ライフサイエンスコーパス: clonal evolution

1 somal abnormalities and their changes during clonal evolution.

2 tterns of nonexpressed genes to characterize clonal evolution.

3 ions may coevolve rather than compete during clonal evolution.

4 hich may cause genomic instability and drive clonal evolution.

5 role of this region in disease phenotype and clonal evolution.

6 e of positive selection and neutral drift in clonal evolution.

7 role of this region in disease phenotype and clonal evolution.

8 cells protected them from TNF-alpha-induced clonal evolution.

9 ession may be more likely to experience such clonal evolution.

10 marked resistant clones selected during the clonal evolution.

11 s the only clinical variable associated with clonal evolution.

12 (range, 10-135 months); 4 patients (11%) had clonal evolution.

13 ting ability and suppresses the tendency for clonal evolution.

14 ions confers a strong advantage during tumor clonal evolution.

15 hogenesis of stem cell diseases and leukemic clonal evolution.

16 ide and copy number variants along the tumor clonal evolution.

17 or blood vessels follow a pattern of dynamic clonal evolution.

18 rates, which drive relapse by Darwinian-type clonal evolution.

19 ts to a model most consistent with divergent clonal evolution.

20 rom 59 patients demonstrated highly frequent clonal evolution.

21 A can allow real-time sampling of multifocal clonal evolution.

22 t of cancer microenvironment and the role of clonal evolution.

23 that persistent lymphocytes do not represent clonal evolution.

24 iscriminant value for identifying cases with clonal evolution.

25 ntial role of ALK mutations in neuroblastoma clonal evolution.

26 apoptosis, promote differentiation, or drive clonal evolution.

27 ignant cells acquire a CSC phenotype through clonal evolution?

28 to 70 years), median time from diagnosis to clonal evolution 14 months (range, 0 to 145 months), and

29 ch an approach can potentially help to avert clonal evolution, a major cause of therapeutic resistanc

30 evaluated for the suppression of cytogenetic clonal evolution after therapy, the cytogenetic response

31 Fifteen patients had clonal evolution alone (AP-CE), 32 had AP features but n

32 However, the dynamic nature of clonal evolution, along with potential fitness costs and

33 Clonal evolution analysis indicates that myeloid related

34 risingly, this work indicates that PNH has a clonal evolution and architecture strikingly similar to

35 es are frequent in AML and permit tracing of clonal evolution and architecture.

36 Chronic inflammation may both initiate clonal evolution and catalyze its expansion from early d

37 n the phenomenon of heterogeneity in cancer--clonal evolution and cell plasticity.

38 inactive genes is indicative of a protracted clonal evolution and consequently, increased risk for tu

39 tic targeting in breast cancer and implicate clonal evolution and expansion of cancer stem-like cells

40 and noncellular elements) and the concept of clonal evolution and heterogeneity have emerged as impor

41 ostically significant CNAs accumulate during clonal evolution and include gains of 1q21 and deletions

42 Clonal evolution and intratumoral heterogeneity drive ca

43 esistance mechanism against immortalization, clonal evolution and malignant progression.

44 t on the mechanisms associated with leukemic clonal evolution and may fundamentally change approaches

45 Clonal evolution and outgrowth of cellular variants with

46 These genes may provide insights to the clonal evolution and progression of breast cancer and hi

47 and the impact of mutation chronology on the clonal evolution and progression of CNL.

48 ve helped to understand the genetic basis of clonal evolution and relapse and the role of inherited g

49 Sequential sample analysis shows clonal evolution and selection of the malignant driving

50 istance to systemic treatment as a result of clonal evolution and selection.

51 aintained by niches that allow for stem cell clonal evolution and selection.

