ライフサイエンスコーパス: esophageal adenocarcinoma

1 00/CBP and Notch has a synergistic effect in esophageal adenocarcinoma.

2 patients at highest risk for progression to esophageal adenocarcinoma.

3 ivity may be associated with reduced risk of esophageal adenocarcinoma.

4 on of the effect of neoadjuvant treatment in esophageal adenocarcinoma.

5 35.7% in high grade dysplasia, and 16.7% in esophageal adenocarcinoma.

6 lastic progression of Barrett's esophagus to esophageal adenocarcinoma.

7 60-fold increase in the risk to evolve into esophageal adenocarcinoma.

8 s representative of the genomic landscape of esophageal adenocarcinoma.

9 a substantially decreased risk of death from esophageal adenocarcinoma.

10 ireflux surgery regarding risk of developing esophageal adenocarcinoma.

11 ients who despite antireflux surgery develop esophageal adenocarcinoma.

12 ate their abilities to reduce mortality from esophageal adenocarcinoma.

13 16q24 and extend our findings to now include esophageal adenocarcinoma.

14 ondition that is the only known precursor to esophageal adenocarcinoma.

15 , little is known about the role of Bmi-1 in esophageal adenocarcinoma.

16 pment sustains oncogenic lineage-survival of esophageal adenocarcinoma.

17 ach to the management of patients with early esophageal adenocarcinoma.

18 an important role in early carcinogenesis in esophageal adenocarcinoma.

19 hagus and are associated with progression to esophageal adenocarcinoma.

20 sophageal strictures, Barrett esophagus, and esophageal adenocarcinoma.

21 arrett's esophagus (BE), and reduce rates of esophageal adenocarcinoma.

22 n intestine-like metaplasia and precursor of esophageal adenocarcinoma.

23 roposed as a viable treatment for submucosal esophageal adenocarcinoma.

24 small proportion of patients, development of esophageal adenocarcinoma.

25 tases is critical to planning therapy for T1 esophageal adenocarcinoma.

26 gus, is associated with an increased risk of esophageal adenocarcinoma.

27 well as allelic imbalances in chromosomes in esophageal adenocarcinoma.

28 ave been developed to predict development of esophageal adenocarcinoma.

29 arrett's esophagus (BE) is a risk factor for esophageal adenocarcinoma.

30 a), columnar-lined esophagus, dysplasia, and esophageal adenocarcinoma.

31 risk of Barrett's esophagus, a precursor to esophageal adenocarcinoma.

32 risk of Barrett's esophagus, a precursor to esophageal adenocarcinoma.

33 esophagus is a well-recognized precursor of esophageal adenocarcinoma.

34 d stage III) and one individual had stage II esophageal adenocarcinoma.

35 agus is a risk factor for the development of esophageal adenocarcinoma.

36 cating a protective effect of NSAIDs against esophageal adenocarcinoma.

37 Barrett's esophagus is a precursor of esophageal adenocarcinoma.

38 reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma.

39 a markedly increased risk of development of esophageal adenocarcinoma.

40 for GERD symptoms, erosive esophagitis, and esophageal adenocarcinoma.

41 identify means of decreasing mortality from esophageal adenocarcinoma.

42 During follow-up, 52 patients developed esophageal adenocarcinoma.

43 rett esophagus to prevent the development of esophageal adenocarcinoma.

44 n to decrease the risk of the development of esophageal adenocarcinoma.

45 ples of screening to Barrett's esophagus and esophageal adenocarcinoma.

46 nd the pathogenesis of Barrett esophagus and esophageal adenocarcinoma.

47 ntal architecture of Barrett's esophagus and esophageal adenocarcinoma.

48 s utilizing the average lipidomic profile of esophageal adenocarcinoma.

49 GERD) is the strongest known risk factor for esophageal adenocarcinoma.

50 ly undiagnosed condition that predisposes to esophageal adenocarcinoma.

51 is and eventually by Barrett's esophagus and esophageal adenocarcinoma.

52 revent reflux reduces the progression toward esophageal adenocarcinoma.

53 de dysplasia (HGD), and 8 from patients with esophageal adenocarcinoma.

54 r the development of Barrett's esophagus and esophageal adenocarcinoma.

55 velopment of Barrett's esophagus followed by esophageal adenocarcinoma.

56 h resolution across the tumor margin area of esophageal adenocarcinoma.

57 and development of the intestine as well as esophageal adenocarcinomas.

58 hageal epithelium, Barrett's metaplasia, and esophageal adenocarcinomas.

59 ated fusions occurring in 3.33% to 11.67% of esophageal adenocarcinomas.

