ライフサイエンスコーパス: mitoses

1 le bundling in interphase cells and aberrant mitoses.

2 w a 92.3% increase in neonatal cardiomyocyte mitoses.

3 are recruited to kinetochores during normal mitoses.

4 resent a new mechanism for regulating closed mitoses.

5 nd is degraded during the embryonic cleavage mitoses.

6 r eukaryotes, PUF proteins promote continued mitoses.

7 LANA expression, and an increased number of mitoses.

8 rogenitor cells had completed their terminal mitoses.

9 cation, centrosome duplication, and abortive mitoses.

10 iated with the highest frequency of abnormal mitoses.

11 chromosome missegregation through multipolar mitoses.

12 abnormal numbers of centrosomes and aberrant mitoses.

13 ich proliferation continued without terminal mitoses.

14 cyclins is required for exit from syncytial mitoses.

15 mosome duplication occur without intervening mitoses.

16 that accumulates during the rapid embryonic mitoses.

17 interphase severely disturbs the subsequent mitoses.

18 ditional S phases without intervening normal mitoses.

19 have finished their developmental program of mitoses.

20 in caps grow into dome-like compartments for mitoses.

21 extended mitosis or successive less extended mitoses.

22 NN classifier "MitosRes-CNN" to filter false mitoses.

23 ion (OXPHOS) module in GC B cells undergoing mitoses.

24 , and hence their identity, through multiple mitoses.

25 ad no consequence on the timing of the early mitoses.

26 ration with an increased number of polyploid mitoses.

27 ts from chromosome damage during error-prone mitoses.

28 remained low during meiosis II and following mitoses.

29 k of human cancers originating from abnormal mitoses.

30 cells initially expand exponentially through mitoses.

31 s centrosome clustering, yielding multipolar mitoses.

32 roper chromosome alignment during Drosophila mitoses.

33 agents may lead to completed but inaccurate mitoses.

34 nation but not for condensation in embryonic mitoses.

35 ty, and Smc5-Smc6-null mutants die in lethal mitoses.

36 defined mechanisms that suppress multipolar mitoses.

37 ficient to cause the formation of multipolar mitoses.

38 exhibited an increased incidence of abnormal mitoses.

39 cause of mechanisms that suppress multipolar mitoses.

40 [vs superficial spreading]), and presence of mitoses (1.7 [1.1-2.6]) (P < .05 for all).

41 AS+ melanoma was associated with presence of mitoses (1.8 [1.0-3.3]), lower tumor-infiltrating lympho

42 ly a result of the difference between 0 to 2 mitoses/10 high-power fields (HPF; 5-year recurrence of

43 F; 5-year recurrence of 31%) and more than 2 mitoses/10 HPF (5-year recurrence of 52%).

44 The 0 to 2 mitoses/10 HPF group was independently associated with i

45 ognosis may be identified using a lower (< 3 mitoses/10 HPF) mitotic count than is usually performed.

46 and graded (low grade: no necrosis and < two mitoses/50 high-powered fields [HPF]; or intermediate gr

47 intermediate grade: necrosis and/or >/= two mitoses/50 HPF) with a simplified schema.

48 cumulate syntelic attachments in unperturbed mitoses, a defect that is partially corrected by BIR1 or

49 mal hepatocytes in vivo triggered dysplastic mitoses, accumulation of supernumerary centrosomes, abno

50 trioles whose presence results in multipolar mitoses and aneuploidy.

51 ome evolution in single cells, during single mitoses and at single-strand resolution.

52 We compare mitoses and CA in patient tumors, xenografts, and tumor

53 to arrest proliferation, leading to abnormal mitoses and cell death, whereas p53 wild-type tumors arr

54 phosphoThr288Aurora-A and increased abnormal mitoses and cellular ploidy, consistent with on-target a

55 y, giant nuclei, multinucleation, multipolar mitoses and centrosome hyperamplification.

