ライフサイエンスコーパス: centrosome amplification

1 n the presence of more than two centrosomes (centrosome amplification).

2 nce of aneuploidy, chromosome aberration and centrosome amplification.

3 on of p53 leads to an increased frequency of centrosome amplification.

4 nue to reduplicate centrosomes, resulting in centrosome amplification.

5 sence of cyclin E, cyclin A is important for centrosome amplification.

6 ary and sufficient mediator of MYCN-mediated centrosome amplification.

7 on signal led to low CHK1 activation and low centrosome amplification.

8 oss of FoxM1 resulted in spindle defects and centrosome amplification.

9 ng p53 responses to DNA damage, facilitating centrosome amplification.

10 lt in deregulated centrosome duplication and centrosome amplification.

11 hosphorylation after irradiation and reduced centrosome amplification.

12 m underlying centrosome duplication leads to centrosome amplification.

13 severe chromosome segregation defects due to centrosome amplification.

14 ed, centrosome index (CI) as a surrogate for centrosome amplification.

15 centrosomes and that PML deficiency leads to centrosome amplification.

16 s that KAT2A/2B acetylation of PLK4 prevents centrosome amplification.

17 ally inhibit KLF4, gamma-irradiation induced centrosome amplification.

18 ogether with inactivation of p53, results in centrosome amplification.

19 checkpoint integrity, and the development of centrosome amplification.

20 targeting drugs will be arrested and undergo centrosome amplification.

21 Gadd45A-null mutation (Gadd45a(-/-)) suffer centrosome amplification.

22 pe and Gadd45a(-/-) cells repressed abnormal centrosome amplification.

23 ernumerary centrosomes, a condition known as centrosome amplification.

24 well as to overexpression of ratAurA and to centrosome amplification.

25 KLF14 is sufficient to induce Plk4-directed centrosome amplification.

26 normal p53 null cells was not accompanied by centrosome amplification.

27 lity in vivo may be associated with abnormal centrosome amplification.

28 ication and the PLK4 overexpression-mediated centrosome amplification.

29 ndent ubiquitination of gamma-tubulin causes centrosome amplification.

30 for inhibiting tumorigenesis associated with centrosome amplification.

31 I42V resulted in BRCA1 proteins that caused centrosome amplification.

32 ssion of LMO2 in DLBCL cell lines results in centrosome amplification.

33 l cycle and promotes cyclin D1 stability and centrosome amplification.

34 its centrosomal retention and regulation of centrosome amplification.

35 neither cytokinesis failure nor increase in centrosome amplification.

36 trosome duplication and for the induction of centrosome amplification.

37 of this key centriole protein and preventing centrosome amplification.

38 ot RhoB, promoted centrosome duplication and centrosome amplification.

39 4 self-limits Plk4 activity so as to prevent centrosome amplification.

40 mosome missegregation, anaphase bridges, and centrosome amplification.

41 on, cellular spindle assembly checkpoint and centrosome amplification.

42 Genotoxic stresses lead to centrosome amplification, a frequently-observed feature

43 These findings demonstrate that centrosome amplification, a structural alteration of the

44 Finally, cells with DRT/DMC chromosomes have centrosome amplification, abnormal spindle assembly, end

45 Centrosome amplification, accompanied by the overexpress

46 ied by loss of p53 integrity, development of centrosome amplification, acquired estrogen receptor (ER

47 Centrosome amplification after hydroxyurea treatment inc

48 y ablates the MYCN-dependent contribution to centrosome amplification after ionizing radiation.

49 or the p53 alleles (HCT116 p53-/-) exhibited centrosome amplification after irradiation.

50 ession data correlated well with IF detected centrosome amplification allowing us to derive a, gene e

51 s carrying defective p53, the development of centrosome amplification also occurred following treatme

52 n mitotic cells, knockdown of Kif5b leads to centrosome amplification and a chromosomal segregation d

53 ollowing mitogen stimulation, they developed centrosome amplification and a higher frequency of aberr

54 Centrosome amplification and aberrant mitosis with misal

55 The loss or mutation of BRCA1 causes centrosome amplification and abnormal mitotic spindle as

56 cells leads to chromosomal polyploidization, centrosome amplification and abnormal mitotic spindle fo

57 Marked centrosome amplification and an increased frequency of a

58 ation promotes the ability of Pin1 to induce centrosome amplification and cell transformation.

59 DAPK1 inhibits the ability of Pin1 to induce centrosome amplification and cell transformation.

60 Centrosome amplification and chromosomal instability occ

61 tionally, ablation of Cdk4 or Cdk2 abrogates centrosome amplification and chromosome instability in p

62 gether with loss of p53, efficiently induces centrosome amplification and CIN in human bladder cancer

63 Deletion of Gadd45a leads to centrosome amplification and consequent abnormal mitosis

64 rs with compromised p53 function may develop centrosome amplification and consequent chromosomal inst

65 alities: (1) Morgana underexpression induces centrosome amplification and cytogenetic abnormalities,

66 ons, mediated by the MAPK pathway, including centrosome amplification and formation of mitotic chromo

67 for efficient cell proliferation, control of centrosome amplification and genome stability.

