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1 h midzone organization by EWSR1/FLI1 induces aneuploidy.
2 athway could influence the risk of embryonic aneuploidy.
3 may occur at the transition from euploidy to aneuploidy.
4 gation without deleterious outcomes, such as aneuploidy.
5 osomes can contribute to chromosome-specific aneuploidy.
6 which can increase the chance of developing aneuploidy.
7 whole-chromosome gains and losses, known as aneuploidy.
8 spindle morphogenesis and dynamics, inducing aneuploidy.
9 ciated with chromosome instability (CIN) and aneuploidy.
10 tics of development, and genetic testing for aneuploidy.
11 isition of tolerance to antifungal drugs via aneuploidy.
12 ociation between histone gene expression and aneuploidy.
13 on cellular defects that are associated with aneuploidy.
14 mitosis as well as protecting cells against aneuploidy.
15 approach can accurately detect low levels of aneuploidy.
16 rotein levels, leading to mitotic errors and aneuploidy.
17 eve optimal chromosome alignment and prevent aneuploidy.
18 rved deletions, duplications, and chromosome aneuploidy.
19 ults in chromosome missegregation leading to aneuploidy.
20 eguard against chromosome missegregation and aneuploidy.
21 sperm have reduced levels of DNA damage and aneuploidy.
22 rise to embryos that fail to develop due to aneuploidy.
23 with the same Gleason score and no predicted aneuploidy.
24 st and causes chromosome mis-segregation and aneuploidy.
25 n the fidelity of chromosome segregation and aneuploidy.
26 ide a second safeguard against brain somatic aneuploidy.
27 osis maintains genome stability and prevents aneuploidy.
28 neuploid cells and cells with natural random aneuploidy.
29 explore cellular mechanisms associated with aneuploidy.
30 h lead to chromosome gains/losses and random aneuploidy.
31 the development of genomic instability with aneuploidy.
32 ous to normal cells because of the burden of aneuploidy.
33 , succumb to enhanced tumour development and aneuploidy.
34 hments that could lead to missegregation and aneuploidy.
35 ty is essential for its function in limiting aneuploidy.
36 synapsis, thereby minimizing transmission of aneuploidy.
37 nd treatment responses of diseases caused by aneuploidy.
38 r activities by producing massive chromosome aneuploidy.
39 ar organization in health and sex chromosome aneuploidy.
40 ome segregation errors to the development of aneuploidy.
41 , and the most frequent survivable autosomal aneuploidy.
42 a B during anaphase, leading to induction of aneuploidy.
43 , affects the genesis of chromosome-specific aneuploidy.
44 surprisingly, this only rarely causes lethal aneuploidy.
45 idies and 23 (31%) embryos possessed meiotic aneuploidies.
46 changes, including 56 with whole chromosome aneuploidies.
48 GSs on 11 RGDs including four sex-chromosome aneuploidies (47,XXX; 47,XXY; 47,XYY; 45,X) that affect
50 dicate that while FISH tended to over-report aneuploidies, a modified 2-probe approach can accurately
54 omere features can translate into non-random aneuploidy, a hallmark of cancer and genetic diseases.
55 les from patients with cirrhosis to quantify aneuploidy, a possible outcome of polyploid cell divisio
56 increased loss of a minichromosome; elevated aneuploidy; a down-regulation of the protein levels of c
57 evelopment could help explain the paradox of aneuploidy abundance in tumors despite somatic fitness c
60 ring that 55 (74%) embryos possessed mitotic aneuploidies and 23 (31%) embryos possessed meiotic aneu
62 rage whole-genome sequencing to detect fetal aneuploidies and copy-number variants (CNVs) at ~1 Mb re
64 and multipolar spindle formation, leading to aneuploidy and apoptosis, which could relate to depletio
66 re, we investigated the relationship between aneuploidy and cancer development using cells engineered
72 ionally, we demonstrate that miR-26a induces aneuploidy and centrosome defects and enhances tumorigen
79 e review the molecular mechanisms underlying aneuploidy and discuss its contributions to B-ALL initia
81 a separate cluster for which chromosomal-arm aneuploidy and driver mutations are mutually exclusive.
84 orrelated with the tissue-specific levels of aneuploidy and genetic heterogeneity observed in primary
87 expression-based score that correlates with aneuploidy and has prognostic value in many types of can
88 e in uncovering the cellular consequences of aneuploidy and how aneuploid cancer cells self-adapt to
89 characterise chromosome-specific patterns of aneuploidy and identified extensive structural variation
97 contribute to increased incidence of oocyte aneuploidy and spontaneous abortion in aging females.
