ライフサイエンスコーパス: aneuploidy

1 the development of genomic instability with aneuploidy.

2 d to spindle microtubule disorganization and aneuploidy.

3 d to alleviate the fitness defect induced by aneuploidy.

4 F depletion show a lag in the cell cycle and aneuploidy.

5 py of the genome is better tolerated than is aneuploidy.

6 ochore attachments, lagging chromosomes, and aneuploidy.

7 PC/C), to delay anaphase, thereby preventing aneuploidy.

8 al question relevant to maternal age-related aneuploidy.

9 ecocious chromosome segregation and suppress aneuploidy.

10 incorrect chromosome segregation, generating aneuploidy.

11 induces defective chromosome segregation and aneuploidy.

12 d congression, putting the oocyte at risk of aneuploidy.

13 cocious onset of anaphase, which can lead to aneuploidy.

14 cal carcinogenesis that predisposes cells to aneuploidy.

15 of microtubules, abnormal nuclear shape, and aneuploidy.

16 rvival of telomerase loss and occurs through aneuploidy.

17 ld affect chromosome segregation and lead to aneuploidy.

18 yploidies in the same cell and low levels of aneuploidy.

19 s precocious sister-chromatid separation and aneuploidy.

20 l cycle regulation, proliferation, death and aneuploidy.

21 te chromosome segregation and for preventing aneuploidy.

22 of CDKN2A followed by TP53 inactivation and aneuploidy.

23 ous to normal cells because of the burden of aneuploidy.

24 d insights into the genetic risk factors for aneuploidy.

25 , succumb to enhanced tumour development and aneuploidy.

26 hments that could lead to missegregation and aneuploidy.

27 ty is essential for its function in limiting aneuploidy.

28 synapsis, thereby minimizing transmission of aneuploidy.

29 nd treatment responses of diseases caused by aneuploidy.

30 r activities by producing massive chromosome aneuploidy.

31 ar organization in health and sex chromosome aneuploidy.

32 ncer, but not in in a manner associated with aneuploidy.

33 ting cells with mitotic aberrations to limit aneuploidy.

34 nated with chromosome segregation to prevent aneuploidy.

35 ome instability gene expression patterns and aneuploidy.

36 int maintains genomic stability and prevents aneuploidy.

37 hromosome segregation failure and consequent aneuploidies.

38 for understanding the maternal age effect on aneuploidies.

39 osity (LOH), and whole or partial chromosome aneuploidies.

40 e use of cfDNA testing detected all cases of aneuploidy (5 for trisomy 21, 2 for trisomy 18, and 1 fo

41 Aneuploidy, a condition that results from unequal partit

42 ckpoint acts during cell division to prevent aneuploidy, a hallmark of cancer.

43 Chromosome instability leads to aneuploidy, a state in which cells have abnormal numbers

44 Aneuploidy, a state of karyotype imbalance, is a hallmar

45 Specifically, X-chromosome aneuploidy accentuated normative rightward inferior fron

46 However, development of specific aneuploidies allows rapid adaptation to cellular stresse

47 Aneuploidy, also known as somatic copy number alteration

48 Patients with chromatin-spliceosome and TP53-aneuploidy AML had poor outcomes, with the various class

49 Aneuploidy, an abnormal chromosome number that deviates

50 Aneuploidy, an imbalanced karyotype, is a widely observe

51 and cells, vary in their ability to tolerate aneuploidy, an unbalanced chromosome complement.

52 existing theories about the origin of human aneuploidies and highlighting a novel reverse segregatio

53 hanisms that can withstand gross chromosomal aneuploidy and (2) X and Y chromosomes can exert focal,

54 ls, and yet the precise relationship between aneuploidy and a cell's proliferative ability, or cellul

55 paradox and share an unexpected link between aneuploidy and aging that was discovered through attempt

56 ds to neurodegeneration in FTLD, we measured aneuploidy and apoptosis in brain cells from patients wi

57 FTLD-causing mutations in human MAPT induce aneuploidy and apoptosis in the mammalian brain.

58 MAPT mutations and identified both increased aneuploidy and apoptosis in the same brain neurons and g

59 s a direct relationship between MAPT-induced aneuploidy and apoptosis, we expressed FTLD-causing muta

60 nic mice led to aberrant mitosis followed by aneuploidy and apoptosis.