68 Further characterization of SCCs revealed centrosome amplification and genomic alterations by arra

69 promotes LSC development, partly by causing centrosome amplification and genomic instability.

70 nesis failure as a primary event, leading to centrosome amplification and gross chromosomal abnormali

71 human breast cancer tissues correlates with centrosome amplification and higher nuclear grade.

72 proteins E6 and E7 have been shown to cause centrosome amplification and lagging chromosomes during

73 sion of MAK leads to mitotic defects such as centrosome amplification and lagging chromosomes.

74 bulin complex that is critically involved in centrosome amplification and microtubule aster formation

75 ably include prior genome tetraploidization, centrosome amplification and mitotic checkpoint defects.

76 SP33 destabilizes CP110 and thereby inhibits centrosome amplification and mitotic defects.

77 ebrates, but not yeast, its depletion causes centrosome amplification and multinucleate division, but

78 oss of PC1 function is sufficient to produce centrosome amplification and multipolar spindle formatio

79 but not the CHC22 clathrin isoform, induced centrosome amplification and multipolar spindles.

80 y, we show a significant correlation between centrosome amplification and MYCN amplification in prima

81 a-A gene expression has been correlated with centrosome amplification and proliferation; thus, inhibi

82 s and ubiquitinates gamma-tubulin to inhibit centrosome amplification and promote microtubule nucleat

83 ltured Brca1(FL/FL) cells exhibited abnormal centrosome amplification and reduction of G(1) populatio

84 uses mitotic arrest, micronucleus induction, centrosome amplification and tubulin disruption, even th

85 4 reduction serves as a mechanism leading to centrosome amplification and tumorigenesis.

86 d centrosome index (CI) that correlated with centrosome amplification and was an independent prognost

87 H-RAS(V12) and activated MEK1 also induced centrosome amplification, and chromosome misalignment.

88 indle checkpoint, abnormal mitotic spindles, centrosome amplification, and chromosome missegregation.

89 ia (aCML), preceded by ROCK hyperactivation, centrosome amplification, and cytogenetic abnormalities

90 NA interference resulted in multinucleation, centrosome amplification, and mitotic defects, although

91 al chromosome condensation failure, aberrant centrosome amplification, and substantial DNA damage.

92 romosome aberrations, gene amplification and centrosome amplification, and was accompanied by abnorma

93 he i(3q) induces a 'cut' phenotype, abnormal centrosome amplification, aneuploidy and loss of G1 arre

94 l-like factor 14 (KLF14) gene in mice causes centrosome amplification, aneuploidy and spontaneous tum

95 This leads to centrosome amplification, aneuploidy, and tumorigenesis,

96 reast cancer cell lines, increased levels of centrosome amplification are accompanied by efficient cl

97 mechanisms downstream of MYCN that generate centrosome amplification are incompletely characterized.

98 ence, the molecular mechanisms that underlie centrosome amplification are only beginning to emerge.

99 for experimental carcinogenesis, we analyzed centrosome amplification as a cellular marker for early

100 53, Plk4 overexpression generated widespread centrosome amplification, but did not drive additional t

101 53 function alone is not sufficient to drive centrosome amplification, but plays a critical role in t

102 Absence of Cdk2 or Cdk4 prevents centrosome amplification by abrogating excessive centrio

103 en (ST), a reported PP2A inhibitor, promotes centrosome amplification by an unknown mechanism.

104 Here, we test the consequence of centrosome amplification by creating mice in which centr

105 Centrosome amplification (CA) contributes to carcinogene

106 Centrosome amplification (CA) is a hallmark of cancer, o

107 s, we constructed and analyzed mice in which centrosome amplification can be induced by a Cre-recombi

108 In mouse cells, centrosome amplification can be readily induced by loss

109 ls, and it has been previously proposed that centrosome amplification can drive genetic instability a

110 Thus, centrosome amplification can initiate tumorigenesis in f

111 of satellite DNA can phenocopy BRCA1 loss in centrosome amplification, cell-cycle checkpoint defects,

112 ested for correlation with three measures of centrosome amplification: centrosome size, centrosome nu

113 encoding gene, whose overexpression leads to centrosome amplification, chromosomal instability and tr

114 der estrogen control, and is coincident with centrosome amplification, chromosomal instability, and a

115 f aurora kinase A in mammalian cells induces centrosome amplification, chromosome instability and onc

116 duplication and its deregulation can induce centrosome amplification, chromosome instability, and on

117 C function in MDCK and mIMCD3 cells leads to centrosome amplification, chromosome lagging and multipo

118 led to genetic instability, characterized by centrosome amplification, chromosome tetraploidization a

119 ogen receptor alpha to Aur-A overexpression, centrosome amplification, CIN, and aneuploidy leading to

120 ults demonstrate that independent aspects of centrosome amplification correlate with chromosomal inst

121 However, centrosome amplification could be suppressed in irradiat

122 cells exposed to VR23 underwent an abnormal centrosome amplification cycle caused by the accumulatio

123 persal of the Golgi apparatus and concurrent centrosome amplification during the interphase.

