ライフサイエンスコーパス: subclone

1 bsequent kinetics of the mutant subclone (or subclones).

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

3 near succession with retention of a dominant subclone.

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

5 leads to a strong selection for the fittest subclone.

6 and median number of cells in each resistant subclone.

7 t is present within the genetically distinct subclones.

8 ls and small clusters of treatment-resistant subclones.

9 4) for patients with three or more resistant subclones.

10 spatial and morphological context of mutant subclones.

11 and PDAC driver mutations are shared by all subclones.

12 erve spatial context and may not detect rare subclones.

13 l subclones or functional hierarchies within subclones.

14 uggesting the emergence of several resistant subclones.

15 s to determine aggressive and non-aggressive subclones.

16 antage, to form large or spatially disparate subclones.

17 ting with more contiguous growth of advanced subclones.

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

19 stant niche that encompasses different tumor subclones.

20 functional differences in genetically unique subclones.

21 without strict interdependence between cell subclones.

22 intratumoral and intertumoral heterogenetic subclones.

23 en TP53 mutations are frequently mapped into subclones.

24 enes or copy number abnormality in different subclones.

25 and interclonal cooperation between multiple subclones.

26 ranching evolution with invasion of multiple subclones.

27 n the initiation and maintenance of leukemic subclones.

28 cally harbours multiple genetically distinct subclones.

29 onstructs the phylogenetic tree relating the subclones.

30 ns between drug-sensitive and drug-resistant subclones.

31 ples were collections of genetically diverse subclones.

32 are needed to track the spread of the ST131 subclones.

33 dence for selective sweeps favoring multiple subclones.

34 al metastases composed of driver and neutral subclones.

35 y associated with a selective sweep of unfit subclones.

36 iple-mutated from DNMT3A/NPM1 double-mutated subclones.

37 s identified by whole plasmid sequencing and subcloning.

38 through automation followed by single-colony subcloning.

39 lation and capable of matrix mineralization, subclones 14 and 24 do not faithfully replicate these ke

40 The majority of subclones (29/46, 60%) share superficial and invasive ph

41 erved between the gene expression profile of subclone 4 and primary calvarial osteoblasts.

42 Specifically, whereas subclone 4 is responsive to PTH stimulation and capable

43 compare the commercially available MC3T3-E1 subclones 4, 14, and 24 in terms of responsiveness to os

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

45 tumor development that includes mixtures of subclones, accumulation of somatic aberrations, infiltra

46 tains them through early drug exposure, rare subclones acquire genetic changes that enable their rapi

47 clones, particularly relationship with T790M subclone, affect patients' outcomes.

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

49 O cells had impaired expansion of the CD133+ subclone and its enrichment after chemotherapy, reduced

50 O cells had impaired expansion of the CD133+ subclone and its enrichment after chemotherapy, reduced

51 tion stimulated by the IL11-expressing minor subclone and showed that the depletion of neutrophils pr

52 at may shape the emergence of immune-evading subclones and aggressive clinical phenotypes.

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

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

55 They consist of varying cell populations or subclones and each subclone is characterized with a dist

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

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

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

59 sters single cells into genetically distinct subclones and reconstructs the phylogenetic tree relatin

60 ecent studies, selection is often present on subclones and that multiple evolutionary models can oper

61 Understanding the number of distinct subclones and the evolutionary relationships between the

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

63 fining the landscape of heterogeneous tumour subclones and their biological functions using radiogeno

64 lineage trees based on SHM semblance between subclones and their discordance from the germline sequen

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

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

67 one, that jointly estimates the genotypes of subclones and their proportions in the samples.

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

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

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

71 ccurrence rates, wide presence in many tumor subclones, and are predicted to bind to the most frequen

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

73 However, cryptic subclones are frequently revealed by additional patient

74 g an integrated evolutionary analysis, minor subclones are identified in 9 patients that expanded in

75 Both subclones are required for efficient tumour propagation,

76 step, possible clusterings of mutations into subclones are scored and a user defined number are selec

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

78 varial cell line MC3T3-E1 and its derivative subclones are widely used models of osteoblast biology.

79 clonal invasion, and invasive and metastatic subclones arise early along the ancestral trees.