52 Intraclonal variation, followed by clonal evolution and the appearance of a second clone ov

53 -tumour genetic heterogeneity resulting from clonal evolution and the emergence of subclonal tumour p

54 al-time and noninvasive approach to tracking clonal evolution and the emergence of treatment-resistan

55 ith intrinsic chromosomal instability, favor clonal evolution and the frequent emergence in their tee

56 in a cohort of 197 MPN patients and followed clonal evolution and the impact on clinical outcome.

57 ims being to dampen chronic inflammation and clonal evolution and thereby also diminish concurrent di

58 nitors could serve as reservoirs for further clonal evolution and thereby contribute to therapeutic r

59 Evidence for clonal evolution and/or polyclonal secondary kinase muta

60 d: 100 in chronic phase (15 with cytogenetic clonal evolution) and five in accelerated phase.

61 cts are associated with genomic instability, clonal evolution, and chemoresistance in chronic lymphoc

62 ns, are associated with genomic instability, clonal evolution, and chemoresistance in chronic lymphoc

63 A for the identification of DLBCL mutations, clonal evolution, and genetic mechanisms of resistance.

64 matic mutations address tumor heterogeneity, clonal evolution, and mechanisms of resistance to guide

65 telomere length was associated with relapse, clonal evolution, and mortality.

66 nse but was associated with risk of relapse, clonal evolution, and overall survival.

67 ntage of abnormal metaphases, longer time to clonal evolution, and presence of other accelerated-phas

68 development of "premature atherosclerosis," clonal evolution, and second cancer in patients with MPN

69 modulation of disease tempo, disease burden, clonal evolution, and tumor microenvironment in SMM rema

70 tinct cancer subclones, many aspects of this clonal evolution are poorly understood, including the di

71 The two main manifestations of clonal evolution are strong linkage disequilibrium (LD)

72 AR-indifferent' cell state through divergent clonal evolution as a mechanism of treatment resistance

73 Age more than 10 years at time of HSCT, clonal evolution as an indication for transplantation, p

74 iagnosed early-stage CLL or the frequency of clonal evolution as determined by interphase FISH.

75 In conclusion, in patients with clonal evolution as the sole criterion of disease accele

76 at a median interval of 36 months, to study clonal evolution at single-cell resolution.

77 ease after relapse, which is associated with clonal evolution at the cytogenetic level.

78 isotypes suggested ongoing switch events and clonal evolution at the M-PC level.

79 We show that whereas clonal evolution can be summarized as a tree, reticulate

80 Markers of clonal evolution can be used to determine patient risk f

81 Patients with cytogenetic clonal evolution can respond to IFN-alpha therapy, and t

82 Cytogenetic clonal evolution (CE) is a known poor prognostic factor

83 loid leukemia (AML) arises through multistep clonal evolution characterized by stepwise accumulation

84 As clonal evolution could allow Bcr-Abl independent prolife

85 ber changes combined with different modes of clonal evolution create extensive somatic genome diversi

86 mal metaphases (cutoff, 24%), longer time to clonal evolution (cutoff, 24 months), other accelerated-

87 A prognostic classification for cytogenetic clonal evolution defined three groups with complete resp

88 s are frequent in PNH, suggesting a stepwise clonal evolution derived from a singular stem cell clone

89 Multiple genetic events and subsequent clonal evolution drive carcinogenesis, making disease el

90 ated that early HSC pools were permissive to clonal evolution driven by drift.

91 s generally thought to result from branching clonal evolution driven by random mutations that accumul

92 nct senescence barriers to permit unfettered clonal evolution during cancer development: (1) stress-

93 e understanding of genetic heterogeneity and clonal evolution during cancer progression.

94 Continued clonal evolution during disease progression is an import

95 Eighteen patients experienced clonal evolution during follow-up.

96 Among 73 patients assessable for clonal evolution during stable chronic phase, those who

97 lowing monitoring of disease progression and clonal evolution during therapy.

