ライフサイエンスコーパス: EAC

1 EAC cells become resistant to trastuzumab and pertuzumab

2 EAC cells cultured for 2 months with a combination of tr

3 EAC cells incubated with ERBB inhibitors began to secret

4 EAC cells incubated with trastuzumab decreased expressio

5 EAC has one of the fastest rising incidences of cancers

6 EAC is a leading cause of cancer death, and current trea

7 EAC patient-derived xenograft tumors grew more slowly in

8 EAC patients who underwent nCRT and surgery, between Jan

9 EAC prevalence in controls increased by 25%; whereas, pr

10 ysis, comparison of 189 cases with stage 0-1 EAC to 520 controls produced an adjusted OR of 0.85 (95%

11 The prevalent Type 1 EAC commonly harbors loss of the tumor suppressor, Pten,

12 diagnostic mouthwash samples from n = 81/160 EAC and n = 25/50 ESCC cases/matched controls.

13 within the EAC cases; specifically, 22 of 25 EAC-only insertions were present identically in distinct

14 amples and clinical data from 150 BE and 285 EAC cases from the Oesophageal Cancer Classification and

15 We compared 311 EAC cases to 856 controls.

16 atched RNA sequencing data, we discovered 77 EAC driver genes and 21 noncoding driver elements.

17 We derived 8 organoids from 8 EAC tissues and tested their sensitivity to different dr

18 Among 9 EAC deaths, 6 (67%) had baseline HGD, and 3 (33%) had ba

19 Reanalysis of additional EAC exome data showed that the majority (62.5%) of EACs

20 develop from the endometrial adenocarcinoma (EAC) through epithelial-mesenchymal transition (EMT).

21 cologic cancer, endometrioid adenocarcinoma (EAC), continue to rise, mirroring the global epidemic of

22 ay play a role in esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC), alth

23 ationship between esophageal adenocarcinoma (EAC) and its precursor lesion, Barrett's esophagus, is p

24 ghly expressed in esophageal adenocarcinoma (EAC) and precancerous lesions.

25 linical course in esophageal adenocarcinoma (EAC) are still not implemented.

26 esophagus (BE) or esophageal adenocarcinoma (EAC) based on genetic and non-genetic factors.

27 splasia (CP-B) to esophageal adenocarcinoma (EAC) cell lines (OE33, OE19) and primary specimens of sq

28 ate resistance of esophageal adenocarcinoma (EAC) cells and patient-derived xenograft tumors to ERBB

29 ithelia (IEE) and esophageal adenocarcinoma (EAC) cells cultured in normal media with or without ciga

30 sease (GERD), yet esophageal adenocarcinoma (EAC) disproportionately affects European American indivi

31 Esophageal adenocarcinoma (EAC) has a dismal prognosis, and survival benefits of re

32 Esophageal adenocarcinoma (EAC) has a poor outcome, and targeted therapy trials hav

33 The incidence of esophageal adenocarcinoma (EAC) has increased in many Western countries and is high

34 GAV expression in esophageal adenocarcinoma (EAC) has not been analyzed so far.

35 o protect against esophageal adenocarcinoma (EAC) in patients with Barrett's esophagus (BE).

36 ysplasia (HGD) or esophageal adenocarcinoma (EAC) in patients with LGD of the esophagus.

37 Esophageal adenocarcinoma (EAC) is a growing problem with a rapidly rising incidenc

38 Esophageal adenocarcinoma (EAC) is a highly lethal cancer with limited treatment op

39 Esophageal adenocarcinoma (EAC) is a poor-prognosis cancer type with rapidly rising

40 er to controlling esophageal adenocarcinoma (EAC) is identifying those most likely to benefit from sc

41 Esophageal adenocarcinoma (EAC) is one of the most frequent causes of cancer death,

42 Esophageal adenocarcinoma (EAC) is rapidly increasing in incidence in Western cultu

43 The incidence of esophageal adenocarcinoma (EAC) is rapidly rising in the United States and Western

44 Esophageal adenocarcinoma (EAC) is resistant to standard chemoradiation treatments,

45 poor outcomes in esophageal adenocarcinoma (EAC) prompted us to interrogate the pattern and timing o

46 splasia (HGD) and esophageal adenocarcinoma (EAC) through endoscopic screening, during which multiple

47 locally advanced esophageal adenocarcinoma (EAC) treated with neoadjuvant chemoradiotherapy followed

48 esophagus (BE) to esophageal adenocarcinoma (EAC) vary.

