ライフサイエンスコーパス: subclone

1 leads to a strong selection for the fittest subclone.

2 and median number of cells in each resistant subclone.

3 the time required for growth of the improved subclone.

4 ggesting that it was associated with a small subclone.

5 near succession with retention of a dominant subclone.

6 ed cytarabine resistance of a KRAS wild-type subclone.

7 ncides with the re-expansion of the dominant subclone.

8 borious especially if many inserts are to be subcloned.

9 functional differences in genetically unique subclones.

10 without strict interdependence between cell subclones.

11 intratumoral and intertumoral heterogenetic subclones.

12 en TP53 mutations are frequently mapped into subclones.

13 spatial and morphological context of mutant subclones.

14 enes or copy number abnormality in different subclones.

15 and interclonal cooperation between multiple subclones.

16 n the initiation and maintenance of leukemic subclones.

17 cally harbours multiple genetically distinct subclones.

18 basal Hras mutant and luminal Hras wild-type subclones.

19 mutations cause the expansion of cancer cell subclones.

20 emorefractoriness of very small TP53 mutated subclones.

21 ectable lesions harbor at least 10 resistant subclones.

22 and PDAC driver mutations are shared by all subclones.

23 e selection drives the expansion of more fit subclones.

24 ns being present as either dominant or minor subclones.

25 e found in both founding clones and daughter subclones.

26 n of drug-resistant and leukaemia-initiating subclones.

27 erve spatial context and may not detect rare subclones.

28 l subclones or functional hierarchies within subclones.

29 uggesting the emergence of several resistant subclones.

30 s to determine aggressive and non-aggressive subclones.

31 antage, to form large or spatially disparate subclones.

32 ting with more contiguous growth of advanced subclones.

33 ciated with the re-emergence of the dominant subclones.

34 stant niche that encompasses different tumor subclones.

35 through automation followed by single-colony subcloning.

36 s identified by whole plasmid sequencing and subcloning.

37 We subcloned a 4868 base pair (bp) fragment from human BAC

38 agment with a 340 pb upstream pheA1 gene was subcloned, a similar biotransformation rate was attained

39 er-daughter evolution, whereas for >/= three subclones, a branched pattern prevailed.

40 t M2 cells but not in the FLNA-expressing M2 subclone A7; this suggests a role for FLNA in stabilizat

41 the novel approach of ordering the resistant subclones according to their time of appearance, here we

42 The H30 subclone accounted for >/=95% of FQ-R and ESBL-producing

43 Among US veterans, ST131, primarily its H30 subclone, accounts for most antimicrobial-resistant E. c

44 rapy favours selection and expansion of rare subclones already present before ibrutinib treatment, an

45 nolone resistance and was the most prevalent subclone among current E. coli clinical isolates, overal

46 dictable relationship between the engrafting subclone and the evolutionary hierarchy of the leukemia.

47 repetitive and purine-rich ORF15 of RPGR was subcloned and sequenced in heterozygous female subjects

48 ook a unique approach by deriving fibroblast subclones and clonal iPSC lines from the same fibroblast

49 cases have multiple epigenetically distinct subclones and determine the primary subclone from which

50 onstrate the presence of ibrutinib-resistant subclones and estimate subclone size before treatment in

51 s despite the routine emergence of resistant subclones and experience in blast-phase chronic myeloid

52 at least frequently, present within genomic subclones and independent of mutational subclone differe

53 cess, involving the interplay between cancer subclones and the local immune microenvironment.

54 Tect particularly useful for studying cancer subclones and their evolution in standard exome and geno

55 geneity, evaluating the importance of tumour subclones and their growth through both Darwinian and ne

56 n phylogenomic methods to accurately dissect subclones and their phylogenies from noisy and impure bu

57 Minor subclones and/or clonal evolution were also observed, th

58 sduction conditions, followed by single-cell subcloning and a round of antibiotic selection, we find

59 Subcloning and sequencing of ORF15 of RPGR in female sub

60 Sanger sequencing but were validated through subcloning and subsequent sequencing of the subcloned DN

61 n human colon organoids, followed by delayed subcloning and whole-genome sequencing.