98 may sequentially accumulate during stem cell clonal evolution either through drift (passenger mutatio

99 cing on bone marrow samples and investigated clonal evolution from clonal haemopoiesis to the develop

100 AP crypt diversity is consistent with slower clonal evolution from enhanced stem cell survival, eithe

101 This study aimed to discover if clonal evolution from heterozygous to homozygous mutatio

102 Clonal evolution from lower to higher risk implicated th

103 There is evidence for a distinct clonal evolution from metaplasia to dysplasia in the hum

104 diagnostic and relapse neuroblastomas showed clonal evolution from the diagnostic tumor, with a media

105 hieved a complete suppression of cytogenetic clonal evolution had a median survival of 66 months, wit

106 Patients showing clonal evolution had significantly shorter survival afte

107 Recent studies aimed at defining patterns of clonal evolution have revealed that serial tumors in som

108 lution (HEM-AP), and 24 had AP features plus clonal evolution (HEM-AP + CE).

109 P-CE), 32 had AP features but no evidence of clonal evolution (HEM-AP), and 24 had AP features plus c

110 l diversity are the cancer stem cell and the clonal evolution hypotheses.

111 nsplanted before the age of 10 years, before clonal evolution (ie, myelodysplastic syndrome or acute

112 Because AML is likely preceded by clonal evolution in "preleukemic" hematopoietic stem cel

113 To better understand clonal evolution in AML, we sequenced the genomes of M3-

114 We conclude that AID accelerates clonal evolution in BCR-ABL1 ALL by enhancing genetic in

115 We present a cellular automaton model of clonal evolution in cancer aimed at investigating the em

116 resolution view of genetic heterogeneity and clonal evolution in cancer.

117 astatic melanomas supports a linear model of clonal evolution in cancer.

118 ted and whole-exome sequencing and described clonal evolution in cases for whom paired CHIP and thera

119 od, Rossi et al provide further evidence for clonal evolution in chronic lymphocytic leukemia (CLL) a

120 Our study thus uncovers patterns of clonal evolution in CLL, providing insights into its ste

121 The prognostic significance of clonal evolution in CML is not uniform and is related to

122 characterize genomic architecture and infer clonal evolution in eight tumour biopsies and nine plasm

123 f which, TNFalpha, can induce BM failure and clonal evolution in Fancc-deficient mice.

124 constitutes a new paradigm for the study of clonal evolution in human cancers.

125 Clonal evolution in longitudinal samples mainly occurred

126 , we present current concepts on the role of clonal evolution in lymphoid and myeloid leukemia as a d

127 We propose that clonal evolution in micropathogens be defined as restrai

128 To study clonal evolution in myeloproliferative disorders, we use

129 usion, our study reveals novel insights into clonal evolution in NPM1mut AML.

130 H gene replacement as a mechanism generating clonal evolution in one group.

131 he biology of stem and progenitor cells, and clonal evolution in patients with myeloproliferative neo

132 To address the role of clonal evolution in relapsed NPM1-mutated (NPM1mut) AML,

133 High-dose Cy does not prevent relapse or clonal evolution in SAA.

134 es provides new opportunities for addressing clonal evolution in solid cancers, in particular those w

135 specially regarding secondary malignancies), clonal evolution in the absence of significant BM dyspla

136 le-agent clinical efficacy may be limited by clonal evolution in the advanced leukemic phase of this

137 umor provides data to analyze the process of clonal evolution in the population of cells that give ri

138 dysplasia and provide functional support for clonal evolution in these mice.

