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 is a leading cause of cancer death, and current trea

6 EAC patient-derived xenograft tumors grew more slowly in

7 EAC patients who underwent nCRT and surgery, between Jan

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 -control and 1 cohort), with a total of 1226 EAC and 1140 EGJA cases, on aspirin and/or NSAID use.

13 n spectra from whole-exome sequencing of 149 EAC tumor-normal pairs, 15 of which have also been subje

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

15 Targeted sequencing of all exons from 20 EAC-associated genes was performed on metaplasia biopsie

16 WGS of 22 EAC cases show that catastrophes may lead to oncogene am

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

18 We compared 311 EAC cases to 856 controls.

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

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

21 ce the susceptibility for esophageal adeno- (EAC) and squamous cell carcinoma (ESCC) in Caucasians.

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

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

24 the incidence of esophageal adenocarcinoma (EAC) after RFA, factors associated with the development

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

26 o reduce risks of esophageal adenocarcinoma (EAC) and esophagogastric junctional adenocarcinoma (EGJA

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

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

29 of patients with esophageal adenocarcinoma (EAC) and/or esophagogastric junction adenocarcinoma afte

30 splasia (HGD) and esophageal adenocarcinoma (EAC) are highly variable.

31 Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like

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

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

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

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

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

37 The incidence of esophageal adenocarcinoma (EAC) has risen 600% over the last 30 years.

38 duces the risk of esophageal adenocarcinoma (EAC) in patients with Barrett's esophagus (BE) with high

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

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

41 own a low risk of esophageal adenocarcinoma (EAC) in patients with nondysplastic Barrett's esophagus

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

43 Esophageal adenocarcinoma (EAC) is a highly aggressive disease with poor long-term

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

45 Esophageal adenocarcinoma (EAC) is an aggressive malignancy with a poor outcome.

46 Esophageal adenocarcinoma (EAC) is characterized by resistance to chemotherapy and

47 s (BE)-associated esophageal adenocarcinoma (EAC) is increasing.

48 esophagus (BE) to esophageal adenocarcinoma (EAC) is low and difficult to calculate.

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

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

51 Esophageal adenocarcinoma (EAC) is the most prevalent esophageal cancer type in the

52 ost patients with esophageal adenocarcinoma (EAC) or squamous cell cancer (ESCC) present with advance

53 tt's esophagus to esophageal adenocarcinoma (EAC) provides an ideal model to study the ordering of so

54 ht to progress to esophageal adenocarcinoma (EAC) through a stepwise progression with loss of CDKN2A

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

56 esophagus (BE) to esophageal adenocarcinoma (EAC) to rationalize the surveillance programs in patient

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

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

59 of which 142 were esophageal adenocarcinoma (EAC), 176 were esophageal squamous cell carcinoma (ESCC)

60 ly predisposes to esophageal adenocarcinoma (EAC), a tumor with a very poor prognosis.

61 increased risk of esophageal adenocarcinoma (EAC), but the appropriate histologic definition of Barre

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

63 splasia and early esophageal adenocarcinoma (EAC), the reported incidence of EAC in Barrett's esophag

64 eases the risk of esophageal adenocarcinoma (EAC).

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

66 als to developing esophageal adenocarcinoma (EAC).

67 ith dysplasia and esophageal adenocarcinoma (EAC).

68 sophagus (BE) and esophageal adenocarcinoma (EAC).

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

70 in patients with esophageal adenocarcinoma (EAC).

71 or progression to esophageal adenocarcinoma (EAC).

72 ndard of care for esophageal adenocarcinoma (EAC).

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

74 ndard of care for esophageal adenocarcinoma (EAC).

75 Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countrie

76 sophageal cancer (esophageal adenocarcinoma [EAC] and/or esophageal squamous cell carcinoma [ESCC]).

77 occurs in 21% of esophageal adenocarcinomas (EAC).

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

79 was also associated with protection against EAC.

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

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

82 on occurs early in many patients with BE and EAC and indicate that early events occurring even in his

83 Our data suggest that BE and EAC arise from gastric progenitors due to a tumor-promot

84 Although miRNA expression profiles in BE and EAC have been reported, it has not been established whic

85 inhibitor prevents the development of BE and EAC in an in vivo model of GDER.

