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1 ogy, we identified mechanisms that eliminate aneuploid cells.
2 into the underlying molecular physiology of aneuploid cells.
3 in vivo, mechanisms exist to select against aneuploid cells.
4 polyploid cells is error-prone and produces aneuploid cells.
5 rturbed condensation similar to that seen in aneuploid cells.
6 les can predict protein level attenuation in aneuploid cells.
7 lantation embryos are mosaics of euploid and aneuploid cells.
8 in aggregates accumulate within lysosomes in aneuploid cells.
9 nuously elevated levels of DNA damage affect aneuploid cells.
10 wild-type p53 suppresses the accumulation of aneuploid cells.
11 and cell proliferation were downregulated in aneuploid cells.
12 owever, these models are based on studies in aneuploid cells.
13 cytokinesis, and formation of polyploid and aneuploid cells.
14 these genes are involved in the survival of aneuploid cells.
15 its traits that are shared between different aneuploid cells.
16 checkpoint activity and high percentages of aneuploid cells.
17 7 was used to identify small populations of aneuploid cells.
18 s in the formation of tetraploid rather than aneuploid cells.
19 ptosis, leading to a greater accumulation of aneuploid cells.
20 regated during cell division, giving rise to aneuploid cells.
21 ith a marked decrease in the accumulation of aneuploid cells.
22 multiple levels to prevent the formation of aneuploid cells, a phenotype frequently observed in canc
23 21WAF1/CIP1-infected cells and inhibition of aneuploid cell accumulation; and an alteration of the ma
25 nown exceptions to the involvement of p53 in aneuploid cells and that tissue context may be important
27 depletion also resulted in the appearance of aneuploid cells and the formation of internuclear chroma
28 aurora result in the generation of severely aneuploid cells and, in the case of aurora, monopolar sp
29 of mutability to select specific tumor-prone aneuploid cells, and open unique avenues toward the unde
31 ease of enhanced proliferative capacity, and aneuploid cells are frequently recovered following the e
33 /+ or p53-/-) had an increased percentage of aneuploid cells as well as an increase in cells with sup
34 loid mouse cells could not, we conclude that aneuploid cells become drug resistant via specific chrom
35 that nondisjunction does not directly yield aneuploid cells, but rather tetraploid cells that may su
36 We provide evidence that p21 is activated in aneuploid cells by reactive oxygen species (ROS) and p38
39 hways that are essential for the survival of aneuploid cells could serve as a new treatment strategy
40 d and euploid cells, reveal that the fate of aneuploid cells depends on lineage: aneuploid cells in t
41 oncluding that nondisjunction does not yield aneuploid cells directly, but instead gives rise to tetr
43 the recent observation of inappropriate and aneuploid cell division in cell lines expressing high le
44 ome segregation errors and the appearance of aneuploid cells due to the presence of VirD5 could be vi
45 turn, results in increased apoptosis of the aneuploid cells during subsequent cell division cycles.
49 unrestrained propagation of tetraploids into aneuploid cells, further undermines genomic stability an
53 romosomal missegregation and accumulation of aneuploid cells in 53BP1-/- p53+/+ and 53BP1-/- p53-/- t
54 a metaanalysis on gene expression data from aneuploid cells in diverse organisms, including yeast, p
55 tment also reduced the steady-state level of aneuploid cells in HPV-16 E7-expressing cell populations
56 pathway in many tumors, but the presence of aneuploid cells in some normal human and mouse tissues i
58 12 controls revealed a higher proportion of aneuploid cells in the exposed group (median, 18.8% [int
59 fate of aneuploid cells depends on lineage: aneuploid cells in the fetal lineage are eliminated by a
61 ted against suggests that the persistence of aneuploid cells in tumors requires not only chromosome m
63 s were identified with altered expression in aneuploid cells, including overexpression of the cellula
64 e-specific phenotypes and global stresses of aneuploid cells, including oxidative and proteotoxic str
67 ggest that the generation and maintenance of aneuploid cells is a widespread, if not universal, prope
69 that the fitness ranking between euploid and aneuploid cells is dependent on context and karyotype, p
72 more find that although DNA damage is low in aneuploid cells, it nevertheless has dramatic consequenc
75 ckpoint activity, increased mitotic defects, aneuploid cells marked by a specific transcriptional sig
76 early human embryo, including management of aneuploid cells, may paradoxically promote embryo develo
78 totic centrosomes, may induce an increase of aneuploid cell population and contribute to tumorigenesi
79 neuploidy in 13 of 15 patients (87%) who had aneuploid cell populations detected in premalignant epit
80 on status of the p16 promoter in flow-sorted aneuploid cell populations from 21 patients with premali
86 ntaneous chromosome missegregation events in aneuploid cells promote chromosomal instability (CIN) th
88 cells was observed in confluent cultures in aneuploid cells relative to their diploid counterparts.
89 chromosome 3q that occurs in HPV16-infected, aneuploid cells represents a pivotal genetic aberration
92 eight-cell division, we efficiently generate aneuploid cells, resulting in embryo death during peri-i
95 lic conditional gene knockouts in diploid or aneuploid cells, such as pluripotent stem cells, 3D orga
96 e demonstrate that certain drugs that act on aneuploid cells synergize with inhibitors of Aurora B to
98 nerate a diverse population of proliferative aneuploid cells that have the potential to contribute to
99 and a 70-gene signature derived from primary aneuploid cells was defined as a strong predictor of inc
103 sely resembles the stressed state of primary aneuploid cells, yet CIN is not benign; a subset of gene
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