56 s led to an increased frequency of defective mitoses and chromosome transmission errors.

57 in A2-deficient CECs appeared to be abnormal mitoses and DNA damage.

58 tein deposits are essential for proper early mitoses and for viability.

59 Endosperm defects include aberrant mitoses and giant polyploid nuclei.

60 ed both in regulating the number of germline mitoses and in the process of oocyte differentation.

61 fication of centrosomes, leading to aberrant mitoses and increased chromosome transmission errors.

62 cell tumors with Homer-Wright rosettes, high mitoses and karyorrhectic index, and strong PHOX2B stain

63 yonic germband in Drosophila, where oriented mitoses and local cell rearrangements appear to direct m

64 vector tumors were infiltrating and had high mitoses and microvessel density, HYAL1-v1 tumors were ne

65 infiltrated with neutrophils, and showed low mitoses and microvessel density.

66 zation of APC2 in postcellularized embryonic mitoses and misorientation of epithelial mitotic spindle

67 irregularity develops quickly, and since no mitoses and only rare possible postmitotic cells were sc

68 showed a significant increase of multipolar mitoses and other spindle pole defects.

69 ant risk stratifier for LN metastases, after mitoses and thickness.

70 n of cell cycle progression, with incomplete mitoses, and a premalignant-like transformation.

71 rganization, nuclear pleomorphism, increased mitoses, and abnormal DNA content.

72 Irradiated cultures contained abnormal mitoses, and after 5 days IGF-1R-inhibited cells showed

73 induced centrosome abnormalities, multipolar mitoses, and aneuploidy often occur at early stages duri

74 play abnormal centrosome numbers, multipolar mitoses, and aneusomy.

75 s were established to measure proliferation, mitoses, and apoptosis.

76 Numerous foci of cellular infiltration, mitoses, and hepatocellular death were observed in liver

77 rnal genome unable to participate in zygotic mitoses, and leads to the development of haploid embryos

78 mis displayed hyperproliferation, suprabasal mitoses, and multinucleated cells.

79 4 mutants exhibit fewer centrioles, aberrant mitoses, and reduced basal bodies in sensory organs.

80 RGPs in the VZ and ensuring their efficient mitoses, and reveal the robust adaptability of RGPs in t

81 ther independent predictors were ulceration, mitoses, and scalp location.

82 of > or =3 centrosomes-generates multipolar mitoses, aneuploidy, and chromosome instability to promo

83 Centrosome aberrations (CA) and abnormal mitoses are considered beacons of malignancy.

84 In homozygous mutant embryos, mitoses are disorganized with an increase in mitotic fig

85 Fourth, germline mitoses are not oriented reproducibly, even within the i

86 We find that mitoses are rare in patient tumors compared with xenogra

87 Abnormal mitoses associated with multiple functional centrosomes,

88 tion of bromo-deoxyuridine incorporation and mitoses at 24 hours after PHx.

89 fferentiate soon after they are generated by mitoses at the surface of the ventricular zone (VZ).

90 ng centre (MTOC) dynamics during the unusual mitoses at various stages of the Plasmodium spp. life cy

91 For species with many mitoses between each meiotic event, mitotic gene convers

92 However, owing to the large number of mitoses between zygote and gamete and because of long mi

93 ounds of DNA replication without intervening mitoses by manipulating the activity of the cyclin-depen

94 We show that the abnormal mitoses can be ameliorated by inhibiting RhoA, the activ

95 ised the possibility that somatic 'reductive mitoses' can also happen in normal hepatocytes.

96 ccumulation of CIN that induces catastrophic mitoses, cell cycle exit, and cell death.

97 nd then reiteratively lost during subsequent mitoses, correlating with transient adhesion disengageme

98 1 KO cells present with evidence of aberrant mitoses coupled to p53 pathway activation.

