ライフサイエンスコーパス: CIN

1 CIN can be induced by tissue oxidative stress, which is

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

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

4 CIN deficiency has been independently associated with ti

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

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

7 CIN has been linked to carcinogenesis, metastasis, poor

8 CIN is driven by chromosome segregation errors and a tol

9 CIN is generally considered to drive tumorigenesis, but

10 CIN leads to mosaic embryos that contain a combination o

11 CIN responses coincide with phasic firing of DAergic neu

12 CIN significantly increased during TKI treatment in T790

13 CIN was absent from all Scottish wildcats.

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 es for PLK1 as a potent proto-oncogene and a CIN gene and provide insights for the development of eff

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

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

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

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

21 a tumor-inhibiting role in AML that affects CIN via MAD2 and CDC20.

22 oplasia (CIN2+) detection at follow-up after CIN management among women living with HIV (WLHIV).

23 ation and EZH2 transcription and ameliorated CIN in AML.

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 olochia fimbriata point to a role of CYC and CIN genes in maintaining differential perianth expansion

27 zed trial conducted among women with HIV and CIN grade 2 or 3.

28 Women with HIV infection and CIN grade 2 or 3 were randomized 1:1 to receive cryother

29 center study of women with HIV infection and CIN grade 2 or 3, treatment with LEEP compared with cryo

30 utes to defects in kinetochore integrity and CIN.

31 cells elevates chromosome missegregation and CIN.

32 y resulting in chromosome missegregation and CIN.

33 ule assembly, chromosome missegregation, and CIN.

34 ment regimens across PLK1-overexpressing and CIN-positive cancers.

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

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

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

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

39 y outcome was disease recurrence, defined as CIN grade 2 or higher on cervical biopsy, during the 24-

40 Human papillomavirus transgenic mice bearing CIN lesions were treated with MPA plus 17beta-estradiol.

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

42 gnized significant effects of CIN in cancer, CIN-targeted therapeutics could have a major impact on i

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

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

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

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

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

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

49 like genes and three paralogs of CINCINNATA (CIN) in early diverging angiosperms.

50 ween route of administration and comparative CIN risk.

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

52 ibromin/Ras/MEK pathway regulates a critical CIN developmental milestone.

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

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

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

56 Distinct CIN mechanisms indicated relationships with HGSC-relevan

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

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

59 Multiple mechanisms coexisted to drive CIN in HGSC, including elevated microtubule dynamics and

60 ional characterization of mechanisms driving CIN in HGSC in seven cell lines that accurately recapitu

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

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

63 n does not appear a primary driver of excess CIN in cats.

64 ation of adequate HIV control and excisional CIN treatment.

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

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

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

68 (T2);Kras(G12D/+);Tp53(R172H/+);Smad4(fl/f) (CIN mice), Anxa10-CreER(T2);Cdh1(fl/fl);Kras(G12D/+);Sma

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

70 ghts potential therapeutic opportunities for CIN-positive cancers.

71 2 cats; 15%, 11 of 70 dogs were positive for CIN, respectively).

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

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

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

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

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

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

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

79 hanges in centromere structure and generates CIN.

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

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

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

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

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

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

86 Overall, we show that HGSC CIN is complex and suggest that specific CIN mechanisms

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

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

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

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

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

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

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

94 We analyzed 87 samples (normal = 16, HPV +/- CIN = 50, cancer = 21 patients).

95 with 100% accuracy normal (100%) vs. HPV +/- CIN (100%) vs. cancer (100%) when compared to histology

96 liferation and the promotion of apoptosis in CIN lesions.

97 Changes in CIN activity are thought to encode salient changes in th

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

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

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

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

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

103 rs) to identify additional genes involved in CIN.

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

105 to molecular pathways regulated by miRNAs in CIN.

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

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

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

109 s extra centrioles, potentially resulting in CIN.

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

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

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

113 iome diversity is associated with increasing CIN severity.

114 imal model focusing on mitotic error-induced CIN.

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

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

117 at characterize the chromosomal instability (CIN) and the genomically stable (GS) subtypes of human g

118 e biorientation and chromosomal instability (CIN) and these phenotypes are suppressed by RNH1 overexp

119 Chromosomal instability (CIN) comprises continual gain and loss of chromosomes or

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

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

122 ene expression, and chromosomal instability (CIN) in the host cell.

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

124 Chromosomal instability (CIN) increases a tumor cell's ability to acquire chromos

125 Although chromosomal instability (CIN) is a common phenomenon in cleavage-stage embryogene

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

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

128 Chromosomal instability (CIN) is one of the major forms of genomic instability in

129 red T790M mutation, chromosomal instability (CIN) related genes, including AURKA and TP53 alterations

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

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

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

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

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

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

136 ing accumulation of chromosomal instability (CIN), which resulted in aneuploidy and tumor formation.

137 and other forms of chromosomal instability (CIN), yet how this occurs remains unclear.

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

139 gly associated with chromosomal instability (CIN).

140 type referred to as chromosomal instability (CIN).

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

142 been associated with chromosome instability (CIN) and aneuploidy.

143 th the levels of the chromosome instability (CIN) genes MAD2 and CDC20.

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

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

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

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

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

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

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

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

152 llmarks of cancer is chromosome instability (CIN), which leads to aneuploidy, translocations, and oth

153 tation and extensive chromosome instability (CIN).

154 tage embryos exhibit chromosome instability (CIN).

155 and the emergence of chromosome instability (CIN).

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

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

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

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

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

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

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

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

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

165 onfirmed cervical intraepithelial neoplasia (CIN) grade 2 or higher regardless of HIV status.