98 st; n = 390), we determine the origin of the aneuploidy and the diagnostic predictive value of segmen
101 ive association between driver mutations and aneuploidy, and a characteristic set of mutations that i
102 study relationships among liver polyploidy, aneuploidy, and adaptation, mice lacking E2f7 and E2f8 i
103 of the proteome imbalance that is caused by aneuploidy, and also predicted a relationship between pl
106 mosome missegregation events, propagation of aneuploidy, and genetic heterogeneity in xenograft model
107 ivation and we previously showed DNA damage, aneuploidy, and senescence in somatotroph adenomas, we s
108 This process is tightly controlled to avoid aneuploidy, and we previously showed that active Ran coo
109 py-number data, we demonstrate that specific aneuploidies are associated with distinct outcomes, and
110 ionally been based on assumptions that these aneuploidies are lethal or associated with poor quality
116 dian of 15 years, increasing extent of tumor aneuploidy as predicted from the tumor transcriptome was
118 hanism for EWSR1/FLI1-dependent induction of aneuploidy associated with mitotic dysfunction and the i
121 r, our results indicate a close link between aneuploidy, autophagy, and apoptosis to refine the embry
122 o this end, we extended an approach to infer aneuploidies based on dosage-associated changes in gene
124 servation of common transcriptome changes of aneuploidy by averaging out karyotype-specific dosage ef
125 ized by in situ co-examination of chromosome aneuploidy by FISH and immunostaining of multiple biomar
127 during mitosis and meiosis, and yet specific aneuploidies can be adaptive during environmental stress
128 and psychiatric disorders in sex chromosome aneuploidies can inform appropriate management of these
129 uniform driver of malignancy, and different aneuploidies can uniquely influence tumor progression.
130 cell line, we report that the dose effect of aneuploidy can be further compensated at the translation
135 instability, the process that gives rise to aneuploidy, can promote tumorigenesis by increasing gene
138 century-old hypothesis by demonstrating that aneuploidy characterized by single-chromosome gains acts
139 oprotein induces centrosome overduplication, aneuploidy, chromosome breakage and the formation of mic
140 rized by large-scale genomic rearrangements, aneuploidy, chromothripsis, and other forms of chromosom
142 rmation, the genome-destabilizing effects of aneuploidy confer an evolutionary flexibility that may c
143 BR1 allelic effects beyond protein level and aneuploidy contribute to disease heterogeneity in both M
144 nge of genetic causes, including chromosomal aneuploidy, copy number variations (CNVs; which are dete
146 h carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required
147 ifferent meiotic errors, we fit our model to aneuploidy data from 11,157 blastocyst-stage embryos.
151 the diagnostic predictive value of segmental aneuploidy detection in TE biopsies toward the ICM's chr
152 nt oocytes exhibit an increased frequency of aneuploidy, digyny, progressive delays in preimplantatio
154 the first time the presence and emergence of aneuploidy-driven FLC heteroresistance in human CM, asso
155 ic catastrophe, chromosome mis-segregation / aneuploidy due to premature anaphase, and cytokinesis fa
160 sequencing (scL-WGS) analyses, which showed aneuploidy frequencies at least an order of magnitude lo
161 lows for the accurate detection of segmental aneuploidies from in vitro fertilization embryo biopsies
162 w the existence in budding yeast of a common aneuploidy gene-expression signature that is suggestive
163 ental stress response" (ESR) and the "common aneuploidy gene-expression" (CAGE) signature, in which m
165 of gene expression in cancer can arise from aneuploidy, genome disorganization or abnormal DNA methy
166 ion scale and identifies genes implicated in aneuploidy, genome instability and cancer susceptibility
170 eoformans var. neoformans (serotype AD) such aneuploidies have resulted in loss of heterozygosity, wh
171 the predominant mitotic origin of segmental aneuploidies in preimplantation embryos and develop a ri
174 gene knockdowns that lead to an increase in aneuploidy in checkpoint-deficient human cancer cells.
177 If left unrepaired, meiotic DSBs can cause aneuploidy in gametes and compromise viability in offspr
180 Genomic analysis revealed high rates of aneuploidy in heteroresistant colonies as well as in rel
188 our work provides a high-resolution view of aneuploidy in preimplantation embryos, and supports the
189 Sequencing System (RealSeqS) that can detect aneuploidy in samples containing as little as 3 pg of DN
192 are preferentially associated with increased aneuploidy in young girls, whereas centromeric and more
193 that promoted chromosome missegregation and aneuploidy, including incomplete replication of DNA, cen
194 dle alterations, delayed anaphase onset, and aneuploidy, indicating that PI3K-C2alpha expression is r
195 es in aneuploid cells: protecting cells from aneuploidy-induced cellular stresses and preventing exce
196 ther than the CAGE signature, in response to aneuploidy-induced cellular stresses, resulting in selec
197 ther, these results support the concept that aneuploidy-inducing gene deficiencies contribute to cell
199 within the tumor suppressor gene FHIT Taking aneuploidy into account, we reanalyzed K562 RNA-seq and
200 for metastatic melanoma, we found that tumor aneuploidy inversely correlates with patient survival.
201 nct outcomes, and the acquisition of certain aneuploidies is in fact linked with a favorable prognosi
206 function is unclear, and the degree of liver aneuploidy is debated, with reports showing aneuploidy a
207 the plasticity of the embryo in dealing with aneuploidy is fundamental to normal development, the mec
210 tually all cell types and cellular contexts, aneuploidy is not a universal promoter of tumorigenesis.