62 0.3%) displayed a defined number of distinct subclones, and 166 (39.7%) were classified as composite

63 isolated and subjected to end point RT-PCR, subcloning, and sequencing.

64 in adhesive properties on tumor endothelial subclones are accompanied by decreases in expression of

65 Cytogenetic subclones are frequent in AML and permit tracing of clon

66 However, cryptic subclones are frequently revealed by additional patient

67 This suggests that independent subclones are generated in some patients.

68 Both subclones are required for efficient tumour propagation,

69 and route of metastatic dissemination of the subclones are unknown.

70 rted from the primary tumor and in divergent subclones arising in metastatic foci found in the brain,

71 es diminish in frequency and are replaced by subclones as tumors evolve.

72 d on fimH sequence (fimbrial adhesin gene: H subclone assignments), multilocus sequence typing, gyrA

73 tracking analysis by FISH identified a minor subclone at diagnosis whose genotype matched that observ

74 minant clone at relapse is present as a rare subclone at primary diagnosis.

75 tations acquired at relapse were detected in subclones at diagnosis, suggesting that the mutations ma

76 s of a female premutation carrier, with each subclone bearing exclusively either the normal or the ex

77 that the mutations were present in expanded subclones before the initiation of panitumumab treatment

78 ly comprised of a single genetically defined subclone, but there was no predictable relationship betw

79 tifies the number and genetic composition of subclones by analyzing the variant allele frequencies of

80 virus genotype 1 strain Sar55 replicated in subcloned Caco-2 intestinal cells and Huh7 hepatoma cell

81 from the normal DNA and from multiple tumour subclones-called circulating tumour DNA or ctDNA.

82 llularity samples or in low-proportion tumor subclones can be used for early cancer detection, progno

83 ng numbers of studies are finding that minor subclones can determine clinical disease course, and tha

84 Metastatic subclones can emerge both early and late in the life of

85 selected more aggressive sorafenib-resistant subclones carrying both FLT3-ITD and D835 mutations, and

86 In 5 patients (6.0%), multiple subclones carrying different mutations arose independent

87 oma multiforme, the distribution of sizes of subclones carrying driver mutations had a heavy right ta

88 be provided by temporal ordering of evolving subclones--cellular subpopulations with unique mutationa

89 quencing, clustering of genetic aberrations, subclone combinatorics, and mutational signature analysi

90 tumor, in which various related but distinct subclones compete within the tumor mass.

91 e earliest stages of tumor establishment and subclone competition, fundamentally shifting the way we

92 All founding clones and subclones contained at least one mutation in a coding ge

93 Importantly, the clonal iPSCs and fibroblast subclones contained comparable numbers of de novo varian

94 s in an individual cancer, the nature of the subclones contributing to relapse, and the identity of p

95 ing despite near-complete changes in genomic subclone contribution.

96 ed that the decrease in the size of dominant subclones could be associated with the rise of founding

97 cused attention to ST131, especially its H30 subclone, could reduce infection-related morbidity, mort

98 In order to more accurately identify subclones, define phylogenetic relationships, and probe

99 tors, and heterogeneity can be maintained if subclones depend on each other for survival.

100 on of ctDNA originating from specific tumour subclones depend on multiple factors, making comprehensi

101 e cell phenotypic activity of AR ligands are subclone dependent.

102 proof-of-principle that very minor leukemia subclones detected at diagnosis are an important driver

103 he clinical importance of small TP53-deleted subclones detected at diagnosis in determining the natur

104 under mutation from which multiple, distinct subclones developed.

105 -renewal and proliferative capacities of the subclones differed.

106 omic subclones and independent of mutational subclone differences.

107 Subclones displayed parallel evolution of treatment resi

108 subcloning and subsequent sequencing of the subcloned DNA.