61 hism (SNP) markers for clinical diagnosis of aneuploidy and biomedical research into its causes is be

62 re, we investigated the relationship between aneuploidy and cancer development using cells engineered

63 ssary, but not sufficient to protect against aneuploidy and cancer.

64 such spindle assembly factors can result in aneuploidy and cancer.

65 ights into the complex relationships between aneuploidy and carcinogenesis.

66 ications to address the relationship between aneuploidy and cellular fitness.

67 ionally, we demonstrate that miR-26a induces aneuploidy and centrosome defects and enhances tumorigen

68 We applied this approach to characterize aneuploidy and chromosomal alterations from a series of

69 clear transport, but was a potent inducer of aneuploidy and chromosomal instability.

70 ted MAPT mutations and altered function with aneuploidy and chromosome instability in human lymphocyt

71 Although excess centrosomes can lead to aneuploidy and chromosome instability in tumor cells, ho

72 rs exhibited a significantly higher level of aneuploidy and copy number alterations compared with the

73 Aneuploidy and copy-number alterations (CNAs) are a hall

74 re acts to integrate protection against both aneuploidy and DNA damage by preventing production of ab

75 Aneuploidy and epigenetic alterations have long been ass

76 orrelated with the tissue-specific levels of aneuploidy and genetic heterogeneity observed in primary

77 ells characteristically show a high level of aneuploidy and genomic instability.

78 expression-based score that correlates with aneuploidy and has prognostic value in many types of can

79 enges in data analysis, complicated by tumor aneuploidy and heterogeneity as well as normal cell cont

80 Variability increases with degree of aneuploidy and is partly due to gene copy number imbalan

81 remature progression through mitosis, marked aneuploidy and mitotic catastrophe.

82 normal human cells and found that they cause aneuploidy and mitotic spindle defects that then result

83 ically unstable due to increased chromosomal aneuploidy and more aggressive.

84 Both aneuploidy and polyploidy can arise from multinucleate s

85 Cdc20-binding domains of BubR1 in preventing aneuploidy and safeguarding against cancer.

86 contribute to increased incidence of oocyte aneuploidy and spontaneous abortion in aging females.

87 urthermore, these mice exhibited DNA damage, aneuploidy and spontaneous tumorigenesis in the liver.

88 ene in mice causes centrosome amplification, aneuploidy and spontaneous tumorigenesis.

89 P88-NUP98-RAE1-APC/CCDH1 axis contributes to aneuploidy and suggest that it may be deregulated in the

90 verexpression of Aurora B in vivo results in aneuploidy and the development of multiple spontaneous t

91 numerary centrosomes are sufficient to drive aneuploidy and the development of spontaneous tumors in

92 e findings provide an important link between aneuploidy and the stress pathways activated by Aurora B

93 Polyploidy can lead to aneuploidy and tumorigenesis.

94 t enables the loss of HJURP to induce severe aneuploidy and, ultimately, apoptotic cell death.

95 ed CIN25 and CIN70 gene expression patterns, aneuploidy, and defects in mitosis.

96 wed extensive gene amplifications, pervasive aneuploidy, and fission of chromosomes 30 and 36.

97 mosome missegregation events, propagation of aneuploidy, and genetic heterogeneity in xenograft model

98 ation, leading to chromosome missegregation, aneuploidy, and ultimately cell death.

99 ionally been based on assumptions that these aneuploidies are lethal or associated with poor quality

100 Aneuploidies are prevalent in the human embryo and impai

101 Gains of chromosome arm 12p and aneuploidy are nearly universal in GCTs, but specific so

102 Whole chromosome gains or losses (aneuploidy) are a hallmark of 70% of human tumors.

103 enotypes, extra copies of whole chromosomes (aneuploidy) are generally strongly deleterious.

104 Finally, we will discuss the role of aneuploidy as an inducer of proteotoxic stress and poten

105 ion, Mcph1 deficiency significantly enhanced aneuploidy as well as abnormal centrosome multiplication

106 lae, this centriole retention contributes to aneuploidy, as centrioles amplify during papillar endocy

107 How the aneuploidy-associated stresses affect cells and whether

108 e potential efficacy of this strategy toward aneuploidy-based azole resistance in Candida albicans.