139 rated or blast phase on treatment, including clonal evolution, in the nilotinib groups than in the im

140 2%) achieved some suppression of cytogenetic clonal evolution; in 41 patients (46%), the suppression

141 Serial sampling reveals diverse patterns of clonal evolution, including linear evolution, differenti

142 The rate of clonal evolution increased with duration of follow-up wi

143 Clonal evolution is a key feature of cancer progression

144 Clonal evolution is believed to be a main driver for pro

145 Our results indicate that clonal evolution is more complex than predicted by linea

146 nd that--outside secondary lymphoid tissues--clonal evolution is retarded by diminished BCR-signaling

147 This niche succession or crypt clonal evolution is similar to the clonal succession of

148 in addition to the Philadelphia chromosome (clonal evolution) is considered by many to be a feature

149 , abnormal metaphases < 16%, and interval to clonal evolution < or = 24 months) had an estimated medi

150 del for explaining intratumor diversity, the clonal evolution model, has recently been challenged by

151 umoral heterogeneity can be explained by the clonal evolution model, whereby growth advantageous muta

152 Both the hierarchical cancer stem cell and clonal evolution models have been invoked to help explai

153 Clonal evolution occurred among 10% of ZAP-70-negative a

154 Clonal evolution occurs during the course of chronic lym

155 These data support a model in which minimal clonal evolution occurs in the metastatic tumor cell pop

156 The course of clonal evolution of 2 related clones in the blood of a p

157 of abnormal metaphases, time to cytogenetic clonal evolution of 24 months or less, and absence of ot

158 Here we explore the clonal evolution of a form of childhood precursor-B cell

159 wn how induction chemotherapy influences the clonal evolution of a patient's nonleukemic hematopoieti

160 formalize the problem of reconstructing the clonal evolution of a tumor using single-nucleotide muta

161 light these recent reports investigating the clonal evolution of acute leukemia genomes and discuss t

162 Further evidence of clonal evolution of ALK-mutated cells was provided by es

163 Our results explain the genetic basis for clonal evolution of an ETV6-RUNX1 preleukemic clone to p

164 Here we study the clonal evolution of barcoded glioblastoma cells in an un

165 eity indicated genetic divergence during the clonal evolution of breast cancer, particularly at the t

166 r numbers of tumors should cast light on the clonal evolution of cancers in space and time.

167 Interestingly, clonal evolution of CD5(+)B220(dull) cells (judged by BC

168 ng, suggesting that mosaicism as a result of clonal evolution of cells harboring somatic mutations is

169 The clonal evolution of cells with extra copies of 1q sugges

170 mmon genetic alterations observed during the clonal evolution of high grade malignant gliomas.

171 underlying pathogenic role of MLL-PTD in the clonal evolution of human leukemia, which should facilit

172 Clonal evolution of Ig V regions, expression of activati

173 The persistence and dynamic clonal evolution of leukemia-initiating cells and preleu

174 int, and have potential implications for the clonal evolution of malignancies.

175 sting that the chaperone is required for the clonal evolution of melanomas and other tumors that depe

176 man cancers can aid our understanding of the clonal evolution of metastasis and provide a realistic m

177 nct PILs, which is evidence for the separate clonal evolution of multiple pancreatic neoplasms within

178 In addition, the results indicate that the clonal evolution of mutations that are seen within later

179 uired genomic instability and the subsequent clonal evolution of neoplastic cells with variable patte

180 tionary clades and supported a predominantly clonal evolution of NTHi, with the majority of genetic i

181 iversity of O55:H7 and better understand the clonal evolution of O157:H7, we fully sequenced EPEC O55

182 nt variability in the mutational profile and clonal evolution of pediatric AML from diagnosis to rela

183 in human tissues have been used to trace the clonal evolution of progenitor cells in diseased states.

184 that this mutation was an early event in the clonal evolution of resistance.

185 ow genome variations might accumulate during clonal evolution of somatic cell populations, including

186 prognosis, suggesting that they occur during clonal evolution of the disease.

187 y U-CLL and M-CLL cells could be involved in clonal evolution of the disease.

188 presentation and at relapse suggesting that clonal evolution of the IgH locus is unusual in this dis

189 environment-facilitated clonal expansion and clonal evolution of tumor cell populations.

190 ually described as tumor progression, or the clonal evolution of tumor cell populations.