109 entifying a monophyletic clade of metastatic subclones does not provide sufficient evidence to unequi

110 evelopment of a dominant JAK2V617F-homzygous subclone drives erythrocytosis in many PV patients, with

111 ity presents itself through the evolution of subclones during cancer progression.

112 ctive drugs upfront to target drug-resistant subclones during initial treatment to prevent later rela

113 Nonstandard strategies also consider minor subclones, dynamics, and predicted future tumor states.

114 ds and led to the identification of dominant subclones, each containing a unique pair of interacting

115 Subclones exclusive to baseline or surgical cores occur

116 ty reagents and bypassing the time-consuming subcloning experiments.

117 ed that the observed monophyly of metastatic subclones favored metastasis-to-metastasis spread ("a me

118 for variants present at unequal read depths, subcloning followed by colony sequencing.

119 myeloma we modeled this competition between subclones for predominance occurring spontaneously and w

120 Subgroup analysis showed that subclone formation adds prognostic information particula

121 t in the cytogenetically adverse group, with subclone formation in 69.0%, 67.1%, and 64.8% of patient

122 In non-core binding factor AML, subclone formation was associated with inferior event-fr

123 Subclone formation was particularly frequent in the cyto

124 The acquisition of H3K27ac and activity of subcloned fragments in an enhancer reporter assay indica

125 distinct subclones and determine the primary subclone from which the metastatic lesion(s) originated.

126 tigate the CSCs' diversity, we established 4 subclones from a glioblastoma patient.

127 Our results suggest that single cell-derived subclones from a patient can produce phenotypically hete

128 BL cell lines from different tumors, and BL subclones from a single tumor, to compare EBV-negative c

129 variation, we isolated disomic and trisomic subclones from the same parental iPS line, thereby gener

130 monstrate that SC3 is capable of identifying subclones from the transcriptomes of neoplastic cells co

131 were wiped out by some treatment while some subclones gained selective advantage.

132 Relative stasis and occasional rapid subclone growth may characterize colorectal tumorigenesi

133 Unlike other ST131 subclones, H30 was significantly associated with fluoroq

134 This subclone had a unique and conserved gyrA/parC allele com

135 d the outgrowth or emergence of at least one subclone, harboring dozens to hundreds of new mutations.

136 esent in all leukemic populations (including subclones) has been exemplified by acute promyelocytic l

137 e phenotypic and genetic features of the MRD subclone have never been investigated.

138 heterogeneity within tumors, and found that subclones have a variable contribution to relapse.

139 Current methods for subclone hierarchy inference tightly couple the problem

140 enable substantial progress in the field of subclone hierarchy inference.

141 Subclones homozygous for JAK2V617F are more common in po

142 Without strict interdependence between subclones, however, nonproducer cells can free-ride on t

143 cally comprise a founding clone and multiple subclones (i.e., clonal heterogeneity is common).

144 By longitudinal analysis, small TP53 mutated subclones identified before treatment became the predomi

145 We used targeted sequencing to track AML subclones identified by whole-genome sequencing using a

146 fluoroquinolone resistance in this EMRSA-15 subclone in the English Midlands during the mid-1980s ap

147 er these mutations were derived from a small subclone in the primary tumor or represented new variant

148 The gene was subcloned in Saccharomyces cerevisiae for expression and

149 Ultra-deep-NGS identified small TP53 mutated subclones in 28/309 (9%) untreated CLL that, due to thei

150 clonal competition between 2 or more genetic subclones in 70% of the patients with relapse, and stabl

151 ing expectations for the number of resistant subclones in a tumor, with implications for future studi

152 We use it to detect subclones in acute myeloid leukemia and breast cancer sa

153 ain tumor clone, primary tumor subclones, or subclones in an axillary lymph node metastasis.

154 rstood, including the diversity of different subclones in an individual cancer, the nature of the sub

155 l cooperation between epithelial tumour cell subclones in mammals is lacking.

156 urred as secondary abnormalities, present in subclones in one-half of the cases.