80 o models respectively predict a hierarchy of subclones arranged by phenotype, or multiple subclones w

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

82 Relative prevalence of two subclones associated with cell cycle and primary immunod

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

84 Metastatic subclones at autopsy were present in tissue and blood sa

85 The number of resistant subclones at diagnosis was found to be a significant pre

86 Our data demonstrate that each subclone bears little functional resemblance to the othe

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

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

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

90 enefit of the tumour because non-cooperative subclones can constantly invade and free-ride on the dif

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

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

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

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

95 The outgrowth of tumor subclones carrying mutations in genes responsible for re

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

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

98 Finally, by analysing the growth rates of subclones compared with their parental clones, we quanti

99 classify patients into groups with distinct subclone compositions.

100 ibit clonal dominance with a small number of subclones comprising the vast majority of the tumor; the

101 genes often occur more than once in distinct subclones, consistent with increasing clonal diversity.

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

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

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

105 erlie poor clinical outcomes because diverse subclones could be comprised of metastatic and drug resi

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

107 ess where older patients accumulate distinct subclones defined by recurring somatic mutations in hema

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

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

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

111 Cancer subclones derived from immune cold regions were more clo

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

113 -renewal and proliferative capacities of the subclones differed.

114 omic subclones and independent of mutational subclone differences.

115 Subclones displayed parallel evolution of treatment resi

116 subcloning and subsequent sequencing of the subcloned DNA.

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

118 us musculus, and enabled detection of mutant subclones down to 20% of the cellularity of the crypt (~

119 lorectal cancer wherein a fast-growing tumor subclone downregulated LINE-1, prompting us to examine h

120 Multiple subclones drive disease progression, creating a therapeu

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

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

123 ukemia initiating capabilities of individual subclones evolving in parallel.

124 Subclones exclusive to baseline or surgical cores occur

125 l and irradiated tumors were consistent with subclone expansion and contraction, that is, subpopulati

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

127 surface markers that could be used to purify subclones for further study.

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

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

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

131 naling; however, we were able to grow stable subclones from each population.

132 ation space, diversifying more recently than subclones from immune hot regions.

133 AC showed, in 90% of patients, that multiple subclones from the primary tumor spread very rapidly fro

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

135 ngle-cell analyses reveal that these genetic subclones gain copy number amplifications of the insulin

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

137 Escherichia coli sequence type (ST) 131-H30R subclone (H30) is a leading cause of multidrug-resistant

138 NA-Seq results suggested that the metastatic subclones had greater activation of EMT-related gene net

139 ty can drive the evolution of multiple tumor subclones harboring unique resistance mechanisms in an i

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

141 p of recurrent tumors comprises thousands of subclones, has a clonal architecture similar to primary

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

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

144 Current methods for subclone hierarchy inference tightly couple the problem

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

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

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

148 respect to tree reconstruction accuracy and subclone identification.

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

150 ed H18N11 virus in Madin-Darby canine kidney subclone II cells and detected two mammal-adapting mutat

151 rby canine kidney, Madin-Darby canine kidney subclone II, and human lung adenocarcinoma [Calu-3] cell

152 population that may randomly produce evasive subclones, imparting transient protection against the ef

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

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

155 on the strength of competition among various subclones in a tumor.

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

157 odological inability to detect low-frequency subclones in bulk DNA.

158 es for non-cell-autonomous drivers and minor subclones in metastasis.

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

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

161 undances varied between patients and between subclones in the same tumor.

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

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

164 irectly synthesized as DNA that is ready for subcloning into appropriate delivery vectors, for both i

165 rying cell populations or subclones and each subclone is characterized with a distinct single nucleot

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

167 lection and expansion of only N-gly-positive subclones is evidence of the tumor cells' dependence on

168 g the evolutionary relationships between the subclones is generated.

169 Monitoring genomic subclone kinetics in three patient tumors and correspond

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

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

172 ptomes and genotyping confirmed that genetic subclones mapped to distinct clades, as inferred solely

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

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

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

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

177 T cell levels are negatively associated with subclone number.

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

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

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

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

182 The multidrug-resistant H30 subclone of E. coli ST131 is responsible for the great m

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

184 C3A is a subclone of the human hepatoblastoma HepG2 cell line wit

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

186 high-confidence ASD mutations engineered in subclones of a human pluripotent stem cell line can be i

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

188 Here, we show that minor subclones of breast cancer cells expressing IL11 and FIG

189 molecular signatures of genetically distinct subclones of cancer cells.

190 Recent evidence of within-patient subclones of M. abscessus in adults with CF suggests the

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

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

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

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

195 rrence and subsequent kinetics of the mutant subclone (or subclones).

