ライフサイエンスコーパス: CIN

1 CIN can be induced in the mouse by inactivating the spin

2 CIN CM-induced nephropathy was defined as an increase in

3 CIN developed after 23 procedures (2.4%).

4 CIN grade 1 was detected in 11.6% of women with HPV test

5 CIN grade 3 or more severe (CIN3+) lesions were detected

6 CIN has been linked to carcinogenesis, metastasis, poor

7 CIN is a common complication of PCI and is associated wi

8 CIN is driven by chromosome segregation errors and a tol

9 CIN is generally considered to drive tumorigenesis, but

10 CIN is observed in most solid tumours and is associated

11 CIN responses coincide with phasic firing of DAergic neu

12 CIN tumours are characterised by a large number of somat

13 CIN-suppressor gene silencing leads to DNA replication s

14 ed specificity (with a threshold of grade <2 CIN) was 83% (95% CI, 80% to 86%) for women with ASC-US

15 ervical intraepithelial neoplasia grade 2/3 [CIN 2/3]) and (2) incident transient infections lasting

16 Fbw7(-)/(-); p53(-)/(-) carcinomas exhibit a CIN(+) phenotype.

17 ase is overexpressed in breast tumors with a CIN phenotype, and overexpression of exogenous JMJD2B in

18 -like behaviors and suggesting that accumbal CIN activity is crucial for the regulation of mood and m

19 Acute CIN was defined as an increase in serum creatinine conce

20 We compared the risk of acute CIN and the influence of preventive strategies in patien

21 C or NaHCO3 did not reduce the rate of acute CIN significantly.

22 Our results suggest advancing CIN disease severity is associated with increasing vagin

23 uency of chromosome segregation errors after CIN-suppressor gene silencing, and attenuates segregatio

24 The proposed network architectures and CIN connectivity allow the models to closely reproduce a

25 tem drives to rhythm-generating circuits and CIN pathways.

26 Together, our results link CSCs, EMT, and CIN through the BMI1-AURKA axis and suggest therapeutic

27 The 5-year cumulative incidence of HSIL+ and CIN-2+ was similar in HIV-infected women and HIV-uninfec

28 inine level was measured 3-5 days later, and CIN was defined as an increase of 25% of more from the b

29 h respect to histopathology, metastasis, and CIN.

30 cells elevates chromosome missegregation and CIN.

31 y resulting in chromosome missegregation and CIN.

32 ule assembly, chromosome missegregation, and CIN.

33 es of both cervical screening prevalence and CIN, was used to compute CIN trends from January 1, 2007

34 ase domains spliced from adjacent SH3BP1 and CIN gene loci.

35 reduce incidence and progression of SIL and CIN and ultimately incidence of invasive cervical cancer

36 nock-in HSCs with serial transplantation and CIN in hematopoietic stem and progenitor cells.

37 m (AY-WB) binds and destabilizes Arabidopsis CIN (CINCINNATA) TCP (TEOSINTE-BRANCHED, CYCLOIDEA, PROL

38 ently overexpressed in human tumors that are CIN.

39 ncer, providing a logical connection between CIN and prognostic signature expression.

40 polymerase II TATA-box binding factor, cause CIN when overexpressed in human cells.

41 candidate list to identify genes that cause CIN when overexpressed in cancer, which can then be leve

42 the budding yeast for yeast genes that cause CIN when overexpressed, a phenotype we refer to as dosag

43 t centromere and kinetochore function causes CIN through chromosome missegregation, leading to aneupl

44 rcumstances in which pRB inactivation causes CIN in human cancers are unclear.

45 entromeric chromatin in model systems causes CIN.

46 how that the cofilin phosphatase chronophin (CIN) spatiotemporally regulates cofilin activity at the

47 ween route of administration and comparative CIN risk.

48 ning prevalence and CIN, was used to compute CIN trends from January 1, 2007, to December 31, 2014.

49 NGAL depicted CIN in patients who received iodinated contrast material

50 found to be higher among those who developed CIN CM-induced nephropathy compared with those who did n

51 .60 mumol/L) were not at risk for developing CIN (P = .25, power > 95%).