109 (7 known cancers among 39 cases of multiple aneuploidies by NIPT, 18% [95% CI, 7.5%-33.5%]).

110 ations of noninvasive prenatal screening for aneuploidy by analysis of circulating cell-free DNA (cfD

111 ized by in situ co-examination of chromosome aneuploidy by FISH and immunostaining of multiple biomar

112 oninvasive prenatal testing (NIPT) for fetal aneuploidy by scanning cell-free fetal DNA in maternal p

113 This mechanism of aneuploidy bypasses the known spindle assembly checkpoin

114 However, there is also evidence that aneuploidy can arise in response to specific challenges

115 cell line, we report that the dose effect of aneuploidy can be further compensated at the translation

116 but not others, the dose effect of segmental aneuploidy can be moderately compensated at the mRNA lev

117 Overall, our data show that aneuploidy can confer selective advantage to human cells

118 These results suggest that aneuploidy can directly cause epigenetic instability and

119 These findings indicate that aneuploidy can increase the adaptability of cells, even

120 Overall, our study shows that aneuploidy can induce chromosome mis-segregation.

121 lmarks of cancer, including rapid growth and aneuploidy, can result in non-oncogene addiction to the

122 neration could be in part linked to neuronal aneuploidy caused by 4R-Tau expression during brain deve

123 Aneuploidy causes a variety of cellular stresses, includ

124 Our results show that aneuploidy causes alterations in metabolism and redox ho

125 s shed light on the mechanisms of removal of aneuploidy cells in vivo.

126 century-old hypothesis by demonstrating that aneuploidy characterized by single-chromosome gains acts

127 s rapid adaptation to cellular stresses, and aneuploidy characterizes most human tumors.

128 oprotein induces centrosome overduplication, aneuploidy, chromosome breakage and the formation of mic

129 Aneuploidy-chromosome instability leading to incorrect c

130 Chromosome aneuploidy, concerted chromosome loss, and point mutatio

131 suggest an analogous role to the eukaryotic aneuploidy condition in cancer.

132 rmation, the genome-destabilizing effects of aneuploidy confer an evolutionary flexibility that may c

133 Although it is known that sperm aneuploidy contributes to early pregnancy losses and con

134 process causes chromosome missegregation and aneuploidy, contributing to cancer and birth defects.

135 h carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required

136 xtremely severe deleterious variant (such as aneuploidy) could escape embryonic lethality if the geno

137 edge, this is the first evidence of adaptive aneuploidy counteracting oxidative stress.

138 cancer cases were compared with the types of aneuploidies detected in the overall cohort.

139 ed with the rare NIPT finding of more than 1 aneuploidy detected (7 known cancers among 39 cases of m

140 Understanding the relationship between aneuploidy detection on noninvasive prenatal testing (NI

141 d a potential therapeutic strategy for human aneuploidy diseases involving additional chromosomes.

142 ng likely explains the challenge of treating aneuploidy diseases with a single stress-inducing agent.

143 defects in centromere architecture result in aneuploidy due to severely altered centromeric cohesion.

144 nisms, which would explain the low levels of aneuploidy during adulthood in the cerebral cortex of Bu

145 ur results reveal an unexpected tolerance of aneuploidy during mammalian spermatogenesis, and the sur

146 haracterized the chromosomal arm changes and aneuploidy events in a manner that offers similar inform

147 However, the accurate determination of aneuploidy events in cancer genomes is a challenge.

148 ight; evaluating the fetus for anomalies and aneuploidy; examining the uterus, cervix, placenta, and

149 cell populations harboring the same defined aneuploidy exhibit heterogeneity in cell-cycle progressi

150 flect an evolutionary advantage of increased aneuploidy for human females.

151 ategies to unveil the mechanisms involved in aneuploidy generation.

152 ion scale and identifies genes implicated in aneuploidy, genome instability and cancer susceptibility

153 Increased aneuploidy has been associated with defects in DNA repai

154 Modeling the consequences of aneuploidy has relied on perturbing spindle assembly che

155 n unbalanced karyotype, a condition known as aneuploidy, has a profound impact on cellular physiology

156 eoformans var. neoformans (serotype AD) such aneuploidies have resulted in loss of heterozygosity, wh

157 High levels of aneuploidy have been observed in disease-free tissues, i

158 features related to tumor samples including aneuploidy, heterogeneity and purity.