99 This centrifugal wave of mitoses depends on cell-cell inhibitory interactions med

100 The mitoses do not show any preferential orientation.

101 At the transition from meiosis to cleavage mitoses, Drosophila requires the cell cycle regulators e

102 city in situ and routinely undergo reductive mitoses during regenerative responses.

103 nd amputation triggers two peaks in neoblast mitoses early in regeneration.

104 CD4 locus remained silent through subsequent mitoses, even when the silencer element was excised.

105 r, proceed through unusually short syncytial mitoses, fail to terminate syncytial division following

106 ant increases in multinucleation, multipolar mitoses, failed abscission, asymmetric segregation of da

107 vide, then exhibited an increase in abnormal mitoses followed by massive apoptosis leading to the los

108 on characterized by symmetric and asymmetric mitoses, followed by migration of post-mitotic neurons t

109 integrity, synchronize asymmetric cystocyte mitoses, form interconnected 16-cell germline cysts, and

110 tes by elevating merotely during consecutive mitoses generates CIN in otherwise stable, near-diploid

111 associated with thicker tumors, ulceration, mitoses (>0/mm(2)), nodular histotype, and CNS involveme

112 male gamete formation, after replication and mitoses have been completed and axonemes have been assem

113 ation, fatty change, and apoptosis, abnormal mitoses, hydropic degeneration, and necrosis.

114 to induce increasing degrees of cellularity, mitoses, hypoxia-induced neoangiogenesis and necrosis, f

115 By tracking successive mitoses in a cell lineage, we find that Ret signaling ha

116 One consequence of aberrant mitoses in cfy embryos is an increase in cell death.

117 ex gene expression profiles after successive mitoses in Drosophila development [1].

118 The earliest embryonic mitoses in Drosophila, as in other animals except mammal

119 ent in culture, we demonstrate that tripolar mitoses in early cleavage cause chromosome dispersal to

120 not cell volume, and arises from additional mitoses in larval eye discs.

121 Analysis of mitoses in living and fixed cells reveals that mitotic d

122 Deletion of the USE results in abnormal mitoses in neuroblasts, revealing a role for this sequen

123 k of the Hes1 expression wave, but preceding mitoses in slow dividing CD44(High)CD24(Low) cells appea

124 B3 is the dominant driver of rapid embryonic mitoses in the C. elegans embryo.

125 n in hepatocytes, and the rare occurrence of mitoses in the liver parenchyma.

126 cadian mutants, consistent with asynchronous mitoses in their hair follicles.

127 sion of projections follows that of terminal mitoses in various nuclei, suggesting the consistent use

128 e but undergo a significant number of failed mitoses in which the mitotic spindle does not properly p

129 ne have multiple characteristics of aberrant mitoses, including misaligned chromosomes, lagging chrom

130 tion of amelanotic melanoma with presence of mitoses independently of Breslow thickness and other cli

131 rmore, pole cells enter G1 following induced mitoses, indicating that entry into both mitosis and S p

132 st cancer cells by RNAi resulted in aberrant mitoses, induction of apoptosis, and decreased ability o

133 meiotic divisions in the oocyte to embryonic mitoses is a critical step in animal development.

134 During animal cap mitoses, Kif2a localizes to the spindle poles and centro

135 uently in human cancers, results in abnormal mitoses leading to chromosome instability and possibly t

136 es in host gene expression, cell growth, and mitoses leading to root nodule development.

137 Rather, impaired mitoses led to p53-mediated cell death and contributed t

138 hows a variety of defects including abnormal mitoses, loss of microtubule structures, displacement of

139 chemical damage was accompanied by aberrant mitoses marked by chromosome missegregation.

140 s inherently error-prone, and that polyploid mitoses may help destabilize the cancer genome.