52 Risk of developing CIN CM-induced nephropathy is relatively low in patients

53 c midbrain afferents can evoke the different CIN responses, we recorded from adult olfactory tubercle

54 Furthermore, distinguishing CIN, which consists of elevated rates of chromosome miss

55 Notably, DMS CIN ensembles tracked rats' beliefs about the current st

56 expressed, a phenotype we refer to as dosage CIN (dCIN), and identified 245 dCIN genes.

57 ast three domains are required for efficient CIN-TCP destabilization in plants.

58 ation and discrimination for both endpoints (CIN AUC for full model 0.85 and for reduced model 0.84,

59 ng NEK2 in cancer cells resulted in enhanced CIN, cell proliferation and drug resistance, while targe

60 Here we evaluate CIN in human cells that become polyploid through an expe

61 zation of parallel inhibitory and excitatory CIN pathways and suggest explanations for how these path

62 with elevated human Tdp1 levels also exhibit CIN that can be partially rescued by siRNA-mediated knoc

63 ia and chromatid cohesion genes does explain CIN in the minority of cases.

64 Influenza Clinical Information Network (FLU-CIN) was established to gather detailed clinical and epi

65 For CIN-3+, the cumulative risk averaged 4% (95% CI, 1%-8%)

66 between September 2003 and February 2010 for CIN lesions used topical interferon alfa 1 million IU/ml

67 Understanding a mechanistic basis for CIN is therefore paramount.

68 stration were identified as risk factors for CIN under the current treatment strategy.

69 = 0.82; net reclassification improvement for CIN 2.92%, p = 0.06).

70 itself as a target for Aurora-A relevant for CIN.

71 r of inpatients identified to be at risk for CIN but would reduce misidentification of a large number

72 (>2.0 mg/dL) subgroups of presumed risk for CIN by using baseline serum creatinine (SCr) level.

73 re classified as having high or low risk for CIN on the basis of absolute glomerular filtration rate

74 Iodixanol had a slightly lower risk for CIN than LOCM, but the lower risk did not exceed a crite

75 Most inpatients were considered low risk for CIN with commonly used thresholds: 92.6% (26 285 of 28 3

76 ventive measure in patients at high risk for CIN.

77 We show that treatment for CIN significantly alters the biochemistry of the cervix,

78 ade 2 or greater (CIN-2+; threshold used for CIN treatment) and grade 3 or greater (CIN-3+; threshold

79 distinguish normal cervix from CIN and from CIN to CC.

80 toff value to distinguish normal cervix from CIN and from CIN to CC.

81 hanges in centromere structure and generates CIN.

82 ow-grade CIN (grade 1 [CIN1]) and high-grade CIN (grade 2 [CIN2] and grade 3 [CIN3]).

83 expressed by a high percentage of high-grade CIN and cervical cancers associated with carcinogenic HP

84 were hardly ever associated with high-grade CIN and, almost exclusively, represented false-positive

85 pecified outcome measures included low-grade CIN (grade 1 [CIN1]) and high-grade CIN (grade 2 [CIN2]

86 ositive women had 13-fold (P = .001) greater CIN-3+ risk than oncHPV-negative women (referent), and H

87 ntraepithelial neoplasia grade 2 or greater (CIN-2+; threshold used for CIN treatment) and grade 3 or

88 d for CIN treatment) and grade 3 or greater (CIN-3+; threshold to set screening practices) were measu

89 HIV-infected and 1 HIV-uninfected woman had CIN-3, but none had cancer.

90 rt the idea that tumours with extremely high CIN are less tolerant to specific genotoxic therapies.

91 cells exhibit low CIN, and we generated high CIN by reducing expression of the kinesin-like mitotic m

92 estinal organoid studies confirmed that high CIN does not inhibit tumor cell initiation but does inhi

93 However, whether high CIN inhibits tumor initiation or suppresses the growth a

94 high CA20 score may reflect tumors with high CIN and potentially other aggressive features that may r

95 enign; a subset of genes upregulated in high-CIN cancers predict aggressive disease in human patients

96 ol to the hematopoietic system and highlight CIN as a characteristic feature of HSC dysfunction and m

97 However, how CIN drives tumor progression to metastasis remains elusi

98 0.992; 95% CI: 0.925, 1.000) in identifying CIN 8 hours after iomeprol administration.

99 release of DA itself evoked acute changes in CIN firing.