49 re diagnosed with esophageal adenocarcinoma (EAC) within 1 year of an endoscopic examination that pro

50 he development of esophageal adenocarcinoma (EAC), a particularly lethal cancer.

51 to dysplasia and esophageal adenocarcinoma (EAC), accompanied by mutations in TP53 that increase the

52 ysplasia (HGD) or esophageal adenocarcinoma (EAC), from 1992 through 2015, and performed RNA sequence

53 stic precursor to esophageal adenocarcinoma (EAC), such biomarkers would be particularly useful becau

54 nant condition of esophageal adenocarcinoma (EAC).

55 is a precursor to esophageal adenocarcinoma (EAC).

56 essed in a subset esophageal adenocarcinoma (EAC).

57 splasia (HGD) and esophageal adenocarcinoma (EAC).

58 ndard of care for esophageal adenocarcinoma (EAC).

59 ysplasia (HGD) or esophageal adenocarcinoma (EAC).

60 eases the risk of esophageal adenocarcinoma (EAC).

61 splasia (HGD) and esophageal adenocarcinoma (EAC).

62 als to developing esophageal adenocarcinoma (EAC).

63 nown precursor to esophageal adenocarcinoma (EAC).

64 BE) progresses to esophageal adenocarcinoma (EAC).

65 he development of esophageal adenocarcinoma (EAC).

66 cancers, such as esophageal adenocarcinoma (EAC).

67 cal precursor of oesophageal adenocarcinoma (EAC), is a condition in which the squamous epithelium of

68 LY3023414 demonstrates efficacy against EAC in a preclinical model, establishing the rationale f

69 was also associated with protection against EAC.

70 ce were given subcutaneous injections of AMC-EAC-007B cells and also given injections of single or co

71 creased the AUC values for BE (to 0.799) and EAC (to 0.754).

72 cell line CP-A towards dysplasia (CP-B) and EAC (OE33 and OE19), confirmed by a lower staining index

73 Knockdown of Iso1 in BE and EAC cells led to degradation of the mutant form of p53 a

74 BE and EAC samples shared genome-wide methylation features, com

75 analyzed methylation profiles of all BE and EAC tissues and assigned them to subgroups using non-neg

76 We performed epigenetic analyses of BE and EAC tissues and combined these data with transcriptome a

77 and genome profiles of more than 400 BE and EAC tissues, along with clinical data, we identified 4 s

78 e been associated with development of BE and EAC, but little is known about epigenetic alterations.

79 cation of individuals with vs without BE and EAC.

80 ein inflammation pathways that affect BE and EAC.

81 e EAC incidence and mortality (all-cause and EAC-specific) were calculated, and adjusted all-cause mo

82 uencing on 23 paired Barrett's esophagus and EAC samples, together with one in-depth Barrett's esopha

83 aimed to determine the incidence of HGD and EAC in patients with irregular Z line with intestinal me

84 ogression to a combined end point of HGD and EAC were lower among those treated with RFA than among u

85 analyses with time to progression to HGD and EAC were performed.

86 g index of WNT3A in Barrett's metaplasia and EAC, than in squamous epithelium specimens.

87 imens of squamous epithelium, metaplasia and EAC.

88 ticipants in the international Barrett's and EAC consortium as well as the United Kingdom's BE gene s

89 mined the association between statin use and EAC in conditional logistic regression models.

90 We analyzed publicly available EAC gene expression datasets to correlate expression of

91 Interestingly, four BE/EAC-associated genes within the TOH regions consistently

92 le nucleotide polymorphisms (SNPs) to map BE/EAC genes has previously provided insufficient genetic i

93 nsive understanding of the development of BE/EAC.

94 to moderate penetrance predisposition to BE/EAC.

95 sing SNPs and tested for association with BE/EAC.