141 These observations suggest that non-apical mitoses might play a role in cell delamination.

142 In contrast to the earlier mitoses, mitosis 16 (M16) is followed by G1, and MCMs do

143 dose paclitaxel induces aberrant, multipolar mitoses, mitotic slippage and multinucleation, triggerin

144 lanomas that were </=2 mm thick and had </=2 mitoses/mm(2) (40 ulcerated; 289 without ulceration), pa

145 ess, mitotic rate (histologically defined as mitoses/mm(2)), and ulceration were the most dominant pr

146 d tumor ulceration with a mitotic rate of 37 mitoses/mm(2).

147 increasing cellular pleomorphism, number of mitoses, nuclear size, and nuclear hyperchromatism.

148 is process is different from the postmeiotic mitoses observed in other fungi.

149 The terminal mitoses occurred in three bursts separated by two 10-h i

150 rea hypersensitivity and associated aberrant mitoses of an rqh1(-) mutant.

151 efficient spindle assembly during subsequent mitoses of daughter cells.

152 king advantage of the naturally synchronized mitoses of Drosophila early embryos, we provide evidence

153 ly, our data demonstrate that while oriented mitoses of individual cells determine neural tube archit

154 nesis: cytokinesis events that follow apical mitoses of NSCs; coordinating abscission with delaminati

155 The stereotyped cross-midline mitoses of progenitors in the zebrafish neural keel prov

156 in the mammalian cortex depends on extensive mitoses of radial glial progenitors (RGPs) residing in t

157 e fragments and bridges were observed in the mitoses of the hemizygous lines.

158 with tumors that had mitotic counts of three mitoses or fewer per 30 high-power fields (HPF), more th

159 .01), satellitosis (P = .03), and increasing mitoses (P = .03).

160 ents with synovial sarcoma with less than 10 mitoses per 10 high-power fields (hpf) had a 10-year can

161 A proliferative threshold of five mitoses per 10 high-power fields (HPF) was of greater pr

162 ter prognostic value than a threshold of two mitoses per 10 HPF for discriminating between low- and i

163 and/or mean mitotic activity greater than 10 mitoses per 10 hpf should be targeted for new therapeuti

164 azard ratio [HR] = 4; P =.006), more than 15 mitoses per 30 HPF (HR = 18; P =.0001), mixed histology

165 <or= 15 mitoses per 30 HPF, and more than 15 mitoses per 30 HPF were 89% +/- 7%, 49% +/- 12%, and 16%

166 wer fields (HPF), more than three to <or= 15 mitoses per 30 HPF, and more than 15 mitoses per 30 HPF

167 .9 cm with a mitotic count of less than 11.5 mitoses per 5 mm(2) or for those with small GISTs (<5.4

168 ) of any site with a count of less than 11.5 mitoses per 5 mm(2).

169 ], 2.3; 95% CI, 1.0 to 5.1; P = .04) and > 5 mitoses per 50 high-power fields (AHR, 2.5; 95% CI, 1.1

170 There were eight to 10 mitoses per 50 high-power fields (Fig 1D).

171 DSS in univariate analysis included < or = 2 mitoses per 50 high-power fields (P =.001, P =.002), vas

172 regrouped on the basis of mitotic rate (< 2 mitoses per 50 high-power fields v higher) and necrosis

173 or other), and mitotic index (<5 or > or =5 mitoses per 50 high-power fields) was developed from 127

174 R 2.72, 95% CI 1.13-6.69, P = 0.026) and > 5 mitoses per 50 HPF (HR 4.77, 95% CI 1.86-13.2, P = 0.001

175 yping of NE tumors is based on the number of mitoses per high powered field and the presences of necr

176 for those with sarcomas with greater than 10 mitoses per hpf (P = .04).

177 Mitotic rate was measured as number of mitoses per mm2 and analyzed as ordered categories (0, <

178 It was proposed that apical progenitor mitoses physically drive these basal translocations non-

179 e labeling method (CLM), the percent labeled mitoses (PLM) method, and a comparison of the time neede

180 egradation ensures that the proper number of mitoses precede the MBT.