60 insights into the molecular pathogenesis of esophageal adenocarcinomas.

61 71% of patients had high-grade dysplasia or esophageal adenocarcinoma, 15% had low-grade dysplasia,

62 ophageal squamous cell carcinoma (ESCC), 151 esophageal adenocarcinoma, 166 gastric cardia adenocarci

63 and 2000, 97 incident cases of ESCC, 205 of esophageal adenocarcinoma, 188 of gastric cardia, and 18

64 subtypes.We identified 966 incident cases of esophageal adenocarcinomas, 323 cases of esophageal squa

65 0.89) for ESCC, 58% (95% CI: 0.38, 0.72) for esophageal adenocarcinoma, 47% (95% CI: 0.27, 0.63) for

66 with Barrett's esophagus, we identified 351 esophageal adenocarcinoma: 70 in persons who had a prior

67 ociated with an increased risk of developing esophageal adenocarcinoma, a cancer with a rapidly incre

68 flux disease (GERD), predisposes patients to esophageal adenocarcinoma, a tumor that has increased in

69 rrett's esophagus is a major risk factor for esophageal adenocarcinoma, a tumor whose incidence rate

70 In patients with operable gastric or lower esophageal adenocarcinomas, a perioperative regimen of E

71 lidated using gene expression data on BE and esophageal adenocarcinoma accessed through National Cent

72 tify which of these patients later developed esophageal adenocarcinoma, adenocarcinomas of the gastri

73 sociated with a decreased risk of death from esophageal adenocarcinoma (adjusted odds ratio, 0.99; 95

74 ily with 14 members affected (3 members with esophageal adenocarcinoma and 11 with Barrett esophagus)

75 Genomic DNA was analyzed from 116 esophageal adenocarcinoma and 26 precancerous lesion pat

76 sophagitis, 224 Barrett's esophagus, and 227 esophageal adenocarcinoma and 260 population controls we

77 e RNA sequencing (RNAseq) of 55 pretreatment esophageal adenocarcinoma and 49 nonmalignant biopsy tis

78 hagus (BE) show increased risk of developing esophageal adenocarcinoma and are routinely examined usi

79 tablish that AXL promotes CDDP resistance in esophageal adenocarcinoma and argue that therapeutic tar

80 d biopsy specimens of Barrett's esophagus or esophageal adenocarcinoma and associated normal esophagu

81 ptibility variants in a familial syndrome of esophageal adenocarcinoma and Barrett esophagus, termed

82 tra-abdominal distribution of fat) to detect esophageal adenocarcinoma and Barrett esophagus.

83 genetic and environmental exposure data for esophageal adenocarcinoma and Barrett's esophagus from t

84 a combinatorial chemoprevention strategy for esophageal adenocarcinoma and characterize the underlyin

85 Rates of esophageal adenocarcinoma and gastric cardia adenocarcin

86 However, the level changes of cyclin E in esophageal adenocarcinoma and its precancerous lesion ha

87 Importance: Esophageal adenocarcinoma and its precursor lesion Barre

88 cted on known and potential risk factors for esophageal adenocarcinoma and on the use of NSAIDs, incl

89 hat high expression Bmi-1 is associated with esophageal adenocarcinoma and precancerous lesions, whic

90 chemistry from tissue microarrays containing esophageal adenocarcinoma and precancerous lesions.

91 an association with overall survival in both esophageal adenocarcinoma and squamous cell carcinoma.

92 ociated clinicopathologic characteristics in esophageal adenocarcinoma and squamous cell carcinoma.

93 astases for intramucosal and submucosal (T1) esophageal adenocarcinoma and to analyze factors potenti

94 suggest that Notch signaling is critical for esophageal adenocarcinoma and underlies resistance to ch

95 tors associated with high-grade dysplasia or esophageal adenocarcinoma and various biomarkers that wo

96 may have contributed to recent increases in esophageal adenocarcinoma and, more speculatively, other

97 study group consisted of 83 patients with 44 esophageal adenocarcinomas and 39 squamous cell carcinom

98 as A-to-C mutations at 5'AA dinucleotides in esophageal adenocarcinomas and complex mutational patter

99 , 6 of 7 found significant associations with esophageal adenocarcinoma, and 4 of 6 found significant

100 chanisms underlying obesity's role in BE and esophageal adenocarcinoma, and suggest that weight loss

101 mors, 156 glioblastoma multiform samples, 27 esophageal adenocarcinomas, and 269 prostate cancer samp

102 Increasingly, patients with superficial esophageal adenocarcinoma are being treated endoscopical

103 Esophageal adenocarcinoma arises from Barrett's esophagu

104 his cohort, we identified 21 novel candidate esophageal adenocarcinoma-associated fusions occurring i

105 tributes to genomic instability in Barrett's esophageal adenocarcinoma (BAC).