100 enuates segregation errors and DNA damage in CIN(+) cells.

101 Population-level decreases in CIN among cohorts partially vaccinated for HPV may be co

102 This drop in ERalpha in CIN and tumor cells was confirmed at the protein level.

103 No differences were found in CIN risk among types of LOCM.

104 ld level exists whereby further increases in CIN frequency in fact hinder tumor growth.

105 Reducing GTSE1 levels in CIN cancer cell lines reduces chromosome missegregation

106 are subject to frequent copy number loss in CIN(+) CRC.

107 to molecular pathways regulated by miRNAs in CIN.

108 ation of core regulators of proliferation in CIN-associated cancer genomes.

109 we investigated the role of APC proteins in CIN.

110 ontrolled trials found a slight reduction in CIN risk with the iso-osmolar contrast media agent iodix

111 The greatest reduction in CIN was seen with N-acetylcysteine plus IV saline in pat

112 -/-) mouse embryonic fibroblasts resulted in CIN gene regulatory region occupancy by the DNA-bound fo

113 ts modifications may have a critical role in CIN in human cancers.

114 sion and increased DNA replication stress in CIN(+) colorectal cancer (CRC) cells relative to CIN(-)

115 herapeutic exploitation, drugs that increase CIN beyond this therapeutic threshold are currently limi

116 centromere-associated H3K9me3 and increased CIN.

117 romote disease progression through increased CIN, but the mechanistic role of APC in preventing CIN r

118 iome diversity is associated with increasing CIN severity.

119 imal model focusing on mitotic error-induced CIN.

120 centromere-associated kinesin) can influence CIN through its impact on MT stability, but how its pote

121 ch are hallmarks of chromosomal instability (CIN) and Bub1 insufficiency.

122 phenotypes such as chromosomal instability (CIN) and invasiveness.

123 Chromosomal instability (CIN) contributes to cancer evolution, intratumor heterog

124 some missegregation/chromosomal instability (CIN) determines the effect of aneuploidy on tumors; wher

125 tance that contains chromosomal instability (CIN) genes.

126 tutional trisomy or chromosomal instability (CIN) in vivo using hematopoietic reconstitution experime

127 pression results in chromosomal instability (CIN) including premature chromatid separation (PCS), lag

128 Chromosomal instability (CIN) is a hallmark of cancer that contributes to tumour

129 Chromosomal instability (CIN) is a major driving force of microsatellite stable (

130 Chromosomal instability (CIN) is associated with poor outcome in epithelial malig

131 Chromosomal instability (CIN) is widely considered a hallmark of cancer, but its

132 Cancer chromosomal instability (CIN) results in an increased rate of change of chromosom

133 errors and elevated chromosomal instability (CIN), but the genetic defects responsible remain largely

134 Whole chromosomal instability (CIN), manifested as unequal chromosome distribution duri

135 Chromosomal instability (CIN), the persistent inability of a cell to faithfully s

136 can be causative of chromosomal instability (CIN), which is a hallmark of many types of cancers.

137 ancer cells exhibit chromosomal instability (CIN), which is associated with tumorigenesis and therapy

138 ncer cells leads to chromosomal instability (CIN), which is defined as a perpetual gain or loss of wh

139 tion errors lead to chromosomal instability (CIN), with deleterious consequences.

140 t [PSI (+)] induces chromosomal instability (CIN).

141 type referred to as chromosomal instability (CIN).

142 neuploidy caused by chromosomal instability (CIN).

143 a phenomenon called chromosomal instability (CIN).

144 ably metastasis and chromosomal instability (CIN).

145 gly associated with chromosomal instability (CIN).

146 res associated with chromosomal instability (CIN); we investigated associations with overall survival

147 Chromosome instability (CIN) has been detected in pNETs from patients with poor

148 Whole chromosome instability (CIN) is a common feature of cancer cells and has been li

149 Chromosome instability (CIN) is deleterious to normal cells because of the burde

150 Chromosome instability (CIN) is observed in 80% to 90% of colon cancers and is t

151 Chromosome instability (CIN) is the most striking feature of human cancers.

152 Chromosome instability (CIN), a common feature of solid tumors, promotes tumor e

153 One form of chromosome instability (CIN), the recurrent missegregation of whole chromosomes

154 ne overexpression on chromosome instability (CIN), we performed genome-wide screens in the budding ye

155 s-segregation termed chromosome instability (CIN), which is likely to be a potent driver of tumor pro

156 Chromosome instability (CIN), which is often mutually exclusive from hypermutati

157 tage embryos exhibit chromosome instability (CIN).