157 ons, and even growth promotion of nonmutated subclones in some cases.

158 nd distant metastases arose from independent subclones in the primary tumor, whereas in 35% of cases

159 d us to study the properties of distinct AML subclones, including differential drug susceptibilities

160 n situ hybridization (FISH) of infected cell subclones indicated the retention of het DNA in an integ

161 characterise the TcNr, the coding region was subcloned into an expression vector and transformed into

162 are generated by phage display are typically subcloned into an expression vector for further biochemi

163 region of the MG192 gene was PCR amplified, subcloned into plasmids, and sequenced.

164 e GEM2010MAS65 study and showed that the MRD subclone is enriched in cells overexpressing integrins (

165 e same parental iPS line, thereby generating subclones isogenic except for chromosome 21.

166 tion improved the prognosis of patients with subclone karyotypes as shown in landmark analyses.

167 cell line KB-3-1 and its multidrug-resistant subclone KB-V1.

168 Monitoring genomic subclone kinetics in three patient tumors and correspond

169 drug initially modulates the distribution of subclones, loss of treatment efficacy coincides with the

170 tumor correlated strongly with the number of subclones (<10% of the tumor).

171 distinguishing and isolating distinct cancer subclones, many aspects of this clonal evolution are poo

172 Thus, characterization of the minor MRD subclone may represent a unique model to understand chem

173 We derived a series of subcloned MCF7 cell lines that were either highly sensit

174 idence is emerging for parallel evolution of subclones, mediated through distinct somatic events conv

175 Alternatively, breast cancer subclones might interact cooperatively to gain a selecti

176 ly high intratumoral heterogeneity (ITH) and subclone mixing in distant regions, as postulated by our

177 r, some tumors appear 'born to be bad', with subclone mixing indicative of early malignant potential.

178 Computational modeling suggests that subclones must arise sufficiently early, or carry a cons

179 Lastly, using subcloned normal fibroblast cells, we demonstrated the h

180 T cell levels are negatively associated with subclone number.

181 ical data on the relative sizes of resistant subclones obtained from liquid biopsies of colorectal ca

182 Minimal expansion of these subclones occurs until many hundreds to thousands of mut

183 not seen with equivalent growth of the 66C4 subclone of 4T1, in which MDSC expansion does not occur.

184 exclusive or occur sequentially in the same subclone of cells.

185 c SC population, which was also present in a subclone of CML-SCs during the chronic phase in a patien

186 te to the epidemiologic success of the H30Rx subclone of E. coli ST131.

187 on, allows HCV to replicate in HRP1 cells, a subclone of Huh-7 cells permissive for HCV replication.

188 gene, is responsible for HRP4 cells, another subclone of Huh-7 cells, being permissive for HCV replic

189 icating that gastric cancer can arise from a subclone of the founder mutation.

190 and evolved into the relapse clone, or (2) a subclone of the founding clone survived initial therapy,

191 associated with tumor cells or a particular subclone of tumor cells.

192 ly high, and for identifying lesions in rare subclones of a tumor when tumor purity is sufficient to

193 etastatic potential, arose within detectable subclones of antecedent lesions.

194 invasive infections were caused by multiple subclones of epidemic emm59 GAS strains likely spread to

195 at understanding the mechanism through which subclones of Huh-7 cells become permissive for HCV repli

196 cells, but it replicates robustly in certain subclones of Huh-7 cells.

197 dividual patients there are multiple genetic subclones of leukemia-initiating cells, with a complex c

198 Moreover, genetically diverse evolving subclones of mutant SF3B1 exist in mice, indicating a br

199 Distinct subclones of PK1 cells mediate swainsonine inhibition to

200 tent stem cell-derived neurons from isogenic subclones of primary fibroblasts of a female premutation

201 ome sequences for two geographically distant subclones of the cancer.

202 We generated a model of bortezomib-adapted subclones of the MCL cell lines JEKO and HBL2 that were

203 ighted effect of dominant neoantigens in the subclones of the tumour.