106 e following neoadjuvant chemoradiotherapy in esophageal adenocarcinoma because most existing studies

107 Patients with cN+ esophageal adenocarcinoma benefit significantly from neo

108 In esophageal adenocarcinoma, Bmi-1 amplification was detec

109 oking has been implicated in the etiology of esophageal adenocarcinoma, but it is not clear if smokin

110 flammatory drugs (NSAIDs) reduce the risk of esophageal adenocarcinoma, but it is not known at what s

111 rett's esophagus is a strong risk factor for esophageal adenocarcinoma, but little is known about its

112 have been associated with a reduced risk of esophageal adenocarcinoma, but little is known about the

113 ased cohort, statin use after a diagnosis of esophageal adenocarcinoma, but not esophageal squamous c

114 ling components activates Notch signaling in esophageal adenocarcinoma, but the basis for this effect

115 sophageal reflux is the main risk factor for esophageal adenocarcinoma, but there is no strong suppor

116 ulmonary adenocarcinomas, and seven of seven esophageal adenocarcinomas, but not corresponding normal

117 the number of cases of incident symptomatic esophageal adenocarcinoma by 19%, compared with 17% for

118 rrett's esophagus, high-grade dysplasia, and esophageal adenocarcinoma by microchip electrophoresis w

119 S6KB1-VMP1 as a genetic fusion that promotes esophageal adenocarcinoma by modulating autophagy-relate

120 abundant in patients progressing through the esophageal adenocarcinoma cascade compared to controls.

121 a genome-wide association study, we compared esophageal adenocarcinoma cases (n = 2,390) and individu

122 Notably, esophageal adenocarcinoma cases harboring RPS6KB1-VMP1 f

123 We estimated the number of incident esophageal adenocarcinoma cases prevented and the increm

124 rent event occurring in approximately 10% of esophageal adenocarcinoma cases.

125 significantly enhanced potency against three esophageal adenocarcinoma cell lines compared with the t

126 ly, myeloid dendritic cells co-cultured with esophageal adenocarcinoma cell lines stimulated regulato

127 ls, co-cultured with Barrett's esophagus and esophageal adenocarcinoma cell lines, display a toleroge

128 us, AGR2 expression promotes tumor growth in esophageal adenocarcinoma cells and is able to transform

129 In contrast, reintroduction into esophageal adenocarcinoma cells of beta2SP and a dominan

130 AGR2 expression in SEG-1 esophageal adenocarcinoma cells was reduced with RNA int

131 ely, SOX9 silencing rescued the phenotype of esophageal adenocarcinoma cells with loss of beta2SP.

132 with reflux, decreases the proliferation of esophageal adenocarcinoma cells, and downregulates a key

133 h in vivo were increased in beta2SP-silenced esophageal adenocarcinoma cells.

134 nd its target SOX9 in primary fibroblasts or esophageal adenocarcinoma cells.

135 roliferative effects in Barrett's-associated esophageal adenocarcinoma cells.

136 ageal cancer from squamous cell carcinoma to esophageal adenocarcinoma coincided with popularization

137 ional processes molding the cancer genome in esophageal adenocarcinoma compared to squamous cell carc

138 st effective and would reduce mortality from esophageal adenocarcinoma compared with no screening.

139 Subsequently, the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON) identified

140 's esophagus from the Barretts Esophagus and Esophageal Adenocarcinoma Consortium (BEACON), and disco

141 ation-based studies within the Barrett's and Esophageal Adenocarcinoma Consortium to evaluate the ass

142 included in the international Barrett's and Esophageal Adenocarcinoma Consortium.

143 mune evasion in Barrett's esophagus favoring esophageal adenocarcinoma development.

144 Esophageal adenocarcinoma develops through a cascade of

145 Survival duration of esophageal adenocarcinoma did not significantly differ b

146 l of Bmi-1 was significantly associated with esophageal adenocarcinoma differentiation.

147 progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA) are not fully understood.

148 progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA) are not known.

149 the progression from Barrett's esophagus to esophageal adenocarcinoma (EA) by increasing cell prolif

150 oking have been individually associated with esophageal adenocarcinoma (EA) development.

151 Esophageal adenocarcinoma (EA) is a rapidly fatal cancer

152 Esophageal adenocarcinoma (EA) is characterized by a poo

153 BACKGROUND & AIMS: Esophageal adenocarcinoma (EA) is increasingly common am

154 1980s, an alarming rise in the incidence of esophageal adenocarcinoma (EA) led to screening of patie

155 metaplasia (BM) is a recognized precursor of esophageal adenocarcinoma (EA) with an intermediary stag

156 in the management of patients with localized esophageal adenocarcinoma (EA).

