesis of indeterminate potential, clonal
260 , acquired somatic mutations associated with clonal hematopoiesis of indeterminate potential, leukocy
262 ave been characterized as frequent events in clonal hematopoiesis of indeterminate potential, suggest
263 atients without MDS/AML also had evidence of clonal hematopoiesis of indeterminate potential-related
265 ng individuals with idiopathic cytopenias or clonal hematopoiesis of undetermined significance, the i
266 nt somatic genetic rescue (SGR) resulting in clonal hematopoiesis, of which 95% was maladaptive (mono
268 in hematopoietic stem and progenitor cells (clonal hematopoiesis or CH) are associated with advanced
270 hieve AML cure and the impact of preleukemic clonal hematopoiesis persistence in predisposing to seco
272 ously illuminates the clonal architecture of clonal hematopoiesis/preleukemic and leukemic cells surv
273 a cross-sectional cohort study, we compared clonal hematopoiesis prevalence in PWH on stable antiret
274 ction, not drift, is the major force shaping clonal hematopoiesis, provide bounds on the number of he
281 In contrast to mutations associated with clonal hematopoiesis (such as Tet2 deletion), the leukem
283 Here, we will review recent studies linking clonal hematopoiesis to altered immune function, inflamm
284 s drives disease evolution from asymptomatic clonal hematopoiesis to frank MDS, and, ultimately, to s
285 Factors that control the conversion from clonal hematopoiesis to MPN disease include inherited pr
286 d across a phenotypic continuum ranging from clonal hematopoiesis to myelodysplastic syndrome (MDS) a
287 ancies exist on a spectrum from asymptomatic clonal hematopoiesis to overt leukemia and exhibit subst
288 re, we developed ArCH, an Artifact filtering Clonal Hematopoiesis variant calling pipeline for detect
292 screened included 40 regions known to drive clonal hematopoiesis when mutated and 64 novel candidate
293 al alterations (mCAs) represent two forms of clonal hematopoiesis where clones bearing expanded somat
294 rom normal, healthy elderly individuals with clonal hematopoiesis who are at increased risk of subseq
295 f ctDNA dynamics in EAC, taking into account clonal hematopoiesis with indeterminate potential (CHIP)
297 n morphologic remission may continue to have clonal hematopoiesis with populations closely related to