124 n mouse mammary glands also potently induces centrosome amplification, eventually leading to mammary

125 Tumors arising from centrosome amplification exhibit frequent mitotic errors

126 ke transcription factor, KLF4, in preventing centrosome amplification following DNA damage caused by

127 both necessary and sufficient in preventing centrosome amplification following gamma-radiation-induc

128 Centrosome amplification frequently occurs in human canc

129 ase, Aurora-A/STK15, have been implicated in centrosome amplification, genome instability and cellula

130 ssion of Aurora-A in mammalian cells induces centrosome amplification, genomic instability and transf

131 a support a direct causal relationship among centrosome amplification, genomic instability, and tumor

132 comparison, other BRCA1 variants that caused centrosome amplification had clustering of supernumerary

133 Centrosome amplification has been extensively associated

134 Centrosome amplification has been implicated as the caus

135 Centrosome amplification has long been recognized as a f

136 Aurora-A (Aur-A), a centrosome kinase, and centrosome amplification have been implicated in the ori

137 omagenesis, and patients with more extensive centrosome amplification have shorter survival, the mech

138 The molecular mechanisms that underlie centrosome amplification, however, are poorly characteri

139 s issue by generating a mouse model inducing centrosome amplification in a naturally proliferative ep

140 Herein we show that MYCN mediates centrosome amplification in a p53-dependent manner.

141 s to Aurora A kinase activation and abnormal centrosome amplification in a Pak1-independent manner.

142 this is an important adaptation mechanism to centrosome amplification in cancer.

143 transient event establishes an incidence of centrosome amplification in cell populations.

144 cyclin E greatly influences the frequency of centrosome amplification in cells lacking functional p53

145 ncer drugs that target DNA synthesis induces centrosome amplification in cells lacking p53 tumor supp

146 pproximately 25% of Klf4(-/-) MEFs exhibited centrosome amplification in contrast to the less than 5%

147 s, we here report that mutant Pik3ca induces centrosome amplification in cultured cells (through a pa

148 free centrosomes in Drosophila embryos, and centrosome amplification in cultured Drosophila and huma

149 how that Pin1 overexpression correlates with centrosome amplification in human breast cancer tissues.

150 elated with DAPK1 levels and negatively with centrosome amplification in human breast cancer.

151 of correlation between p53 mutation and CIN/centrosome amplification in human cancer can be detected

152 inally, Plk1 depletion significantly reduces centrosome amplification in hydroxyurea-treated U2OS cel

153 We found that centrosome amplification in interphase and mitotic cells

154 ectively; however, lead oxide did not induce centrosome amplification in interphase or mitotic cells.

155 export sequence blocked BRCA1 regulation of centrosome amplification in irradiated cells.

156 levels in mice with functional p53 produced centrosome amplification in liver and skin, but this did

157 nscriptional inhibition dramatically affects centrosome amplification in MYCN-induced cells, indicati

158 cell lines, MYCN (N-Myc) expression induces centrosome amplification in response to ionizing radiati

159 ynthesis and Pin1 inhibition also suppresses centrosome amplification in S-arrested CHO cells.

160 ng vertebrate cells, a role that also limits centrosome amplification in S-phase-arrested cells.

161 with our in vitro findings, we also observed centrosome amplification in the kidneys from human ARPKD

162 ociating cyclins, namely cyclins E and A, in centrosome amplification in the p53-negative cells.

163 formed human cell cultures did not establish centrosome amplification in the short or long terms.

164 oduced a modest increase in the incidence of centrosome amplification in the short term, which did no

165 tested whether cleavage failure established centrosome amplification in transformed cell populations

166 The presence of extensive centrosome amplification in tumors and hyperplastic glan

167 lack of Cebpd causes genomic instability and centrosome amplifications in primary embryonic fibroblas

168 ncreased centrosomal microtubule nucleation, centrosome amplification increases Rac1 activity, which

169 Centrosome amplification induced by DNA damage or by PLK

170 of the centrosome cycle and that it mediates centrosome amplification induced by various altered tumo

171 (2)-arrested cells, cyclin A is important in centrosome amplification irrespective of the cyclin E st

172 Recognizing that centrosome amplification is a common feature of aneuploi

173 Centrosome amplification is a common feature of human tu

174 Centrosome amplification is a common feature of human tu

175 Centrosome amplification is a common feature of many can

176 Centrosome amplification is a common feature of many typ

177 Given that centrosome amplification is already observed in MGUS and

178 n in situ ductal carcinomas, suggesting that centrosome amplification is an early event in these lesi

179 these functions contribute to prevention of centrosome amplification is being investigated.