158 and the emergence of chromosome instability (CIN).

159 Distinct cortical interneuron (CIN) subtypes have unique circuit functions; dysfunction

160 Intriguingly, CIN induction in lower eukaryotic cells and human cells

161 Apc(Min/+) cells exhibit low CIN, and we generated high CIN by reducing expression of

162 In HIV-infected women with LSIL, CIN-3+ risk was 7% (95% CI, 3%-11%).

163 developed a quantitative assay for measuring CIN based on the use of a nonessential human artificial

164 ement used to compare full and reduced model CIN prediction after grouping in low-, intermediate-, an

165 Moreover, CIN was a feature of fatal T-cell malignancies that ulti

166 ent for cervical intra-epithelial neoplasia (CIN) is linked to significant adverse sequelae including

167 en with cervical intra-epithelial neoplasia (CIN).

168 gh-grade cervical intraepithelial neoplasia (CIN) and the influence on biopsy and treatment rates of

169 ied with cervical intraepithelial neoplasia (CIN) grade 2+ (CIN2+) (n = 102) or CIN3+ (n = 55) within

170 onfirmed cervical intraepithelial neoplasia (CIN) in 2.5 years after the baseline testing were determ

171 (HPVs), cervical intraepithelial neoplasia (CIN) is common, and current treatments are ablative and

172 (SIL) or cervical intraepithelial neoplasia (CIN) prevalence, incidence, progression, or regression;

173 on-based cervical intraepithelial neoplasia (CIN) trends when adjusting for changes in cervical scree

174 n of conjunctival intraepithelial neoplasia (CIN) vs SCC revealed SCC with greater diffuse involvemen

175 rmal, 52 cervical intraepithelial neoplasia (CIN), and 68 cervical cancer (CC) tissues, for the expre

176 gh-grade cervical intraepithelial neoplasia (CIN).

177 cancers [cervical intraepithelial neoplasia (CIN)] and cancers near the ectoendocervical squamocolumn

178 everity (cervical intraepithelial neoplasia [CIN] 3, 17.9% [+/-7.2] vs CIN2, 11.6% [+/-6.5], P < .001

179 icting risk of contrast-induced nephropathy (CIN) in patients undergoing contemporary percutaneous co

180 Contrast-induced nephropathy (CIN) is a serious condition in patients with ST-segment-

181 d for reducing contrast-induced nephropathy (CIN).

182 side effect is contrast-induced nephropathy (CIN).

183 RNAs in cyclosporine-induced nephrotoxicity (CIN) and the gene pathways they regulate.

184 or contrast material-induced nephrotoxicity (CIN; SCr increase >/=0.5 mg/dL [44.20 mumol/L] or >/=25%

185 We identify three new CIN-suppressor genes (PIGN (also known as MCD4), MEX3C (

186 n the generation of structural and numerical CIN, which may inform new therapeutic approaches to limi

187 There were four cases (5%) of CIN CM-induced nephropathy : three (4%) at 24 hours and

188 with verification of presence or absence of CIN at the resection margins; were tested by cytology or

189 This included 1 case of CIN-2+ in 44 oncogenic HPV-negative HIV-infected women w

190 No cases of CIN CM-induced nephropathy occurred in the control group

191 There were 6 cases of CIN-2+ in 145 HIV-uninfected women (cumulative incidence

192 and NGAL levels, and there were no cases of CIN.

193 at the loss of pRB may be a general cause of CIN in tumors.

194 efects in DNA repair genes, but the cause of CIN is still elusive.

195 The most common cause of CIN is the persistence of aberrant kinetochore-microtubu

196 Causes of CIN are poorly understood but probably include prior gen

197 ledge of the mechanisms and contributions of CIN in cancer has been elusive.