204 ovides an effective strategy for directional subcloning of DNA fragments from Bacteria Artificial Chr

205 Further, to facilitate the subcloning of the fragment cloned into other targeting o

206 nce of a substitute Wnt source, the original subclones often evolve to rescue Wnt pathway activation

207 ected differential kinetics among individual subclones or functional hierarchies within subclones.

208 o either the main tumor clone, primary tumor subclones, or subclones in an axillary lymph node metast

209 alysis estimated that the population of this subclone over the last 20 yr has grown four times faster

210 evolution and the waxing and waning of tumor subclones over time in advanced metastatic epithelial ma

211 We report here the subcloning, overexpression, and a robust but novel metho

212 Two-subclone patterns typically followed a mother-daughter e

213 alysis revealed at least two to four genetic subclones per sample.

214 The conventional hybridoma screening and subcloning process is generally considered to be one of

215 o detect ST131 and its ESBL-associated H30Rx subclone, pulsed-field gel electrophoresis, extended vir

216 r regression and relapse revealed that basal subclones recruit heterologous Wnt-producing cells to re

217 Viral subclones representing these forms were isolated by limi

218 g the emergence of genetically heterogeneous subclones, rescue signals in the microenvironment, and t

219 t given the need to understand the nature of subclones responsible for the refractory and relapsed di

220 et of cancer growth and not in later-arising subclones, resulting in numerous passenger mutations tha

221 netically distinct CSCs exist on top of each subclone, revealing a highly complex cellular compositio

222 guingly, three metastatic and chemoresistant subclones, S2-CP9, S2-LM7AA, and S2-013, exhibit up-regu

223 We present subclone sensitive cell phenotypic pharmacology of ligan

224 In this study, we subcloned, sequenced, and expressed the genes encoding 5

225 The MRD subclone showed significant downregulation of genes rela

226 Bortezomib-adapted subclones showed increased proteasome activity and toler

227 Patients harboring small TP53 mutated subclones showed the same clinical phenotype and poor su

228 Subclones showed variable engraftment potential in immun

229 with PHF6 expression in three TMZ-resistant subclones significantly enhanced TMZ-induced cell kill i

230 f ibrutinib-resistant subclones and estimate subclone size before treatment initiation.

231 ity of bloodstream infections, including one subclone (ST131-H30) responsible for 28% of bacteremic E

232 Other alterations that could define subclones such as structural variants or epigenetic modi

233 conditioned medium of T24 vs. its metastatic subclone T24M bladder cancer cells allowed the identific

234 ts in the emergence of a more drug-resistant subclone that exhibits ERK activation.

235 are consistent with emergence of a resistant subclone that has acquired spontaneous mutations largely

236 nostic biomarker strategies, where the tumor subclone that may ultimately influence therapeutic outco

237 ases typically arose from a common ancestral subclone that was not detected in the primary tumor biop

238 hat the B-LBLs developed from preexistent FL subclones that accumulated additional genetic damage.

239 entire disease course identified 2 competing subclones that alternate in a back and forth manner for

240 ngle expansion producing numerous intermixed subclones that are not subject to stringent selection an

241 these phenotypes pre-exist in pre-treatment subclones that become dominant after chemotherapy, indic

242 e additional cooperating mutations, yielding subclones that can contribute to disease progression and

243 patterns of subclonal evolution, to identify subclones that decline or expand over time, and to detec

244 ce that a brain tumor contains heterogeneous subclones that exhibit dissimilar morphologies and self-

245 appropriately restricted to cells generating subclones that have established malignant properties.

246 miR-135a expression in paclitaxel-resistant subclones that were established in vivo.

247 ns, pocketed with occasional newly generated subclones that were the result of recent rapid clonal ex

248 ntities; (2) mutations, typically arising in subclones, that may influence prognosis but are unlikely

249 rom ET by expansion of a dominant homozygous subclone, the selective advantage of which is likely to

250 In a mouse model featuring xenografts of the subclones, the progression and invasion of tumors and an

251 Expansion of the dominant subclone to an appreciable mass may therefore represent

252 Moreover, the sensitivities of the subclones to an inhibitor of epidermal growth factor rec

253 onstruct the phylogeny of metastases and map subclones to their anatomic locations.