96 Athymic nude mice bearing EAC xenograft tumors (grown from OE-33 cells) were given

97 markers would be particularly useful because EAC risk may change with BE dwell time and it is general

98 after BE diagnosis and up to 90 days before EAC diagnosis for cases and controls (during the corresp

99 We found no association between EAC and non-statin lipid-lowering medications.

100 tor to compare the risk distribution between EAC cases and controls from six population-based studies

101 en shows surprisingly little overlap between EAC and adjacent Barrett's esophagus; and (iii) despite

102 capacity (EDC), electron accepting capacity (EAC), and redox state) of HS.

103 , these data provide a new way to categorize EAC at a genome scale and implicate HNF4A activation as

104 g hazard ratios (HRs) with 95% CIs, compared EAC risk in GERD patients with antireflux surgery with t

105 Barrett's esophagus, and 2 studies comparing EAC risk after antireflux surgery to the background popu

106 matic review identified 10 studies comparing EAC risk after antireflux surgery with nonoperated GERD

107 ochemistry on tissue microarrays, containing EAC, high grade dysplasia (HGD), low grade dysplasia (LG

108 Crude EAC incidence and mortality (all-cause and EAC-specific)

109 ous levels of miR-217 expression in cultured EAC cells (EACC)/primary EACs were significantly lower t

110 Pacific Ocean, the East Australian Current (EAC), transports microbial assemblages that maintain tro

111 Among 4982 patients, 100 (2%) developed EAC (7.8/1000 person-years [PY]) and 9 patients (0.2%) d

112 2 BE patients developed HGD and 62 developed EAC.

113 rast, no cPten(f/f)Grp78(f/f) mice developed EAC, even after more than 8 months of observation.

114 precisely their absolute risk of developing EAC, interpret this estimate in the context of risk of d

115 f/f)) deletion developed well-differentiated EAC by 4 weeks.

116 Understanding of the genetic events driving EAC development is limited, and there are few molecular

117 let cell maturation, a feature of BE, during EAC pathogenesis.

118 egrates relevant cell-level processes during EAC development with a spatial screening process to prov

119 ents within and between several dysregulated EAC pathways, a result suggestive of strong functional r

120 fective for treating dysplastic BE and early EAC, whereas esophagectomy is indicated for patients wit

121 patients with BE who have dysplasia or early EAC, from surgical resection to endoscopic resection and

122 h mainly HER2 phosphorylation, and the ESO51 EAC cell line with mainly MET phosphorylation, profound

123 OR dual inhibitor, LY3023414, on established EAC in an in vivo model.

124 lex atypical hyperplasia, a well-established EAC precursor.

125 in-vitro and in-vivo models of experimental EAC.

126 First, EAC risk after antireflux surgery in the cohort was comp

127 ification improvement for BE of 3.0% and for EAC of 5.6%.

128 d called the multistage clonal expansion for EAC (MSCE-EAC) screening model that is used for screenin

129 Some risk factors for EAC have been identified-mainly gastroesophageal reflux

130 apy as an efficacious therapeutic option for EAC.

131 variants have been associated with risk for EAC, but their overall contribution is low.

132 d the University of Washington, Seattle) for EAC to match the 0.18% annual rate of progression from p

133 pCR after trimodality therapy for EAC is infrequent but associated with improved prognosis

134 antitumor efficacy in vitro and in vivo for EAC, suggesting the need for human clinical trials.

135 cultured primary tumor cells, isolated from EAC patient samples, and OE19 and OE33 EAC cell lines wi

136 Human EAC (FLO-1 and EsoAd1), dysplastic BE (CP-B, CP-C, CP-D)

137 MET and HER2 activation in a panel of human EAC cell lines, and the differential susceptibility of t

138 ritoneal metastatic survival models of human EAC.

139 , we examined the expression of Claudin-2 in EAC and precancerous lesions and its association with VD

140 4, Fzd5, Fzd7, and the co-receptor LRP5/6 in EAC cells, while Fzd3 and Fzd7 were rarely expressed in

141 athways that are differentially activated in EAC vs nonmalignant dysplastic tissues; pathway activiti

142 e responses to neoadjuvant chemoradiation in EAC patients.