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

197 composition and relationship among resistant subclones, particularly relationship with T790M subclone

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

199 servation of N-gly sites in more than 96% of subclone populations within and across diagnostic, progr

200 ing indicates these two tumors had resistant subclones prior to treatment and rates of resistance-rel

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

202 r cell lines and their oxaliplatin-resistant subclones, promoted DNA single- and double-strand break

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

204 Evaluation of mutation rates on the level of subclones rather than individual genes allows to capture

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

206 ce, especially in the absence of preexisting subclones, remains unclear.

207 Viral subclones representing these forms were isolated by limi

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

209 cal resection of early-stage NSCLC represent subclones responsible for subsequent disease relapse.

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

211 ial, along with two metastatic Suit2-derived subclones, S2-013 and S2-LM7AA, which have upregulated S

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

213 The selected subclone SCAP-O(BCOR-mut) expressed only the mutated BCO

214 We found that after reprogramming SCAP-O or subclone SCAP-O(BCOR-mut) into iPSCs, some of the iPSC c

215 We reprogrammed SCAP-O and subclone SCAP-O(BCOR-mut) into transgene-free iPSCs usin

216 We subcloned SCAP-O and separated SCAP-O(BCOR-WT) and SCAP-

217 We present subclone sensitive cell phenotypic pharmacology of ligan

218 The MRD subclone showed significant downregulation of genes rela

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

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

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

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

223 experimental conditions, though the specific subclone studied is often not specified.

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

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

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

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

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

229 is in part caused by Darwinian selection of subclones that arise by random (epi)genetic aberrations.

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

231 progression and metastasis often arise from subclones that can develop naturally or during therapy,

232 we identified the mosaic of malignant B-cell subclones that coexist within a FL and examined the char

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

234 ing methods by allowing the deconvolution of subclones that have independent copy number variation ev

235 entify the biological activities of specific subclones that predict prognosis in a noninvasive and cl

236 ure dramatically selected for rare resistant subclones that were initially undetectable.

237 expanded during transformation and stem cell subclones that were not detectable in MDS blasts became

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

239 integrates prior belief about the number of subclones, the composition of the tumor and the process

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

241 Subcloning these late passage cells to clonal density, t

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

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

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

245 eterminants governing the evolution of tumor subclones toward phylogenetic branches or fixation remai

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

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

248 rence of mutation rates of individual cancer subclones using single-cell sequencing data.

249 ize the behavior of FastClone in identifying subclones using stage III colon cancer primary tumor sam

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

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

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

253 A hierarchy of subclones was visualized through lineage trees based on

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

255 Overall, these subclones were frequently below current standard detecti

256 Rare N-gly-negative subclones were lost or negligible from successive events

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

258 Few subclones were present based on PyClone analysis.

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

260 These subclones were subsequently propagated and analyzed.

261 Minor subclones were validated by independent approaches.

262 own as HIF1B), TERT and MYC) within separate subclones, were present in 37% of tumours.

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

264 h samples usually mix several distinct tumor subclones, which confounds the discovery of the tumor ph

265 essive events, in contrast to N-gly-positive subclones, which could additionally migrate between anat

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

267 S and IDH2 arise, mostly as FLT3-independent subclones, while TET2 and IDH1 predominantly co-occur wi

268 y defined by the expansion or emergence of a subclone with a unique set of mutations.

269 Minor subclones with alternative post-switch isotypes suggeste

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

271 Ongoing SHM of the N-gly sites resulted in subclones with different amino acid compositions across

272 resent within the patient, which can include subclones with differing antimicrobial resistance profil

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

274 at some primary melanomas may be composed of subclones with differing mutational profiles.

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

276 Reprogramming preferentially captured early subclones with fewer mutations, which were rare among si

277 (ITH) could represent clonal evolution where subclones with greater fitness confer more malignant phe

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

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

280 53 mutations is linked with the expansion of subclones with metastatic potential which we can detect

281 rsity and did not allow for the detection of subclones with mutations previously associated with macr

282 nstrates treatment resistance, selecting for subclones with mutations to the remaining copies of PTEN

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

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

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

286 subclones arranged by phenotype, or multiple subclones with shared phenotypes.

287 umors indicates the expansion of co-evolving subclones with similar malignant potential in absence of

288 to decompose the tumor samples into several subclones with the objective of forming a minimum perfec

289 mours are often heterogeneous, consisting of subclones with various genetic alterations and functiona

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

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

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

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

294 ar, parallel clonal evolution, with distinct subclones within pre-MDS-SC and MDS-SC contributing to g

295 oroquinolone-resistant [FQR]) H30R and H30Rx subclones within sequence type 131 (ST131).

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

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

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

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

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