211 amage without generating mitotic errors, and aneuploidy is not commonly observed in cirrhotic livers.
217 the cellular and organismal consequences of aneuploidy, it is important to determine how altered gen
219 ains acts to suppress tumorigenesis and that aneuploidy itself is a nidus for genomic instability.
220 t as confounders between gene expression and aneuploidy, leading to spurious correlations between the
221 oupled with the endocytic defect inherent to aneuploidy, leads to a marked alteration of intracellula
223 Further, scL-WGS tends to underestimate aneuploidy levels, especially in a polyploid background.
224 for any dysplasia, colon segment resection, aneuploidy, male sex, and age was classified as weak.
225 Even though embryos with CIN-derived complex aneuploidies may arrest between the cleavage and blastoc
226 MM both accounts for the impact of purity on aneuploidy measurements and identifies a new association
227 ity, eliciting mitotic failures that trigger aneuploidy, mitosis-dependent DNA damage responses, p53
228 Our method thus allowed the detection of aneuploidy mosaicism, and provides a solid basis which c
229 rity with human pediatric gliomas per robust aneuploidy, mutational rates, relative timing of mutatio
231 BUB1B are responsible for mosaic variegated aneuploidy (MVA), a human congenital disorder characteri
232 ades of phenotype-driven research, 80-90% of aneuploidy-negative holoprosencephaly individuals with a
235 tion leads to rDNA bridges, rDNA damage, and aneuploidy of an rDNA-containing acrocentric chromosome.
236 investigating the immediate consequences of aneuploidy on cell physiology, we identified mechanisms
238 iseases, complementing current screening for aneuploidies or carrier screening for recessive disorder
240 tionary model for the dynamics of cells with aneuploidy or other fitness-reducing mutations during he
241 n the multitude of diseases linked to either aneuploidy or protein aggregation, this study could serv
244 ling that two mechanisms could underlie this aneuploidy peak: rapid expansion of the engrafted HSPC p
245 d aneuploidy rates ranging from 0.01 to 0.05 aneuploidies per gamete; crossovers partially protected
246 ironment is favorable to retrotransposition, aneuploidy predisposes tumor cells to L1 insertions, and
248 The study of individuals with sex chromosome aneuploidies provides a promising framework for studying
249 in oocytes and could contribute to the high aneuploidy rate observed during female meiosis, a leadin
251 h resolution, SNVs and Indels (corrected for aneuploidy), regions with loss of heterozygosity, phased
253 e common in solid tumors, different forms of aneuploidy represent the initiating oncogenic lesion in
255 can significantly improve the prediction of aneuploidy risk in the ICM in over 86% of clinical cases
256 ly used to study how maternal ageing impacts aneuploidy risk, however the differences in reproductive
257 um biomarkers (AMSB), identified through the aneuploidy screening programme, are frequent incidental
258 2,208 samples sent for non-invasive prenatal aneuploidy screening to detect CMV and precisely measure
259 = 0.94, specificity = 0.92), chromosome 7/10 aneuploidies (sensitivity = 0.90, specificity = 0.88), a
260 ve PCR-based assay called Repetitive Element AneupLoidy Sequencing System (RealSeqS) that can detect
262 general and seemingly detrimental effect of aneuploidy, slowed proliferation, provides a selective b
263 We show that the CAGE signature is not an aneuploidy-specific gene-expression signature but the re
264 mere data and DNA index correlated well with aneuploidy status at higher sensitivity than cytogenetic
268 cribe here an original mode of generation of aneuploidies that could be very common in oocytes and co
272 he preferred method for studying single cell aneuploidy, this method was applied in a second step, on
273 The MLPA telomere kit was used to identify aneuploidy through detection of whole chromosome loss or
274 ugh our understanding of the contribution of aneuploidy to cancer initiation and progression is incom
275 e find that BCL9L dysfunction contributes to aneuploidy tolerance in both TP53-WT and mutant cells by
280 chromosome instability (CIN), which leads to aneuploidy, translocations, and other chromosome aberrat
281 development of human embryos bearing common aneuploidies using a recently established culture platfo
282 ance of large autosomal CNVs and chromosomal aneuploidies using a standard CNV detection algorithm no
283 colorectal cancer in patients with fLGD and aneuploidy was 5.3 (95% CI, 1.542-24.121) within a mean
289 prevalent meiotic origin of whole-chromosome aneuploidies, we show that sub-chromosomal abnormalities
290 to understand how cells develop tolerance to aneuploidy, we subject disomic (i.e. with an extra chrom
293 rrors lead to an abnormal chromosome number (aneuploidy), which typically results in disease or cell
294 y and paclitaxel treatment induces excessive aneuploidy, which in turn results in elevated cell death
299 Our analysis revealed widespread mosaic aneuploidies, with 59 of 74 (80%) embryos harboring at l
300 d the DNA mutations and chromosome arm-level aneuploidy within tumours with low, intermediate and hig