143 kdown of TGFB or JNK signaling components in EAC cells (FLO-1 or EsoAd1) significantly reduced cell p

144 There was no difference in EAC risk between antireflux surgery and medical treatmen

145 , a family of microRNAs critical for EMT, in EAC cell lines.

146 for our understanding of molecular events in EAC.

147 cer types, but this has not been explored in EAC.

148 t was significantly more highly-expressed in EAC, SCC and glandular lesions than in SE and more in EA

149 and particularly SOX2 protein expression in EAC predicts response to nCRT.

150 enetic events to modulate gene expression in EAC.

151 therapy and serves as a prognostic factor in EAC.

152 tative oncogene not previously implicated in EAC.

153 and glandular lesions than in SE and more in EAC than in BE and CM.

154 ns in regulating gene expression networks in EAC.

155 regulatory networks that are operational in EAC.

156 and were later clonally expanded in BE or in EAC.

157 ted by these pathways to be overexpressed in EAC and dysplastic BE.

158 Inhibiting these pathways in EAC cells reduces their proliferation, migration, and fo

159 o identify deregulated signaling pathways in EAC tissues that might be targeted to slow tumor growth

160 n of phosphorylated JUN and SMAD proteins in EAC tumor tissues compared with nonmalignant tissues.

161 the stromal driver of therapy resistance in EAC.

162 tromal contribution to therapy resistance in EAC.

163 K pathway were overexpressed specifically in EAC and dysplastic BE.

164 eting Mcl-1 may be a therapeutic strategy in EAC.

165 grade, stage, or patients' survival time in EAC and SCC.

166 rkers may help to individualize treatment in EAC patients.

167 The PI3K/mTOR pathway is upregulated in EAC and may be a target for novel therapies.

168 ates several oncoproteins, is upregulated in EAC, and may be a novel target for therapy.

169 roesophageal reflux disease (GERD) increases EAC risk, but whether antireflux surgery prevents EAC is

170 e HGD, and 3 (33%) had baseline intramucosal EAC.

171 a to prevent further progression to invasive EAC.

172 the global epidemic of obesity, a well-known EAC risk factor.

173 ococcus pneumoniae was associated with lower EAC risk.

174 sources should be allocated to detect missed EAC.

175 nalysis to determine the magnitude of missed EAC in cohorts of patients with BE.

176 molecular targets to prevent and/or mitigate EAC is imperative.

177 he multistage clonal expansion for EAC (MSCE-EAC) screening model that is used for screening BE patie

178 EAC microbial assemblages compared with non-EAC assemblages, including strain transitions within the

179 In the OE19 EAC cell line with mainly HER2 phosphorylation, and the

180 from EAC patient samples, and OE19 and OE33 EAC cell lines with trastuzumab (an inhibitor of HER2),

181 The OE33 EAC cell line with strong expression of phosphorylated b

182 (JNK) signaling pathways in more than 80% of EAC samples.

183 In a transcriptome analysis of EAC and nondysplastic BE tissues, we found the TGFB and

184 Diagnostic analysis of EAC usually commences with upper endoscopy followed by c

185 We identified specific characteristics of EAC microbial assemblages compared with non-EAC assembla

186 level of ITGAV in a very large collective of EAC and its impact on individual patients' prognosis.

187 In comparisons of EAC gene expression patterns, we associated high express

188 Comparisons of EAC vs nondysplastic BE tissues showed hyperactivation o

189 Kaplan-Meier curves of EAC incidence were stratified by baseline histology.

190 was inversely associated with development of EAC (adjusted odds ratio [OR], 0.65; 95% confidence inte

191 to clarify the long-term risk development of EAC after antireflux surgery.

192 on-years [PY]) and 9 patients (0.2%) died of EAC (0.7/1000 PY) in a mean 2.7 +/- 1.6 years.

193 our understanding and clinical evaluation of EAC.

194 so1 protein in BE cells and slowed growth of EAC xenograft tumors in mice.

195 The HRs of EAC were stable comparing the surgery group with the non

196 nd more accurately estimate the incidence of EAC among people with BE.

197 The incidence of EAC in nondysplastic BE was 0.5/1000 PY.

198 amage and contribute to the low incidence of EAC in this population.

