ライフサイエンスコーパス: mitoses

1 are recruited to kinetochores during normal mitoses.

2 resent a new mechanism for regulating closed mitoses.

3 nd is degraded during the embryonic cleavage mitoses.

4 r eukaryotes, PUF proteins promote continued mitoses.

5 LANA expression, and an increased number of mitoses.

6 rogenitor cells had completed their terminal mitoses.

7 cation, centrosome duplication, and abortive mitoses.

8 iated with the highest frequency of abnormal mitoses.

9 chromosome missegregation through multipolar mitoses.

10 abnormal numbers of centrosomes and aberrant mitoses.

11 ich proliferation continued without terminal mitoses.

12 cyclins is required for exit from syncytial mitoses.

13 mosome duplication occur without intervening mitoses.

14 that accumulates during the rapid embryonic mitoses.

15 interphase severely disturbs the subsequent mitoses.

16 ditional S phases without intervening normal mitoses.

17 have finished their developmental program of mitoses.

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

19 ration with an increased number of polyploid mitoses.

20 remained low during meiosis II and following mitoses.

21 k of human cancers originating from abnormal mitoses.

22 cells initially expand exponentially through mitoses.

23 s centrosome clustering, yielding multipolar mitoses.

24 roper chromosome alignment during Drosophila mitoses.

25 agents may lead to completed but inaccurate mitoses.

26 nation but not for condensation in embryonic mitoses.

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

28 defined mechanisms that suppress multipolar mitoses.

29 ficient to cause the formation of multipolar mitoses.

30 exhibited an increased incidence of abnormal mitoses.

31 cause of mechanisms that suppress multipolar mitoses.

32 w a 92.3% increase in neonatal cardiomyocyte mitoses.

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

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

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

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

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

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

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

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

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

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

43 trioles whose presence results in multipolar mitoses and aneuploidy.

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

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

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

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

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

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

50 Endosperm defects include aberrant mitoses and giant polyploid nuclei.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 Abnormal mitoses associated with multiple functional centrosomes,

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

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

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

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

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

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

82 The mitoses do not show any preferential orientation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 efficient spindle assembly during subsequent mitoses of daughter cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 ], 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 The abnormal mitoses were associated with biochemical defects in the

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

175 Mitoses were determined by labeling DNA of adult mice wi

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

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

178 Moreover, mitoses were never detected in normal myocardium.

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

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

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

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

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

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

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

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

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