191 he need for novel therapies and suggest that clonal evolution or decreasing platelet counts while on

192 ity to some cancers beyond that explained by clonal evolution or environmental differences.

193 23 months earlier--findings consistent with clonal evolution or multifocal disease.

194 the evolutionary process and the dynamics of clonal evolution over time.

195 We show that clonal evolution patterns are heterogeneous in individua

196 ells at each site, we also proposed distinct clonal evolution patterns between primary and metastatic

197 41 and DAXX) in AML, we also found two major clonal evolution patterns during AML relapse: (1) the fo

198 ing; this allowed us to define clonality and clonal evolution patterns precisely at relapse.

199 iteria that we have proposed for predominant clonal evolution (PCE).

200 state cancer is due to time-dependent cancer clonal evolution (potentially induced by radiation damag

201 ng the timeline of mutations contributing to clonal evolution, pre- and postnatally.

202 e patients have other signs of acceleration, clonal evolution predicts lower response rates and a sho

203 only one of six without treatment) underwent clonal evolution, predominantly involving subclones with

204 may realize its invasive potential through a clonal evolution process driven by definable microenviro

205 Tumorigenesis is a clonal evolution process that is initiated from single c

206 integrated investigations of spatial ITH and clonal evolution provide an important molecular foundati

207 ically occult, altered stem cell turnover or clonal evolution rates may be detected by measuring the

208 ulate more alterations from slower stem cell clonal evolution rather than increased error rates.

209 Our method effectively characterizes clonal evolution, reassortment, and recombination in RNA

210 se to lenalidomide and the drug's effects on clonal evolution remain unknown.

211 However, evidence for various forms of clonal evolution suggests that B-CLL clones may be more

212 Clonal evolution that leads to emergence of a dominant m

213 Here we emphasize a view of clonal evolution that stresses natural selection over de

214 The classic tumor clonal evolution theory postulates that cancers change o

215 nk4a); and (ii) provide an in vitro model of clonal evolution through successive dysfunction of Rb an

216 By taking into account clonal evolution through time-dependent analysis, the ge

217 oid lineage, characterized by cytopenias and clonal evolution to acute myeloid leukemia (AML).

218 ded overall response, survival, relapse, and clonal evolution to myeloid cancer.

219 les AID-induced hypermutation and propagates clonal evolution toward malignant follicular lymphoma.

220 Postnatally acquired mutations then drive clonal evolution toward overt leukemia.

221 roup (*p = 0.018), indicative of a shortened clonal evolution treated sulindac.

222 However, the dynamics of clonal evolution underpinning carcinogenesis remain poor

223 Clonal evolution underpins all facets of adaptive immuni

224 The median survival time following clonal evolution was 19 months.

225 Clonal evolution was analyzed after 4 cycles of treatmen

226 Clonal evolution was defined as the presence of karyotyp

227 Similarly, using SNP-A, earlier clonal evolution was found in 4 of 7 AA patients followe

228 The probability of clonal evolution was higher in patients in the first qua

229 Later in life, clonal evolution was suppressed by stabilizing selection

230 on receptor chromosomes (RCs) and subsequent clonal evolution, we analyzed specimens from 86 patients

231 Minor subclones and/or clonal evolution were also observed, thus potentially li

232 Rates of relapse and clonal evolution were similar to our historical experien

233 resources for the tumour, this gives rise to clonal evolution where only the fittest cells survive.

234 wth regulation and drive successive waves of clonal evolution, whereas a far greater number are funct

235 iated with the addition of new mutations and clonal evolution, which is shaped, in part, by the chemo

236 Ninety patients with CML and cytogenetic clonal evolution who received IFN-alpha-based regimens w

237 trated that AID and RAG1-RAG2 drove leukemic clonal evolution with repeated exposure to inflammatory

238 The software simulates clonal evolution with the emergence of driver and passen

239 ity during therapy demonstrated differential clonal evolution within tumors and putative selection ag