199 The incidence of EAC was markedly lower in this study than in other studi

200 Incubation of EAC cells with trastuzumab and pertuzumab accelerated th

201 Incubation of EAC cells with trastuzumab, followed by 10 days of incub

202 gus (BE), the only known precursor lesion of EAC, is indicated for individuals with increased risk.

203 As the majority of EAC cases are diagnosed in individuals without a known h

204 sent whole-exome sequencing from 25 pairs of EAC and Barrett's esophagus and from 5 patients whose Ba

205 linically relevant sensitivity in a panel of EAC cell lines and organoids.

206 f miR-217 contributes to the pathogenesis of EAC via upregulation of KLK7 and suggest that restoratio

207 els were constructed to assess predictors of EAC and all-cause mortality.

208 Necropsy confirmed the presence of EAC in 50% of treatment animals and 75% of control anima

209 ns for the early detection and prevention of EAC and ESCC.

210 ology, staging, screening, and prevention of EAC as well as endoscopic and surgical management.

211 The prognosis of EAC remains poor because it is usually diagnosed late, a

212 pid means to graphically communicate risk of EAC in the context of other health risks, facilitates "w

213 of statin or SSRI usage reduced the risk of EAC or HGD by 49% or 61%, respectively.

214 ials were used to calculate absolute risk of EAC over 10 years adjusting for competing risks.

215 to address these factors can reduce risk of EAC, although some evidence exists for smoking cessation

216 rsythia to be associated with higher risk of EAC.

217 ose with BE appeared to decrease the risk of EAC.

218 n risk factors and the molecular subtypes of EAC.

219 calized with activated AKT on the surface of EAC, thus providing an opportunity for therapeutic targe

220 pathways might be developed for treatment of EAC.

221 y; however the possible preventive effect on EAC development remains unclear.

222 2.22; 95% confidence interval, 1.89-2.60) or EAC (odds ratio, 2.46; 95% confidence interval, 2.07-2.9

223 sease and 16 with Barrett's esophagus and/or EAC).

224 databases of patients from studies of BE or EAC to develop a risk prediction model based on genetic,

225 accuracy in identifying patients with BE or EAC using the area under the receiver operating characte

226 GERD symptoms identified patients with BE or EAC with AUC values ranging from 0.637 to 0.667.

227 etic variants associated with risk for BE or EAC, and constructed a polygenic risk score (PRS) for ca

228 164 patients, with and without dysplasia or EAC, enrolled in a multicenter study.

229 ned BE tissues from 100 patients with HGD or EAC and normal esophageal squamous mucosa (controls).

230 nical predictors of BE progression to HGD or EAC are poorly understood, with multiple contradictory s

231 Progression of BE to HGD or EAC associated with changes in expression of mRNAs that

232 We calculated rates of progression to HGD or EAC between groups of patients with irregular Z line (n

233 All 71 incident cases of HGD or EAC developed in patients with BE of >/=1 cm in length.

234 the 255 patients, 45 (18%) developed HGD or EAC during a median 42-month follow-up period (interquar

235 ients with irregular Z line developed HGD or EAC during a median follow-up period of 4.8 years (inter

236 he primary outcome was development of HGD or EAC during the follow-up period (median, 5.9 years).

237 time increase risk for development of HGD or EAC in patients with Barrett's esophagus and LGD.

238 model to determine of progression to HGD or EAC in patients with BE, based on demographic data and e

239 Risk factors for HGD or EAC included age, caffeine intake, and low-grade dysplas

240 The risk of progression to HGD or EAC was significantly lower among patients who underwent

241 The annual rates of progression to HGD or EAC were 6.6% in the surveillance group and 0.77% in the

242 d patients with BE that progressed to HGD or EAC with a c-statistic of 0.76 (95% confidence interval,

243 ear of follow-up, were diagnosed with HGD or EAC within the past year, were missing baseline histolog

244 period, 154 patients (5.7%) developed HGD or EAC, with an annual rate of progression of 0.95%.

245 primary end point was development of HGD or EAC.

246 low, intermediate, and high risk for HGD or EAC.