198 adjustment by using reported risk factors of CIN (low risk: odds ratio [OR], 0.93; 95% confidence int

199 screened were significant for all grades of CIN among female individuals 15 to 19 years old, droppin

200 To investigate the impact of CIN on colon cancer development, we developed shugoshin-

201 The low incidence of CIN supports the use of hydration as a preventive measur

202 for presumed risk factors, the incidence of CIN was not significantly different from contrast materi

203 DNA-bound form of cyclin D1 and induction of CIN gene expression.

204 In contrast, inhibition of CIN firing with the mu/delta selective opioid [Met(5)]en

205 this technique, we show that high levels of CIN correlate with the combined inactivation of pRB and

206 cise mechanisms underlying the modulation of CIN firing by dopaminergic afferents remain unclear.

207 tions to determine the epigenetic origins of CIN that lead to congenital birth defects and early preg

208 ) were found to be independent predictors of CIN.

209 ed NAC and NaHCO3 did not reduce the rate of CIN significantly compared with hydration with intraveno

210 f aneuploidy on tumors; whereas low rates of CIN are weakly tumor promoting, higher rates of CIN caus

211 are weakly tumor promoting, higher rates of CIN cause cell death and tumor suppression.

212 ty in chromosome copy number as a readout of CIN.

213 Model performance estimating risk of CIN and new requirement for dialysis (NRD) was evaluated

214 The risk of CIN and NRD among patients undergoing PCI can be reliabl

215 laboratory variables to estimate the risk of CIN in patients undergoing PCI.

216 Patients were stratified for the risk of CIN.

217 m to expand our understanding of the role of CIN in cancer and aging with the long-term objective of

218 It is now evident that the role of CIN in tumor initiation and growth is more complex than

219 BE represses the transcription of a suite of CIN-TCP genes that in turn act to inhibit the number and

220 HSET overexpression had only mild effects on CIN, suggesting that additional defects must contribute

221 One CIN gene in particular, NEK2, was highly correlated with

222 ion, VEs against persistent infection and/or CIN 2/3 due to HPV-31 A/B and HPV-31C variants were -7.1

223 -51 resulting in persistent infection and/or CIN 2/3 were matched (ratio, 1:2) to the more-frequent t

224 (2)=18%), and increased likelihood of SIL or CIN regression among 5261 women living with HIV (1.54, 1

225 Overall, CIN occurred in 141 (21.9%) patients.

226 of the spinal locomotor network and parallel CIN pathways involved in gait control at different locom

227 rises a combination of BAR, GAP, and partial CIN phosphatase domains spliced from adjacent SH3BP1 and

228 The partial CIN domain is a poly-ubiquitin (poly-Ub)-binding module

229 NCINNATA-teosinte branched1, cycloidea, PCF (CIN-TCP) transcription factor lanceolate (LA) restricts

230 brocytes adjacent to normal and precancerous CIN epithelium, and FSP1-, CD34-, SMA+ activated fibrobl

231 sis showed that NGAL independently predicted CIN.

232 viously described risk scores for predicting CIN either have modest discrimination or include procedu

233 ut the mechanistic role of APC in preventing CIN remains controversial.

234 p53 tumor suppressor pathways that promotes CIN.

235 The proposed CIN and diagonal LPN connections contribute to speed-dep

236 of these phenotypes and dramatically reduced CIN in cancer cells lacking functional pRB.

237 ivation of the Mad2l1 SAC gene and resulting CIN.

238 nt pathway, suggesting that miR319-sensitive CIN-TCPs delay flowering in tomato.

239 Several CIN types have been genetically identified, including th

240 sing miR319, a negative regulator of several CIN-TCP genes including LA, flower with fewer leaves via

241 Pathway analyses indicated that the Sgo1-CIN tissues upregulated pathways known to be activated i

242 ith increased tumor prevalence and signature CIN gene profiles.

243 atae together with the catalytically similar CIN of N. suaveolens of section Suaveolentes, thus sugge

244 onsistent with an emerging role for striatal CIN activity in the processing of predictive information

245 n may provide a general strategy to suppress CIN.

246 stered the newly isolated cineole synthases (CIN) of section Alatae together with the catalytically s

247 vely, our findings demonstrate that systemic CIN results in transcriptomic changes in metabolism, pro

248 ad to identification of strategies to target CIN in pancreatic tumors.