180 Centrosome amplification is common in myeloma and may be

181 Centrosome amplification is frequent in cancer, but the

182 Centrosome amplification is poorly tolerated by non-tran

183 ly converges toward a stable ploidy in which centrosome amplification is significantly decreased, tho

184 s to bladder cancer specimens and found that centrosome amplification is strongly correlated with con

185 e et al. (2017) provide strong evidence that centrosome amplification is sufficient to initiate tumor

186 r growth, higher tumor histopathology grade, centrosome amplification, loss of nuclear ERalpha expres

187 hese results further suggest that aspects of centrosome amplification may have clinical diagnostic an

188 chromosomes, anaphase bridges, micronuclei, centrosome amplification, multinucleated cells, gradual

189 ulted in generation of multinucleated cells, centrosome amplification, multipolar mitotic spindles, a

190 in immortalized epithelial cells, including centrosome amplification, multipolar spindles, and chrom

191 Centrosome amplification (number and area/cell) was dete

192 alence of hyperdiploid chromosome number and centrosome amplification observed in many cancers.

193 the first in vivo evidence that significant centrosome amplification occurs in kidneys from conditio

194 ased centrosome numbers (also referred to as centrosome amplification) often accompany genomic instab

195 cing of endogenous p53 alone does not induce centrosome amplification or CIN, although high degrees o

196 Centrosome amplification, or the condition of having mor

197 Thus, the high frequency of centrosome amplification, particularly in more aggressiv

198 1 is associated with an exacerbation of the centrosome amplification phenotype associated with BRCA

199 Centrosome amplification plays a key role in the origin

200 ocesses (beta-adrenergic receptor recycling, centrosome amplification, RalB signaling, and cancer cel

201 uestration and reestablishes control against centrosome amplification, regardless of mutant p53 statu

202 n of the G1/S cell cycle transition leads to centrosome amplification responsible for breast cancer p

203 Centrosome amplification results primarily from overdupl

204 shorter survival, the mechanisms leading to centrosome amplification should be investigated as these

205 Preventing Plk4 autoregulation causes centrosome amplification, stabilization of p53, and loss

206 rgeted disruption of murine BRCA1 results in centrosome amplification, suggesting that BRCA1 serves a

207 Orc6 depletion during the S phase triggers centrosome amplification suppressed by G2 checkpoint inh

208 likely the genetic instability arising from centrosome amplification that is associated, at least in

209 Moreover, in cancer cells with centrosome amplification, the CEP215-HSET complex promot

210 Furthermore, in tumor cells with centrosome amplification, the failure to restrict cortic

211 Centrosome amplification-the acquisition of > or =3 cent

212 k phosphorylation site (NPM(T199A)) prevents centrosome amplification to the same extent as ablation

213 human mammary epithelial cells, we find that centrosome amplification triggers cell invasion.

214 Disruption of this process causes centrosome amplification, unequal segregation of chromos

215 Centrosome amplification was dependent on cdk2/cyclin ac

216 Using immunofluorescent (IF) staining, centrosome amplification was detected in 67% of monoclon

217 Centrosome amplification was detected in in situ ductal

218 Centrosome amplification was found to occur at a very ea

219 Centrosome amplification was initially detected at 3 mo

220 ults suggest that ratAurA overexpression and centrosome amplification were linked to tumor developmen

221 Moreover, isogenic cells with conditional centrosome amplification were more sensitive to GF-15 th

222 e and healthy, although epidermal cells with centrosome amplification were still appreciable.

223 cyclin E, but not cyclin A, is important in centrosome amplification, whereas in the absence of cycl

224 CHK1 is required for DNA damage-induced centrosome amplification, whereas MCPH1 deficiency great

225 that cells stably overexpressing MTA1 showed centrosome amplification which has been long implicated

226 Centrosome amplification, which is frequently observed i

227 ause it immediately produces tetraploidy and centrosome amplification, which is thought to produce ge

228 tumors exhibited aneuploidy associated with centrosome amplification, which may underlie the mechani

229 Absence of Brca2 also led to centrosome amplification, which we found associated with

230 polar spindle frequency that correlated with centrosome amplification, while loss of Hsp72 or Nek6 fu

231 s study, we investigated the relationship of centrosome amplification with aneuploidy, chromosomal in