247 progression to high-grade dysplasia (HGD) or EAC are needed to improve outcomes and identify who will

248 R2 positive patients with MET-overexpressing EAC, and could be a novel treatment strategy for specifi

249 to the corresponding background population, EAC risk did not decrease after antireflux surgery [SIR

250 zumab to nCRT in patients with HER2-positive EAC is feasible and demonstrates potentially promising a

251 t neoplasia (dysplasia and early preclinical EAC) in the esophageal lining.

252 rade dysplasia [HGD] respectively) predicted EAC incidence.

253 Antireflux surgery may prevent EAC better than medical therapy in patients with Barrett

254 k this pathway might be developed to prevent EAC in patients with BE.

255 isk, but whether antireflux surgery prevents EAC is uncertain.

256 al treatment of GERD does not seem to reduce EAC risk.

257 in terms of the long-term impact on reducing EAC incidence.

258 his signaling can be targeted to resensitize EAC to therapy, and its activity can be measured using s

259 n, while reverting their alterations reveals EAC acquired dependencies that can be exploited in thera

260 Significant EAC risk factors included age, abdominal obesity, caffei

261 d be a novel treatment strategy for specific EAC patients.

262 effect was strongest against advanced-stage EAC, and increased with statin dose.

263 nts are at risk of developing advanced-stage EAC.

264 s strongest for patients with advanced-stage EAC: in a stratified analysis, comparison of 189 cases w

265 Among patients with late-stage EAC (stages 2-4, n = 106) and 291 controls, the adjusted

266 rmine whether targeting GRP78 could suppress EAC development, we created a conditional knockout mouse

267 T1a EAC may be treated endoscopically, and some patients wit

268 The EAC risk after antireflux surgery does not seem to rever

269 The EAC risk remained elevated in patients after antireflux

270 ription factors work together to control the EAC transcriptome.

271 , associated with the seasonal impact of the EAC microbial assemblage.

272 n accurate and reliable determination of the EAC of humic acid samples.

273 ith the electrochemical determination of the EAC.

274 e structure and function associated with the EAC, we conclude that climate-driven expansions of WBCs

275 we observed evidence of clonality within the EAC cases; specifically, 22 of 25 EAC-only insertions we

276 and the differential susceptibility of these EAC cell lines to single agent or combination of foretin

277 esity contribute to the progression of BE to EAC in mice.

278 iagnosis, the rate of progression from BE to EAC is likely to more closely approximate the lower esti

279 Progression of BE to EAC was associated with a significant reduction in goble

280 man esophageal tissues, progression of BE to EAC was associated with reduced goblet cell density and

281 As tissues progressed from BE to HGD to EAC, they increased expression of mRNAs encoding isoform

282 mes from patients with BE that progressed to EAC vs patients with BE that did not develop into cancer

283 s esophagus, the putative precursor state to EAC, thereby providing novel molecular evidence in suppo

284 By using EAC patient-derived CAFs, organoid cultures, and xenogra

285 In vitro, EAC cell lines were utilized to evaluate AUY922, alone a

286 samples of this subtype were BE and 17% were EAC.

287 s reported from prospective studies in which EAC is detected by surveillance.

288 onsumption of alcohol is not associated with EAC risk, other exposures, such as physical activity, nu

289 in the inflammatory cascade associated with EAC.

290 is of 388 samples across 18 individuals with EAC showed, in 90% of patients, that multiple subclones

291 ned the relationship of oral microbiota with EAC and ESCC risk in a prospective study nested in two c

292 cted 397 biopsy specimens from patients with EAC and nonmalignant Barrett's esophagus (BE), with or w

293 The prognosis for patients with EAC has slightly improved, but remains poor-screening an

294 Patients with EAC or HGD at the initial endoscopy were excluded.

295 these known associations, most patients with EAC present with symptoms of dysphagia from late-stage t

296 ective database and identified patients with EAC treated with neoadjuvant chemoradiotherapy followed

297 th BE with an AUC of 0.793 and patients with EAC with an AUC of 0.745.

298 om 3288 patients with BE, 2511 patients with EAC, and 2177 individuals without either (controls) from

299 nt chemoradiotherapy (nCRT) in patients with EAC.

300 We selected patients with BE without EAC (controls) using incidence density sampling; 3 contr