181 variety of developmental systems, asymmetric mitoses precede, and are essential for, cellular differe

182 or of angiogenesis, decreasing the number of mitoses present in carcinogen-induced foci of preneoplas

183 cells undergo multiple consecutive abnormal mitoses, producing large cells with giant nuclei and hig

184 e germline of flowering plants undergoes two mitoses, producing two sperm that are carried within a p

185 or N-cadherin results in abnormally oriented mitoses, reduced cross-midline cell divisions, and simil

186 Although tumor size and the number of mitoses remain the best prognostic markers, several stud

187 nds of discrete S phases without intervening mitoses result in polyteny.

188 ernumerary centrosomes to undergo multipolar mitoses resulting in apoptotic cell death.

189 es, increased Breslow thickness, presence of mitoses, severe solar elastosis, and lack of a coexistin

190 interphase basal cells to neighbouring basal mitoses so that they align their horizontal division pla

191 mitotic inhibitors led to increased aberrant mitoses, suggesting a role for these genes in cell cycle

192 eveals catastrophic and highly heterogeneous mitoses, suggesting that analysis of established cell li

193 h the appearance of micronuclei and aberrant mitoses that are a by-product of dissociated chromatin s

194 after the normal cessation of developmental mitoses that produce hair cells.

195 greatest differences seen in the products of mitoses that showed the severest asymmetry in spindle po

196 s demonstrated that in many supposedly equal mitoses the segregation of proteins destined for degrada

197 ing observations of the time elapsed between mitoses, the BAP1 mutation was calculated to occur when

198 incorporation into the DNA, the frequency of mitoses, the expression of cell-cycle control genes, and

199 Although mats depletion leads to aberrant mitoses, this does not seem to be due to compromised mit

200 aughter cell undergoes several amplificatory mitoses, thus generating more cells that embark on the d

201 ucts can lower the number of early embryonic mitoses to 12, whereas increasing maternal Cdc25(twine)

202 dc25(twine) can increase the number of early mitoses to 14.

203 f 0.76 mm or larger, increasing Clark level, mitoses, ulceration, and lymphovascular invasion were in

204 t uses clinicopathologic factors (thickness, mitoses, ulceration, patient age) plus molecular analysi

205 odel with Breslow thickness, sex, age, site, mitoses, ulceration, regression and melanoma subtype.

206 o successive rounds of increasingly aberrant mitoses, ultimately triggering cell death.

207 Further analysis of perturbed mitoses unexpectedly revealed that condensation is a tra

208 A 5-fold increase in abnormal mitoses was observed in the Syk-transfected cells compar

209 The abnormal mitoses were associated with biochemical defects in the

210 ere rare in the IBL and a high proportion of mitoses were asymmetrical, giving rise to one basal daug

211 Mitoses were determined by labeling DNA of adult mice wi

212 Villus height, crypt depth, and crypt cell mitoses were greater in jejunum of transgenics than wild

213 In the PBL, mitoses were more frequent and predominantly symmetrical

214 Moreover, mitoses were never detected in normal myocardium.

215 The postmeiotic mitoses were normal in the homozygous lines; however, ch

216 ation and an increased frequency of aberrant mitoses were observed within 72 h of introduction of p53

217 otypes were not causally linked, and in fact mitoses were prevalent in the sprout field of both wild-

218 tumor thickness and the presence/absence of mitoses were the most powerful predictors of MSS.

219 nia and preleptotene spermatocytes and their mitoses were unaffected by testosterone plus 17beta-estr

220 eby increasing the propensity for multipolar mitoses, which can lead to chromosome missegregation and

221 find that E7-expressing cells undergo normal mitoses with an intact spindle assembly checkpoint and t

222 in nuclear export of BRCA1 protein, aberrant mitoses with extra centrosomes, and genomic instability.

223 protein induces pleomorphic nuclei, aberrant mitoses with extra centrosomes, and tetraploidy.