159 gene Bub1b further support the finding that aneuploidy impairs cell proliferation in vivo.

160 A number of studies have shown that aneuploidy impairs cellular fitness.

161 can be used to accurately detect chromosomal aneuploidies in circulating fetal DNA; however, the nece

162 paraffin-embedded colon tissue, we detected aneuploidy in 15 of 37 samples with fLGD (40.5%).

163 multiple somatic copy number alterations and aneuploidy in approximately 85%, containing oncogenic ac

164 Genetic instability is a hallmark of aneuploidy in budding and fission yeast.

165 f a transient tetraploid state proceeding to aneuploidy in cancer progression.

166 g the resolution processes may contribute to aneuploidy in cancer.

167 functions for RAPGEF2 that may contribute to aneuploidy in cancer.

168 ntly acquire chromosomal aberrations such as aneuploidy in culture.

169 s (iECs) returned to mitosis, it resulted in aneuploidy in daughter cells.

170 ding to micronucleus formation and increased aneuploidy in daughter cells.

171 specific mitotic defects that contribute to aneuploidy in each cell line.

172 Sperm aneuploidy in Faroese men with lifetime exposure to dich

173 Here we present a mechanism for aneuploidy in fission yeast based on spindle pole microt

174 Aneuploidy in human eggs is the leading cause of pregnan

175 Aneuploidy in human eggs is the leading cause of pregnan

176 ide a possible explanation for high rates of aneuploidy in human eggs.

177 ygotic cell division contribute to pervasive aneuploidy in human embryos.

178 This study also confirms aneuploidy in LP cells, provides antigens that may be he

179 may shed light on the early consequences of aneuploidy in mammalian cells.

180 approaches to alleviating the risk of oocyte aneuploidy in maternal ageing.

181 polychlorinated biphenyls (PCBs), and sperm aneuploidy in men from the general population of the Far

182 ed for by the known incidence of chromosomal aneuploidy in miscarriage, and it has been suggested tha

183 Furthermore, we found a high level of aneuploidy in post-mitotic differentiated tissue.

184 bly, inactivation of NORAD triggers dramatic aneuploidy in previously karyotypically stable cell line

185 Surprisingly, the level of aneuploidy in the brain of these murine models of accele

186 vasive prenatal testing for the detection of aneuploidy in the high-risk population.

187 chromosome-specific, age-related increase in aneuploidy in the mouse cerebral cortex.

188 segregation errors in vivo and long-lasting aneuploidy in tumour-derived cell lines.

189 n that lead to extra or missing chromosomes (aneuploidy) in human eggs, a major cause of pregnancy fa

190 he BAM format, and the outputs are calls for aneuploidy, including trisomies 13, 18, 21 and monosomy

191 ers are associated with an increased risk of aneuploidy, including Trisomy 21 in humans.

192 e architecture that could explain why oocyte aneuploidy increases with advanced maternal age.

193 dle alterations, delayed anaphase onset, and aneuploidy, indicating that PI3K-C2alpha expression is r

194 increased levels of these genes underlie the aneuploidy induced by Ulp2 loss.

195 ence a number of stresses that are caused by aneuploidy-induced proteomic changes.

196 The aneuploidy-induced re-balance of the proteome via modula

197 for metastatic melanoma, we found that tumor aneuploidy inversely correlates with patient survival.

198 sults, 3757 (3%) were positive for 1 or more aneuploidies involving chromosomes 13, 18, 21, X, or Y.

