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 l to limit cell proliferation in response to centrosome amplification.

3 ot RhoB, promoted centrosome duplication and centrosome amplification.

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

5 mosome missegregation, anaphase bridges, and centrosome amplification.

6 on, cellular spindle assembly checkpoint and centrosome amplification.

7 n, resultant beta-catenin stabilization, and centrosome amplification.

8 nce of aneuploidy, chromosome aberration and centrosome amplification.

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

10 nue to reduplicate centrosomes, resulting in centrosome amplification.

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

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

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

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

15 lt in deregulated centrosome duplication and centrosome amplification.

16 m underlying centrosome duplication leads to centrosome amplification.

17 severe chromosome segregation defects due to centrosome amplification.

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

19 centrosomes and that PML deficiency leads to centrosome amplification.

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

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

22 checkpoint integrity, and the development of centrosome amplification.

23 targeting drugs will be arrested and undergo centrosome amplification.

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

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

26 ernumerary centrosomes, a condition known as centrosome amplification.

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

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

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

30 Cancer cells often display centrosome amplification.

31 induce multipolar spindles without requiring centrosome amplification.

32 ocesses of centrosome duplication to prevent centrosome amplification.

33 ion to the procentriole assembly and induces centrosome amplification.

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

35 hosphorylation after irradiation and reduced centrosome amplification.

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

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

38 ication and the PLK4 overexpression-mediated centrosome amplification.

39 required for PIDDosome activation following centrosome amplification.

40 ndent ubiquitination of gamma-tubulin causes centrosome amplification.

41 for inhibiting tumorigenesis associated with centrosome amplification.

42 I42V resulted in BRCA1 proteins that caused centrosome amplification.

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

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

45 its centrosomal retention and regulation of centrosome amplification.

46 neither cytokinesis failure nor increase in centrosome amplification.

47 sistant cancers exhibiting high incidence of centrosome amplification.

48 trosome duplication and for the induction of centrosome amplification.

49 of this key centriole protein and preventing centrosome amplification.

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

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

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

53 Centrosome amplification, accompanied by the overexpress

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

55 Centrosome amplification after hydroxyurea treatment inc

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

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

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

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

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

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

62 Centrosome amplification and aberrant mitosis with misal

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

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

65 Marked centrosome amplification and an increased frequency of a

66 oved understanding of the molecular basis of centrosome amplification and aneuploidy.

67 centriole duplication machinery and induces centrosome amplification and aneuploidy.

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

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

70 Centrosome amplification and chromosomal instability occ

71 Uncontrolled centriole duplication leads to centrosome amplification and chromosomal instability, bu

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

73 cluding spindle assembly checkpoint failure, centrosome amplification and chromosome segregation erro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 proliferation and cyst growth; (3) abnormal centrosome amplification and multipolar spindle formatio

92 d consistent and severe mitotic failure with centrosome amplification and multipolar spindle formatio

93 and induces mitotic abnormalities, including centrosome amplification and multipolar spindle formatio

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

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

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

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

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

99 and the mitotic kinase NEK2 in vitro drives centrosome amplification and the accumulation of CIN tha

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

101 4 reduction serves as a mechanism leading to centrosome amplification and tumorigenesis.

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

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

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

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

106 dy, including incomplete replication of DNA, centrosome amplification, and formation of nonperpendicu

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

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

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

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

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

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

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

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

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

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

117 53, Plk4 overexpression generated widespread centrosome amplification, but did not drive additional t

118 53 function alone is not sufficient to drive centrosome amplification, but plays a critical role in t

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

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

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

122 Centrosome amplification (CA) contributes to carcinogene

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

124 e assembly, and elevated PLK4 levels promote centrosome amplification (CA), a founding event of tumor

125 Therapies targeting centrosome amplification (CA), a key mediator of chromos

126 A numerical increase in centrosomes, or centrosome amplification (CA), is common in cancer and c

127 These processes prevent centrosome amplification (CA), mitotic dysfunction, and

128 upernumerary centrosomes, a condition called centrosome amplification (CA).

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

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

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

132 Thus, centrosome amplification can initiate tumorigenesis in f

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

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

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

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

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

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

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

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

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

142 Here, we show that centrosome amplification, commonly observed in cancer an

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

144 However, centrosome amplification could be suppressed in irradiat

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

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

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

148 Tumors arising from centrosome amplification exhibit frequent mitotic errors

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

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

151 Centrosome amplification frequently occurs in human canc

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

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

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

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

156 Centrosome amplification has been extensively associated

157 Centrosome amplification has been implicated as the caus

158 Centrosome amplification has long been recognized as a f

159 The overproduction of centrosomes (known as centrosome amplification) has been reported in a variety

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 We found that centrosome amplification in interphase and mitotic cells

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 nd CETN2 are necessary for infection-induced centrosome amplification, in a manner that requires the

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

194 Centrosome amplification induced by DNA damage or by PLK

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

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

197 Recognizing that centrosome amplification is a common feature of aneuploi

198 Centrosome amplification is a common feature of human tu

199 Centrosome amplification is a common feature of human tu

200 Centrosome amplification is a common feature of many can

201 Centrosome amplification is a common feature of many typ

202 Centrosome amplification is a hallmark of human cancers

203 Given that centrosome amplification is already observed in MGUS and

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

205 Here, we show that centrosome amplification is associated with and sufficie

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

207 Centrosome amplification is common in myeloma and may be

208 Centrosome amplification is frequent in cancer, but the

209 Centrosome amplification is frequently observed in tumor

210 Centrosome amplification is poorly tolerated by non-tran

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

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

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

214 n breast cancer; however, the role of p15 in centrosome amplification is unknown.

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

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

217 Centrosome amplification mediated by CteG-CETN2 interact

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

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

220 pharmacologically, induced aberrant mitosis, centrosome amplification, multipolar spindles, and chrom

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

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

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

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

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

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

227 Centrosome amplification, or the condition of having mor

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

229 1 is associated with an exacerbation of the centrosome amplification phenotype associated with BRCA

230 Centrosome amplification plays a key role in the origin

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

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

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

234 Centrosome amplification results primarily from overdupl

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

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

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

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

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

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

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

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

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

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

245 In non-transformed cells, centrosome amplification triggers PIDDosome activation a

246 over-duplicated centrioles, suggesting that centrosome amplification underlies the development of HI

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

248 Centrosome amplification was dependent on cdk2/cyclin ac

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

250 Centrosome amplification was detected in in situ ductal

251 Centrosome amplification was found to occur at a very ea

252 Centrosome amplification was initially detected at 3 mo

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

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

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

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

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

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

259 Centrosome amplification, which is frequently observed i

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

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

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

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

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