86 of normal squamous epithelium (NSE), BE and EAC obtained from a patient who progressed to adenocarci

87 The development of BE and EAC was accelerated by exposure to bile acids and/or nit

88 pared with controls, the incidence of BE and EAC was decreased in treated animals by 35.7% (relative

89 outcome measure was the incidence of BE and EAC.

90 cation of individuals with vs without BE and EAC.

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

92 associated with the development of EAC, and EAC-specific and all-cause mortality.

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

94 le for up to 3 years, progression to HGD and EAC can occur, highlighting the need for close endoscopi

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

96 98) of NSE, BE, low-grade dysplasia, HGD and EAC tissues, respectively, and was inversely associated

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

98 a stage-specific manner, confined to HGD and EAC, respectively.

99 of esophagitis, Barrett-like metaplasia and EAC.

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

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

102 e association observed between NSAID use and EAC risk, our pooled analysis suggests a possible role f

103 is-inducing ligand are detected in apoptotic EAC cells upon GATA6 deprivation.

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

105 inhibitor can prevent the development of BE/EAC in the Levrat model, in which induced gastroduodenoe

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

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

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

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

110 t associated with overall esophageal cancer, EAC, or ESCC risk, although total flavonoids and some fl

111 ny flavonoid subclass and esophageal cancer, EAC, or ESCC.

112 =885) and the Leiden Early Arthritis Clinic (EAC) cohort (n=581) and Yorkshire Early Arthritis Regist

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

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

115 enign BE, 5 patients with BE and concomitant EAC, and 10 additional patients with EAC to determine L1

116 model named "Escape from Adaptive Conflict" (EAC) includes adaptive processes before and after gene d

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

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

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

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

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

122 the BE patients at high risk for developing EAC.

123 the BE patients at high risk for developing EAC.

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

125 Multifunctional proteins, arising during EAC evolution, allow rapid adaptation independent of gen

126 selective gene amplification of GATA6 during EAC development sustains oncogenic lineage-survival of e

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

128 nes in the management of dysplasia and early EAC in Barrett's esophagus patients today.

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

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

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

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

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

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

135 apy as an efficacious therapeutic option for EAC.

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

137 Genotypes with similar risks for EAC or ESCC were combined and analyzed for multiplicativ

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

139 dentification of new therapeutic targets for EAC is greatly important.

140 also a rationale for combination therapy for EAC.

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

142 underwent RFA of BE, less than 1% died from EAC.

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

144 ted in 15% (3/20) high-grade dysplasia (HGD)/EAC patients.

145 xamined its role in CDDP resistance in human EAC cells.

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

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

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

149 for our understanding of molecular events in EAC.

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

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

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

153 enetic events to modulate gene expression in EAC.

154 ow that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chro

155 the majority of recurrently mutated genes in EAC were also mutated in NDBE.

156 d 1, was 184x higher in BE and 99x higher in EAC compared with normal esophageal tissue (P = 0.0239 a

157 Both have been implicated in EAC risk but this is controversial.

158 tative oncogene not previously implicated in EAC.

159 d PIK3CA) have previously been implicated in EAC.

160 confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations.

161 l genotypes in GST genes are not involved in EAC or ESCC susceptibility in Caucasians, in contrast to

162 nvasion were observed on ARID1A knockdown in EAC cells.

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

164 In conclusion, mutations in EAC driver genes generally occur exceptionally early in

165 ns in regulating gene expression networks in EAC.

166 Hedgehog (HH) pathway, has been observed in EAC.

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

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

169 rkers may help to individualize treatment in EAC patients.

170 rkers may help to individualize treatment in EAC patients.

171 tuzumab resistance remain uncharacterized in EAC.

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

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

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

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

176 While large EAC exome sequencing efforts to date have found recurren

177 of rs26232 was replicated in both the Leiden EAC cohort during the initial 7 years of RA (P=0.04) and

178 ococcus pneumoniae was associated with lower EAC risk.

179 istologic subtypes of esophageal malignancy (EAC, esophagogastric junctional adenocarcinoma, and ESCC

180 sources should be allocated to detect missed EAC.

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

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

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

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

185 Functional analyses of EAC-derived mutations in ELMO1 identifies increased cell

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

187 l activity may decrease the global burden of EAC.

188 New cases of EAC recorded after BE diagnosis were identified during a

189 creased risk of EAC (4 studies, 503 cases of EAC; OR, 0.68; 95% CI, 0.55-0.85) with minimal heterogen

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

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

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

193 was inversely associated with development of EAC (odds ratio = 0.58; 95% confidence interval: 0.39-0.