249 tiple NGATHA (NGA) and CINCINNATA-class-TCP (CIN-TCP) transcription factors act redundantly, shortly

250 Our data demonstrate that CIN in terms of ICL-induced chromosomal breakage and def

251 In addition, we establish that CIN is crucial for the balance of protrusion/retraction

252 We hypothesized that CIN permits accelerated genomic evolution through the ge

253 It stands to reason that CIN enables the acquisition of multiple cancer hallmarks

254 We show that CIN translocates to the leading edge in a PI3-kinase-, R

255 key cancer phenotypes, and they suggest that CIN provides a permissive landscape for selection of cop

256 s a growing body of evidence suggesting that CIN impairs cellular fitness and prevents neoplastic tra

257 ctively, experimental evidence suggests that CIN enables tumor adaptation by allowing tumors to const

258 The CIN populations incorporated in the models include the g

259 tly lost/gained chromosomes out-competes the CIN-imposed mis-segregation.

260 mic symptoms, compared with only 7.7% in the CIN group and 0% in the PTX group (P<0.01).

261 reening across the period, reductions in the CIN incidence per 100000 women screened were significant

262 scovered through attempts to investigate the CIN-cancer relationship.

263 peutic strategies to target and leverage the CIN phenotype in cancer cells.

264 Complete clinical resolution of the CIN lesions was achieved in 87 of the 89 eyes treated (9

265 centromere as a potential contributor to the CIN phenotype.

266 These CIN genes of N. bonariensis, N. forgetiana, N. longiflor

267 Thus, CIN coordinates the leading edge dynamics by controlling

268 loidy and how these mechanisms contribute to CIN are not fully understood.

269 entromeric heterochromatin may contribute to CIN in cancer and be a novel therapeutic target.

270 ture could also be affected, contributing to CIN.

271 lar response of the cleavage-stage embryo to CIN and uncover a mechanism by which centromeric fission

272 ive lengthening of telomeres, are related to CIN in pNETs.

273 +) colorectal cancer (CRC) cells relative to CIN(-) CRC cells, with structural chromosome abnormaliti

274 cellular mechanisms activated in response to CIN.

275 mg/dL [141.44 mumol/L] by using traditional CIN criteria: odds ratio, 1.64; 95% CI: 1.18, 2.28; P =

276 tive to interferon alfa-2b alone in treating CIN.

277 anconi anemia pathway inactivation underlies CIN in HNSCC of non-Fanconi anemia individuals.

278 W-CIN induced DNA double strand breaks and elevated oxidat

279 Although W-CIN is a hallmark of most cancers, mutations in genes in

280 of whole chromosomes during cell division (W-CIN), leads to aneuploidy.

281 sequences of whole chromosome instability (W-CIN) we down-regulated the spindle assembly checkpoint c

282 rigenesis and the clinical implications of W-CIN are also discussed.

283 SAFs of W-CIN cells were remarkably similar to those induced by re

284 senescence features to reveal the fate of W-CIN cells.

285 e highlight the often neglected effects of W-CIN on key non-cell-autonomous entities, such as the imm

286 ting and tumor-suppressing consequences of W-CIN.

287 These findings suggest that W-CIN triggers premature senescence, presumably to prevent

288 stinct tissue-specific susceptibilities to W-CIN-induced tumorigenesis and the clinical implications

289 Loss of DAXX or ATRX is associated with CIN in pNETs and shorter survival times of patients.

290 engthening of telomeres were associated with CIN in pNETs.

291 ve chromosomal abnormalities associated with CIN, its cause is likely a defect in a network of genes

292 ic genetic factors have been associated with CIN.

293 plication, is defective in cancer cells with CIN.

294 ) in patients treated with PTX compared with CIN.

295 Analyses of mice with CIN caused by a hypomorphic mutation in the gene Bub1b f

296 In this group of patients observed with CIN lesions, combination treatment of topical retinoic a

297 52 were treated by OBS; 13 were treated with CIN, and 18 underwent PTX.

298 ive (ER(+)) breast cancer define tumors with CIN and high proliferative potential.

299 The 5-year CIN-2+ cumulative risk in the HIV-infected oncHPV-positi

300 ressed state of primary aneuploid cells, yet CIN is not benign; a subset of genes upregulated in high