254 pproach based on RNA sequencing of resistant subclones, to discover the molecular mechanisms of sensi

255 These two genes were subcloned together as a 2 kb fragment into Escherichia c

256 We found that virtually all AML subclones trafficked from the marrow to the peripheral b

257 orm of several driver genes mutated in small subclones underlying the disease course.

258 sponse (odds ratio [OR] 1.99, P = .036) when subclones unlikely to be detected by Sanger sequencing (

259 Genetic analysis of the AnR subclones versus parental cells via next generation sequ

260 cDNA-microarray analyses revealed that each subclone was composed of distinct populations of cells.

261 The evolution of these subclones was associated with distinct genetic aberratio

262 The paclitaxel-resistant phenotype of these subclones was maintained upon retransplantation in new m

263 ses, selection of dominant, relapse-specific subclones was observed over time.

264 ST131 and its H30 subclone were detected by polymerase chain reaction and

265 Cytogenetic subclones were detected in 418 (15.8%) of 2,639 patients

266 Four stable subclones were established and used to profile a library

267 Overall, these subclones were frequently below current standard detecti

268 In contrast, the vast majority of subclones were present at <10% frequency, many of which

269 Few subclones were present based on PyClone analysis.

270 ants detected in clonal iPSCs and fibroblast subclones were rare variants inherited from the parental

271 These subclones were subsequently propagated and analyzed.

272 Two HMC-1 subclones were used, HMC-1.1 lacking KIT D816V and HMC-1

273 Minor subclones were validated by independent approaches.

274 rs are composed of genetically heterogeneous subclones which may diverge early during tumour growth.

275 pond to tamoxifen in sensitive vs. resistant subclones, which also predicts disease-free survival in

276 cancer and the characterization of emerging subclones, which seed metastatic sites, might offer new

277 se transformation, and links the presence of subclones with adverse clinical outcomes.

278 Minor subclones with alternative post-switch isotypes suggeste

279 d tumour load and selective reduction of CLL subclones with ATM or TP53 alterations.

280 le mutations and are potentially composed of subclones with differing mutational composition, renderi

281 nt clonal evolution, predominantly involving subclones with driver mutations (e.g., SF3B1 and TP53) t

282 The presence or emergence of distinct subclones with drug-resistant genetic and epigenetic phe

283 the CRCs further diversified into different subclones with heterogeneous mutation profiles accumulat

284 ness threshold to prevent the propagation of subclones with high-level BRAF(amp).

285 53 mutations is linked with the expansion of subclones with metastatic potential which we can detect

286 ged leukemia allowed development of leukemic subclones with newly acquired PTEN microdeletions.

287 and spheroids was driven by multiple genomic subclones with profoundly differing growth dynamics and

288 We hypothesized that rare subclones with SETBP1 mutations are present at diagnosis

289 specimens and the difficulties in resolving subclones with whole exome sequencing.

290 The H30 subclone within Escherichia coli sequence type 131 (ST13

291 these additional mutations arose either as a subclone within the PIGA-mutant population, or prior to

292 s epithelial tissue architecture, individual subclones within a malignant microenvironment are common

293 change over time to produce unique molecular subclones within a parent neoplasm, presumably including

294 process, often leading to multiple competing subclones within a single primary tumour.

295 cordance between the typology and fimH-based subclones within ST131, with accurate identification of

296 story of metastases, a complete phylogeny of subclones within the primary tumor facilitates the ident

297 n the absence of a complete phylogeny of the subclones within the primary tumor, a scenario of parall

298 stases should obtain a complete phylogeny of subclones within the primary tumor.

299 ion pathway, or protein complex in different subclones within the same tumor.

300 gely due to drug-refractory sub-populations (subclones) within heterogeneous tumors.