194 , factors associated with the development of EAC, and EAC-specific and all-cause mortality.

195 ients who are at low risk for development of EAC.

196 thway is known to mediate the development of EAC.

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

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

199 nocarcinoma (EAC), the reported incidence of EAC in Barrett's esophagus patients varies widely.

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

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

202 Incubation of EAC cells with trastuzumab and pertuzumab accelerated th

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

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

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

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 was associated with a 32% decreased risk of EAC (4 studies, 503 cases of EAC; OR, 0.68; 95% CI, 0.55

213 The annual risk of EAC in groups 1 to 5 was 0.32%, 0.27%, 0.16%, 0.2%, and

214 than Lewis(x), were associated with risk of EAC or high-grade dysplasia.

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

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

217 rsythia to be associated with higher 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 cant role in the malignant transformation of EAC.

221 s potential importance in clinical trials of EAC.

222 A better understanding of EAC underpins efforts to improve early detection and tre

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

224 2.22; 95% confidence interval, 1.89-2.60) or EAC (odds ratio, 2.46; 95% confidence interval, 2.07-2.9

225 dditional 37 missense mutations in BE and/or EAC, which were confirmed by Sanger sequencing.

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

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

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

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

230 ot significantly modify the risk for ESCC or EAC in our Dutch population.

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

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

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

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

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

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

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

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

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

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

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

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

243 primary end point was development of HGD or EAC.

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

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

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

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

248 ectron-accepting and -donating capacities (Q(EAC) and Q(EDC)) were quantified at applied potentials (

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

250 ypothesized that if NGM and IM infer similar EAC risk, then they would harbor similar genetic aberrat

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

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

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

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

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

256 We find that EAC patients whose tumors carry GATA6 amplification have

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

258 The EAC risk remained elevated in patients after antireflux

259 p), a protein encoded by L1, in eight of the EAC cases for which formalin-fixed paraffin embedded tis

260 ysis, cyclin E was amplified in 19.0% of the EAC samples.

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

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

263 miRNAs associated with progression of BE to EAC were identified using miRNA sequencing analysis.

264 tic test to predict the progression of BE to EAC.

265 tion of the RAC1 pathway as a contributor to EAC tumorigenesis.

266 nual rates of progression of no dysplasia to EAC of 0.12%, 0.33%, or 0.5% per year, respectively.

267 k of progression from Barrett's esophagus to EAC to be significantly lower than previously reported,

268 annual rate of progression rate from LGD to EAC of 0.5%/year.

269 o predict which cases of BE will progress to EAC or high-grade dysplasia and identified those that ca

270 compared with those who did not progress to EAC.

271 Cases who progressed to EAC (n = 89) or high-grade dysplasia >/= 6 months after

272 BE samples from patients with progression to EAC compared with those who did not progress to EAC.

273 ns during BE pathogenesis and progression to EAC, but treatment-naive surgical specimens are scarce.

274 gradually lower likelihood of progression to EAC.

275 resistance, 50 were dysregulated in treated EAC (P < 0.05 for each gene).

276 leaved caspase 3 was no different in treated EAC (P = 0.398).

277 Compared with untreated EAC, Ki-67 was downregulated (P = 0.04) and cleaved casp

278 Using EAC-xenografted mouse model, t-DARPP enhanced tumor grow

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

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

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

282 wn to harbor genetic changes associated with EAC, little is known about NGM.

283 genetic aberrations in genes associated with EAC.

284 in the inflammatory cascade associated with EAC.

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

286 In total, 581 participants with EAC, 213 with esophagogastric junctional adenocarcinoma,

287 Our analyses includes 327 patients with EAC and 106 patients with ESCC.

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

289 enotypes were compared between patients with EAC or ESCC, and controls.

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

291 omitant EAC, and 10 additional patients with EAC to determine L1 activity in this progressive disease

292 Between 2000 and 2010, 518 patients with EAC who completed TMT were analyzed for the frequency of

293 in two independent cohorts of patients with EAC who had undergone curative esophagectomy from the Un

294 ies and costs implications) to patients with EAC who have LRF only after TMT.

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

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

297 sed as a first-line therapy in patients with EAC, resistance remains a major clinical problem.

298 ion with long-term survival in patients with EAC.

299 ) panel for prognostication in patients with EAC.

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