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1 evelopmental impairment, embryonic death and chromosomal instability.
2 s, hypersensitivity to genotoxic agents, and chromosomal instability.
3 evaluation of tumors revealed characteristic chromosomal instability.
4 levels and promoted checkpoint weakness and chromosomal instability.
5 ng of telomeres, seems to be associated with chromosomal instability.
6 VHL with increased miR-28-5p expression and chromosomal instability.
7 mis-segregate whole chromosomes and display chromosomal instability.
8 oplastic tissue, is attributed to continuous chromosomal instability.
9 bipolar spindle assembly and a high rate of chromosomal instability.
10 r and promotes tumor growth, metastasis, and chromosomal instability.
11 atumor heterogeneity, genetic diversity, and chromosomal instability.
12 ploidy single-handedly triggered cancer-like chromosomal instability.
13 cellular cholesterol homeostasis also causes chromosomal instability.
14 he development of HGSOC, and associated with chromosomal instability.
15 nes associated with cancer proliferation and chromosomal instability.
16 in and heterochromatin, and cause widespread chromosomal instability.
17 Human cells lacking RECQL5 display chromosomal instability.
18 cterized by progressive fatal BM failure and chromosomal instability.
19 nt human tumors and strongly correlates with chromosomal instability.
20 kinase A (AURKA) drives tumor aneuploidy and chromosomal instability.
21 em cells, uncoupling cell cycle defects from chromosomal instability.
22 pone DSB repair without accumulating massive chromosomal instability.
23 essive disorders characterized by cancer and chromosomal instability.
24 nd processing, HR-type DSB repair, and overt chromosomal instability.
25 and led to concomitant telomerase-dependent chromosomal instability.
26 No evidence was found of G-CSF-induced chromosomal instability.
27 umor development to drive the acquisition of chromosomal instability.
28 ted MEK1-tubulin in spindle organization and chromosomal instability.
29 s chromosome content, two characteristics of chromosomal instability.
30 61 is associated with higher cancer risk and chromosomal instability.
31 tic event associated with gene silencing and chromosomal instability.
32 evoid of RECQL1 and RECQL5 display increased chromosomal instability.
33 resence of extra centrosomes correlates with chromosomal instability.
34 lium and is characterized by a high level of chromosomal instability.
35 intraepithelial lesions, yet did not exhibit chromosomal instability.
36 sease characterized at the cellular level by chromosomal instability.
37 ve double-strand break repair, and increased chromosomal instability.
38 llular superoxide, to the acute induction of chromosomal instability.
39 ochastic model, driven by the observation of chromosomal instability.
40 arities involving anaphase bridges and gross chromosomal instability.
41 y of p53 lesions, and display high levels of chromosomal instability.
42 a gene expression signature associated with chromosomal instability.
43 to mitomycin C and exhibited high levels of chromosomal instability.
44 ersensitivity to DNA crosslinking agents and chromosomal instability.
45 uence motifs, predispose the human genome to chromosomal instability.
46 radiosensitivity, increased micronuclei, and chromosomal instability.
47 repair pathway that protects the genome from chromosomal instability.
48 severely compromised DSB repair resulting in chromosomal instability.
49 eukemia (AML) is frequently characterized by chromosomal instability.
50 onical Hh signaling through the induction of chromosomal instability.
51 repton reduced liver overgrowth and signs of chromosomal instability.
52 histomorphologic parameters associated with chromosomal instability.
53 checkpoint activity and the potentiation of chromosomal instability.
54 cell cycle checkpoint, resulting in profound chromosomal instability.
55 , but was a potent inducer of aneuploidy and chromosomal instability.
56 centromeres are altered in cancer cells with chromosomal instability.
57 ts in sensitivity to DNA-damaging agents and chromosomal instabilities.
58 athway to propagate structural and numerical chromosomal instabilities.
59 -positive ALT cells were found to have gross chromosomal instabilities.
61 hindered in p27-deficient cells, leading to chromosomal instability, a hallmark of cancers with poor
63 y defects have recently been associated with chromosomal instability, a hallmark of human cancer.
64 ubule attachments during mitosis can lead to chromosomal instability, a hallmark of human cancers.
65 auses polyploidy, which in turn can generate chromosomal instability, a hallmark of many cancers.
66 essing tissues with age, consistent with the chromosomal instability accompanying a polzeta defect.
67 data implicate MAK in both AR activation and chromosomal instability, acting in both early and late p
69 odification may contribute to the prevention chromosomal instability and aneuploidy which frequently
70 meres are associated with the development of chromosomal instability and aneuploidy, the latter being
72 are implicated in hereditary human disease, chromosomal instability and cancer, and underlie the cli
74 rly or late stages of tumorigenesis promotes chromosomal instability and carcinogenesis in telomerase
76 down-regulation of such homologs resulted in chromosomal instability and chromatid cohesion defects i
77 been implicated as an important mediator of chromosomal instability and colon cancer triggered by En
79 pt management of small melanoma might reduce chromosomal instability and could improve overall patien
80 ly, loss of TRAIP function leads to enhanced chromosomal instability and decreased cell survival afte
81 of FA including DNA crosslinker sensitivity, chromosomal instability and defective FA pathway activat
82 ks whose unfaithful repair may contribute to chromosomal instability and disease progression to blast
84 efine genomic heterogeneity of PLC linked to chromosomal instability and evasion of immune surveillan
85 ons disturb mitosis and cytokinesis, causing chromosomal instability and greatly increased susceptibi
87 ) is a rare genetic disease characterized by chromosomal instability and impaired DNA damage repair.