199 However, whether aneuploidy is a driving cause or a consequence of tumor

200 Aneuploidy is a hallmark of breast cancer; however, know

201 Aneuploidy is a hallmark of cancer, although its effects

202 Aneuploidy is a hallmark of most human tumors, but the m

203 Aneuploidy is a hallmark of tumor cells, and yet the pre

204 wing reintroduction of ULP2, suggesting that aneuploidy is a reversible adaptive mechanism to counter

205 nsistent with this observation, incidence of aneuploidy is also markedly increased in Sirt6-depleted

206 Pharmacologic targeting of aneuploidy is an attractive therapeutic strategy, as thi

207 al Center, to determine whether detection of aneuploidy is associated with later development of high-

208 y sensitive to aneuploidy, we show here that aneuploidy is common in wild yeast isolates, which show

209 Aneuploidy is frequently detected in human cancers and i

210 Aneuploidy is linked to myriad diseases but also facilit

211 strains, suggest that dosage compensation of aneuploidy is not general but contingent on genotypic an

212 Aneuploidy is the leading genetic abnormality contributi

213 Aneuploidy is the leading genetic abnormality that leads

214 Aneuploidy is ubiquitous in cancer and plays a pivotal,

215 yeast and mouse fibroblasts have shown that aneuploidy is usually detrimental to cellular fitness.

216 We maintain that aneuploidy is well tolerated in the wild strains of S. c

217 for non-invasive prenatal testing (NIPT) of aneuploidy is widely available.

218 rmal chromosome number, a condition known as aneuploidy, is a ubiquitous feature of cancer cells.

219 An abnormal number of chromosomes, termed aneuploidy, is usually deleterious.

220 the cellular and organismal consequences of aneuploidy, it is important to determine how altered gen

221 ains acts to suppress tumorigenesis and that aneuploidy itself is a nidus for genomic instability.

222 g low levels of DNA damage, whole-chromosome aneuploidies lead to DNA breaks that persist into mitosi

223 To determine whether aneuploidy leads to neurodegeneration in FTLD, we measur

224 Aneuploidy leads to severe developmental defects in mamm

225 However, the overall low incidence of aneuploidy limits the positive predictive value of these

226 To investigate whether aneuploidy may confer a selective advantage to cancer ce

227 e, its contribution to the overall incidence aneuploidy may mask the contribution of other processes.

228 aracteristics such as tumor mutational load, aneuploidy may thus help identify patients most likely t

229 Our results reveal a complex aneuploidy mechanism that adapts cells to loss of the SU

230 As most tumours show some degree of aneuploidy, mechanistic understanding of these pathways

231 Constitutional mosaic aneuploidies, microcephaly, developmental delay and seiz

232 res, which are features of mosaic variegated aneuploidy (MVA) syndrome, were more variably present.

233 read depth used in our standard pipeline for aneuploidy NIPT detected 15/18 (83%) samples with pathog

234 racterized by a highly unstable genome, with aneuploidy observed in nearly all patients.

235 cycles, we identified an association between aneuploidy of putative mitotic origin and linked genetic

236 Here, we quantified the frequency of aneuploidy of three autosomes in the cerebral cortex and

237 rans effects of chromosomal duplications and aneuploidies on epigenetic patterning.

238 investigating the immediate consequences of aneuploidy on cell physiology, we identified mechanisms

239 To test the effects of aneuploidy on chromosome segregation and other mitotic p

240 Here, we examined the effects of aneuploidy on mouse embryonic stem (ES) cells by generat

241 l instability (CIN) determines the effect of aneuploidy on tumors; whereas low rates of CIN are weakl

242 lastocyst stage with no detectable effect on aneuploidy or gene expression.

243 We propose that, similar to aneuploidy or tetraploidy, haploidy triggers a p53-depen

244 etaphase delay that was not a consequence of aneuploidy or the activation of a checkpoint.

245 ients); AML with TP53 mutations, chromosomal aneuploidies, or both (in 13%); and, provisionally, AML

246 Aneuploidy-or an unbalanced karyotype in which whole chr

247 Most human aneuploidies originate maternally, due in part to the pr

248 eiotic errors inherited in the oocyte, these aneuploidies persist at the blastocyst stage and the rea

249 We find that aneuploidy provides a clear ecological advantage to oak

250 role of INPP5E in mitosis and prevention of aneuploidy, providing a new perspective on the function

251 uch concurrence has a vital role in reducing aneuploidy rates by extending MI, probably by allowing t

252 PSCs, but significant differences existed in aneuploidy rates, reprogramming efficiency, reliability

253 hrough chromosome missegregation, leading to aneuploidy, rearrangements and micronucleus formation.