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

167 data on cervical intraepithelial neoplasia (CIN) grades 2-3 and adenocarcinoma in situ (designated C

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

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

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

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

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

173 whether cervical intraepithelial neoplasia (CIN) will regress or progress.

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

175 HPV) +/- cervical intraepithelial neoplasia (CIN), or cervical cancer.

176 ion, and cervical intraepithelial neoplasia (CIN); however, causal inference remains uncertain.

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

178 al lesion is chronic interstitial nephritis (CIN).

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

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

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

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

183 hrough Kenya's Clinical Information Network (CIN) between September 2013 and February 2016.

184 A cluster of cefepime-induced neutropenia (CIN) was identified from June 2017 to May 2018 in a regi

185 ssay that allows the identification of novel CIN genes.

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

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

188 on and evolution can occur in the absence of CIN.

189 ority of human tumors the molecular basis of CIN remains unknown, partly because not all genes contro

190 We sought to develop a biomarker of CIN in circulating tumor cells (CTC) that are more likel

191 resultant computer vision-based biomarker of CIN in CTCs in a pretreatment sample strongly associated

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

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 onnect to specific CIN mechanisms, causes of CIN in most cancer types remain unknown.

196 ional characterization to identify causes of CIN.

197 ngential migration, abnormal distribution of CIN in the neocortex, a marked reduction of CINs express

198 Given the recognized significant effects of CIN in cancer, CIN-targeted therapeutics could have a ma

199 owever, neither the prevalence nor extent of CIN during prenatal development and at birth, following

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

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

202 such as zinc, underpin the high incidence of CIN in domestic cats.

203 The increase of CIN firing by CRF results in the activation muscarinic a

204 In this review, we describe the influence of CIN on the various steps in tumor initiation and develop

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

206 provide models that support interrogation of CIN mechanisms in cells not extensively cultured in vitr

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

208 The majority of CIN regress in young women and since local treatments ar

209 A well-established mechanism of CIN is the overproduction of centrosomes, which promotes

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

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

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

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

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

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

216 push, were associated with a higher 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 Renal lesions were graded by severity of CIN.

219 Identification of the complete spectrum of CIN genes will reveal new insights into mechanisms of ch

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

221 Because our understanding of CIN mechanisms is based largely on analysing established

222 in AML cell lines and assessed the effect on CIN using fluorescence in situ hybridization (FISH).

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

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

225 -51 resulting in persistent infection and/or CIN 2/3 were matched (ratio, 1:2) to the more-frequent t

226 (2)=18%), and increased likelihood of SIL or CIN regression among 5261 women living with HIV (1.54, 1

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

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

229 In our randomly sampled population, CIN was more prevalent in domestic cat versus domestic d

230 t in treating progesterone receptor-positive CIN lesions.

231 WLHIV followed between 6 and 33 months post-CIN management.

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

233 This observation suggests that MPA prevented CIN from progressing to invasive cancer.

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

235 cted MAD2 and CDC20 expression, and promoted CIN in AML cells.

236 p53 tumor suppressor pathways that promotes CIN.

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

238 30%) randomized to cryotherapy had recurrent CIN grade 2 or higher vs 37 (19%) in the LEEP group (rel

239 ress that can be partially rescued to reduce CIN by low doses of paclitaxel and nucleoside supplement

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

241 first time TFs that differentially regulate CIN vs. HIN production.

242 rations that probably arose from IVF-related CIN.

243 ivation of the Mad2l1 SAC gene and resulting CIN.

244 Several CIN types have been genetically identified, including th

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

246 but were not directly predictive of specific CIN mechanisms, underscoring the importance of functiona

247 GSC CIN is complex and suggest that specific CIN mechanisms could be used as functional biomarkers to

248 ne expression landscapes connect to specific CIN mechanisms, causes of CIN in most cancer types remai

249 n may provide a general strategy to suppress CIN.

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

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

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

253 grade 3 or worse, 88 regressed to less than CIN grade 1, and 36 lesions persisted as CIN1/2.

254 grade 3 or worse, 88 regressed to less than CIN grade 1, and 36 persisted as CIN1/2.

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

256 We demonstrate that CIN is not preserved at later stages of prenatal develop

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

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

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

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

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

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

263 The CIN populations incorporated in the models include the g

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

265 The gastric tumors from the CIN mice had an invasive phenotype and formed liver and

266 ant to docetaxel, whereas organoids from the CIN tumors were more resistant to trametinib.

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

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

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

270 e increased over time, likely because of the CIN's feedback to hospitals.

271 f novel therapeutic strategies to target the CIN phenotype in cancer cells.

272 Thus, CIN coordinates the leading edge dynamics by controlling

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

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

275 mechanisms of genome stability that lead to CIN in ovarian cancer and demonstrate the benefit of int

276 Twenty-five lesions progressed to CIN grade 3 or worse, 88 regressed to less than CIN grad

277 Twenty-five lesions progressed to CIN grade 3 or worse, 88 regressed to less than CIN grad

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

279 cellular mechanisms activated in response to CIN.

280 ce that aberrant expression of PLK1 triggers CIN and tumorigenesis and highlights potential therapeut

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

282 en outcomes among young women with untreated CIN grade 2 (CIN2).

283 ong women of childbearing age with untreated CIN grade 2 (CIN2).

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

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

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

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

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

289 It is unclear whether CIN is stable between precursor lesions, primary tumor,

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

291 engthening of telomeres were associated with CIN in pNETs.

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

293 ic genetic factors have been associated with CIN.

294 plication, is defective in cancer cells with CIN.

295 ic was higher in domestic cats and dogs with CIN.

296 Even though embryos with CIN-derived complex aneuploidies may arrest between the

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

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

299 renal arsenic levels in cats with or without CIN, renal arsenic accumulation does not appear a primar

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