88 -deficient B cells also exhibited pronounced chromosomal instability and impaired proliferation capac
89 t CDK inhibitors may have use in suppressing chromosomal instability and in synthetic lethal drug com
90 iferation, while prolonged expression caused chromosomal instability and in vivo tumor suppression.
91 eat shock protein Hsp72 was shown to promote chromosomal instability and increase radiation sensitivi
92 es provide valuable information for studying chromosomal instability and its consequences in cancer.
93 to the vast size of tumour cell populations, chromosomal instability and its potential for phenotypic
94 esulting from these interactions may promote chromosomal instability and leave the hepatocyte unable
96 , they demonstrate that MSH2-MSH3 suppresses chromosomal instability and modulates the tumor spectrum
98 s (ICL), a highly toxic lesion that leads to chromosomal instability and perturbs normal transcriptio
99 bishield emergency program drives evasion of chromosomal instability and phagocytosis checkpoints by
101 lular transformation through accumulation of chromosomal instability and premature progression of the
102 , with seemingly opposing roles in promoting chromosomal instability and protecting genome integrity.
103 ct as posttranscriptional safeguards against chromosomal instability and replication stress by integr
105 , tumors overexpressing Shh exhibited marked chromosomal instability and Smoothened-independent upreg
106 r that plays a key role in the prevention of chromosomal instability and suppresses the acquisition o
107 ntribute to tumor formation by both inducing chromosomal instability and suppressing the DDR pathway.
108 e report that LANA promoted the induction of chromosomal instability and the formation of micronuclei
113 nificant differences in mutational patterns, chromosomal instability, and gene expression that correl
114 ignaling pathway results in excessive ssDNA, chromosomal instability, and hypersensitivity to replica
115 phases of cellular transformation, exhibited chromosomal instability, and promoted increase in nuclea
116 ted hypersensitivity to DNA damage reagents, chromosomal instability, and reduced ATM-dependent phosp
122 useful strategy in cancer therapy, although chromosomal instability associated with pol zeta deficie
123 al to preserve genomic integrity and prevent chromosomal instability-associated diseases including ca
124 uggest that KIF5B is critical in suppressing chromosomal instability at the early stages of female me
125 ongly associated with tumor stage, a mitotic chromosomal instability attractor strongly associated wi
126 a striking association between the degree of chromosomal instability, both numerical and structural,
127 bute to tumor formation not only by inducing chromosomal instability but also by suppressing the func
128 n increases tumor initiation by induction of chromosomal instability, but that initiated tumors need
129 the absence of NORAD, PUMILIO proteins drive chromosomal instability by hyperactively repressing mito
130 that LMW-E expression primes cells to accrue chromosomal instability by shortening the length of mito
131 tastrophe and apoptosis; and 4) induction of chromosomal instability by telomere aggregate formation.
134 mouse Mcm4(Chaos3) mutation associated with chromosomal instability, cancer, and decreased intersubu
135 ity in mouse thymi and small intestines, the chromosomal instability caused by Atf3 deficiency was la
136 rt that Spartan insufficiency in mice causes chromosomal instability, cellular senescence and early o
139 and anaphase bridges, which are hallmarks of chromosomal instability (CIN) and Bub1 insufficiency.
141 lterations in pathways that characterize the chromosomal instability (CIN) and the genomically stable
142 to defects in kinetochore biorientation and chromosomal instability (CIN) and these phenotypes are s
144 The mechanisms that safeguard cells against chromosomal instability (CIN) are of great interest, as
148 d that the rate of chromosome missegregation/chromosomal instability (CIN) determines the effect of a
152 ness of cells with constitutional trisomy or chromosomal instability (CIN) in vivo using hematopoieti
153 euploidy, Separase overexpression results in chromosomal instability (CIN) including premature chroma
165 egregation events in aneuploid cells promote chromosomal instability (CIN) that may contribute to the
166 ve increased segregation errors and elevated chromosomal instability (CIN), but the genetic defects r
168 hways in colorectal cancer pathogenesis: the chromosomal instability (CIN), microsatellite instabilit
170 chromosome segregation, can be causative of chromosomal instability (CIN), which is a hallmark of ma
172 loss of BRCA1 in human cancer cells leads to chromosomal instability (CIN), which is defined as a per
173 -cycle checkpoints, allowing accumulation of chromosomal instability (CIN), which resulted in aneuplo
175 euploidy, chromothripsis, and other forms of chromosomal instability (CIN), yet how this occurs remai
189 s having microsatellite instability (MSI) or chromosomal instability (CIN); herein termed microsatell
190 o search for gene signatures associated with chromosomal instability (CIN); we investigated associati
191 ouble knockout splenocytes displayed reduced chromosomal instability compared with Atm null mice.