254 Since centrosome inaccuracies cause aneuploidies responsible for cancers, birth defects and

255 This aneuploidy resulted from multipolar divisions, chromosom

256 Most aneuploidy results from chromosome segregation errors du

257 This aneuploidy results in increased levels of the telomerase

258 rior frontal asymmetries, while Y-chromosome aneuploidy reversed normative rightward medial prefronta

259 imated across five rare sex (X/Y) chromosome aneuploidy (SCA) syndromes, and (3) clarify brain size-i

260 ic phenotypes associated with sex-chromosome aneuploidy (SCA).

261 ed 137 youth with one of five sex-chromosome aneuploidies [SCAs; XXX (n = 28), XXY (n = 58), XYY (n =

262 NIPT for fetal aneuploidy screening (chromosomes 13, 18, 21, X, and Y).

263 s, we assigned pregnant women presenting for aneuploidy screening at 10 to 14 weeks of gestation to u

264 ll-free DNA sequencing for clinical prenatal aneuploidy screening.

265 n heavy chain enhancer elements, chromosomal aneuploidy, somatic mutations that further affect oncoge

266 results in increased DNA damage, widespread aneuploidy, spontaneous tumor development, accelerated E

267 MC(-) spermatozoa, while evaluation of sperm aneuploidy status indicated an increased level of chromo

268 e complex, respectively-suppresses ulp2Delta aneuploidy, suggesting that increased levels of these ge

269 We propose that aneuploidy suppresses telomerase insufficiency through r

270 DNA has enabled non-invasive prenatal fetal aneuploidy testing without direct discrimination of the

271 that neural cells are much more tolerant of aneuploidy than epithelial cells.

272 ated controls, and may explain the pervasive aneuploidy that characterizes Leishmania chromosome arch

273 of chromosome mis-segregation and resultant aneuploidy that uniquely afflicts human female oocytes (

274 ies-including rearrangements, deletions, and aneuploidy-that contribute to cancer formation.

275 Aneuploidy, the inheritance of an atypical chromosome co

276 Aneuploidy-the gain or loss of one or more whole chromos

277 Chromosomal or segmental aneuploidy-the gain or loss of whole or partial chromoso

278 The presence of aneuploidy therefore identifies patients with fLGD in co

279 Therefore, based on aneuploidy, these adult mice with reduced life span and

280 erived cell lines carrying single-chromosome aneuploidies to assess a number of cancer cell propertie

281 pensation buffers gene amplification through aneuploidy to provide a natural, but likely transient, r

282 e find that BCL9L dysfunction contributes to aneuploidy tolerance in both TP53-WT and mutant cells by

283 Efforts to exploit aneuploidy tolerance mechanisms and the BCL9L/caspase-2/

284 ow cells overcome the deleterious effects of aneuploidy until new phenotypes evolve.

285 colorectal cancer in patients with fLGD and aneuploidy was 5.3 (95% CI, 1.542-24.121) within a mean

286 By comparison, aneuploidy was detected in 14 of 15 samples with flat HG

287 First, aneuploidy was found in brain cells from MAPT mutant tra

288 a genome-sequencing survey and reported that aneuploidy was frequently observed in wild strains of S.

289 t found previously in T. miscellus, in which aneuploidy was more common (69%; Fisher's exact test, P=

290 aboratory strains are extremely sensitive to aneuploidy, we show here that aneuploidy is common in wi

291 Conversely, most aneuploidies were transient and did not correlate with d

292 de duplication of entire chromosome arms and aneuploidy where chromosomes are duplicated beyond norma

293 stability, we utilized an ex vivo system for aneuploidy where primary splenocytes from Casp2(-/-) mic

294 pensation of CCP1 and UTH1 via chromosome XI aneuploidy, wherein these proteins support hydroperoxide

295 rrors lead to an abnormal chromosome number (aneuploidy), which typically results in disease or cell

296 detected foci of shifting CT asymmetry with aneuploidy, which fell almost exclusively within regions

297 normalities, chromosome mis-segregation, and aneuploidy, which then lead to apoptosis.

298 Many isolates display evidence of aneuploidy, which was detected for all chromosomes.

299 The mechanisms that lead to an increase in aneuploidy with advanced maternal age are largely unclea

300 e were found to exhibit increasing levels of aneuploidy with decreasing Tau gene dosage.