192 that macroevolutionary shifts (the onset of chromosomal instability) contribute to the evolution of
193 nd disruption of these complexes can lead to chromosomal instability culminating in cell death or mal
198 uster DNA helicase genetically linked to the chromosomal instability disorder Warsaw breakage syndrom
201 tically stable epithelial cells can initiate chromosomal instability, DNA damage, cell transformation
202 summary, we propose that Hus1 loss leads to chromosomal instability during DNA replication, triggeri
203 imply that multiple oncogenic pathways drive chromosomal instability during osteosarcoma evolution an
206 aling via a DNA-bound form, the induction of chromosomal instability, enhancement of DNA damage sensi
207 during childhood, which along with intrinsic chromosomal instability, favor clonal evolution and the
208 f; that is, whether aneuploidy per se causes chromosomal instability, for example, in patients with i
209 Together, these data identify RanBP2 as a chromosomal instability gene that regulates Topo IIalpha
210 as been no systematic exploration of whether chromosomal instability generated as a result of deregul
213 s) are highly toxic lesions that can lead to chromosomal instability if they are not repaired correct
214 hypersensitivity to DNA cross-linker-induced chromosomal instability in association with developmenta
218 hila epithelial cells to address the role of chromosomal instability in cancer development as they ha
221 progress has been made to identify causes of chromosomal instability in colorectal cells and to deter
226 eveal a previously unrecognized mechanism of chromosomal instability in leukemia progenitors because
227 chromosomal aneuploidy accompanying ongoing chromosomal instability in mice resulting from reduced l
229 how that overexpression of Cyclin B1 induces chromosomal instability in mouse embryonic fibroblasts l
230 mirus provide a second example of prolonged chromosomal instability in natural neoallopolyploid popu
232 eres produce apoptosis, cell senescence, and chromosomal instability in tissue culture and animal mod
236 cancer cells with a growth advantage, caused chromosomal instability in vitro, and promoted tumor dev
238 evel of somatic mosaicism, a proxy marker of chromosomal instability, in patients with constitutional
239 rylation leads to multiple manifestations of chromosomal instability including increased levels of DN
240 sed replication forks, as well as in various chromosomal instabilities, including loss of heterozygos
241 ot only reduced but the cells also exhibited chromosomal instability, including binucleation and aneu
242 ing from primary causes that do not generate chromosomal instability, including loss of the INK4a tum
245 ation of nucleoplasmic bridges and increased chromosomal instability, indicating that inaccurate endo
246 from undergoing programmed cell death (PCD), chromosomal instability induces neoplasic overgrowth.
254 pericentric heterochromatin, with consequent chromosomal instability manifested by increased micronuc
257 cies suggests that substantial and prolonged chromosomal instability might be common in natural popul
259 ecimens and 37 tumor cell lines derived from chromosomal instability neoplasia and microsatellite ins
260 revealed no evidence of aneuploidy or gross chromosomal instability (no difference to adenomas from
261 mb features, and backbone demethylation with chromosomal instability, NSD1 and TP53 mutations, 5q and
262 It corrected the DNA repair defect and the chromosomal instability observed after exposure to a DNA
263 cancer mouse models with persistent mitotic chromosomal instability, observing a decrease in prolife
264 ncer is aneuploidy, which is a result of the chromosomal instability of cancer cells and is thought t
266 ncy did not modify the checkpoint defects or chromosomal instability of Mre11 complex mutants; howeve
267 s are found in many tumors, and the enhanced chromosomal instability of polyploid cells in culture su
269 th in CAFs was significantly associated with chromosomal instability on 4q and 13q and lymphocyte tel
271 r DNA strand separation is the basis for the chromosomal instability or collision of RNA polymerases.
272 early-stage tumors induced by oncoproteins, chromosomal instability, or DNA damage is associated wit
273 ession is a hallmark of cancer cells showing chromosomal instability, particularly in certain breast
275 This hereditary disease is associated with chromosomal instability, premature aging and cancer pred
277 ross 22 tumour types to show that continuous chromosomal instability results in pervasive SCNA hetero
284 ency program and the accumulation of genomic/chromosomal instability that leads to tumorigenesis.
286 e the proteome, the proteins associated with chromosomal instability, the sets of signaling pathways
287 sing disease progression in MPDs by inducing chromosomal instability through the production of DSBs a
288 Overexpression of Mad1 causes aneuploidy and chromosomal instability through weakening mitotic checkp
292 fork stalling in FAN1-deficient cells causes chromosomal instability, we reasoned that the key functi
297 ing during mitosis to prevent aneuploidy and chromosomal instability, which are hallmarks of tumor ce
298 Most human cancers are aneuploid and have chromosomal instability, which contrasts to the inabilit
299 es mitophagy and results in the promotion of chromosomal instability, which enables tumor cells to ef
300 he reported Fanconi anemia (FA) mouse model, chromosomal instability with radial changes can be detec