157 's esophagus (BE) is a major risk factor for esophageal adenocarcinoma (EA).

158 Barrett's esophagus (BE) and progression to esophageal adenocarcinoma (EA).

159 tt esophagus (BE) is a major risk factor for esophageal adenocarcinoma (EA).

160 We assessed the incidence of esophageal adenocarcinoma (EAC) after RFA, factors assoc

161 incidence of high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC) and compared progression

162 Bacteria may play a role in esophageal adenocarcinoma (EAC) and esophageal squamous

163 NSAIDs) has been reported to reduce risks of esophageal adenocarcinoma (EAC) and esophagogastric junc

164 The molecular genetic relationship between esophageal adenocarcinoma (EAC) and its precursor lesion

165 ed receptor5 (TGR5) were highly expressed in esophageal adenocarcinoma (EAC) and precancerous lesions

166 ary purpose of surveillance of patients with esophageal adenocarcinoma (EAC) and/or esophagogastric j

167 rogression to high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC) are highly variable.

168 Esophageal adenocarcinoma (EAC) arises from Barrett esop

169 etermine risk of Barrett's esophagus (BE) or esophageal adenocarcinoma (EAC) based on genetic and non

170 igated mechanisms that mediate resistance of esophageal adenocarcinoma (EAC) cells and patient-derive

171 immortalized esophageal epithelia (IEE) and esophageal adenocarcinoma (EAC) cells cultured in normal

172 gical therapy in patients with mucosal (T1a) esophageal adenocarcinoma (EAC) given the low likelihood

173 Esophageal adenocarcinoma (EAC) has a poor outcome, and

174 The incidence of esophageal adenocarcinoma (EAC) has increased in many We

175 The incidence of esophageal adenocarcinoma (EAC) has risen 600% over the

176 frequency ablation (RFA) reduces the risk of esophageal adenocarcinoma (EAC) in patients with Barrett

177 tatins have been reported to protect against esophageal adenocarcinoma (EAC) in patients with Barrett

178 ct these medications may have on the risk of esophageal adenocarcinoma (EAC) in patients with existin

179 progression to high-grade dysplasia (HGD) or esophageal adenocarcinoma (EAC) in patients with LGD of

180 ation-based studies have shown a low risk of esophageal adenocarcinoma (EAC) in patients with nondysp

181 Esophageal adenocarcinoma (EAC) is a growing problem wit

182 Esophageal adenocarcinoma (EAC) is a highly aggressive d

183 Esophageal adenocarcinoma (EAC) is a highly lethal cance

184 Esophageal adenocarcinoma (EAC) is an aggressive maligna

185 Esophageal adenocarcinoma (EAC) is characterized by resi

186 dence of Barrett's esophagus (BE)-associated esophageal adenocarcinoma (EAC) is increasing.

187 f progression of Barrett's esophagus (BE) to esophageal adenocarcinoma (EAC) is low and difficult to

188 Esophageal adenocarcinoma (EAC) is rapidly increasing in

189 The incidence of esophageal adenocarcinoma (EAC) is rapidly rising in the

190 Esophageal adenocarcinoma (EAC) is the most prevalent es

191 Most patients with esophageal adenocarcinoma (EAC) or squamous cell cancer

192 ion from premalignant Barrett's esophagus to esophageal adenocarcinoma (EAC) provides an ideal model

193 arrett's esophagus is thought to progress to esophageal adenocarcinoma (EAC) through a stepwise progr

194 screened for high grade dysplasia (HGD) and esophageal adenocarcinoma (EAC) through endoscopic scree

195 the progression of Barrett esophagus (BE) to esophageal adenocarcinoma (EAC) to rationalize the surve

196 progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EAC) vary.

197 Barrett's esophagus (BE) are diagnosed with esophageal adenocarcinoma (EAC) within 1 year of an endo

198 t esophageal cancer cases, of which 142 were esophageal adenocarcinoma (EAC), 176 were esophageal squ

199 iatus hernia, and it strongly predisposes to esophageal adenocarcinoma (EAC), a tumor with a very poo

200 ophagus is associated with increased risk of esophageal adenocarcinoma (EAC), but the appropriate his

201 e of BE, which is a metaplastic precursor to esophageal adenocarcinoma (EAC), such biomarkers would b

202 esophagus is the only known risk factor for esophageal adenocarcinoma (EAC), the most rapidly rising

203 though obesity increases risk for developing esophageal adenocarcinoma (EAC), the prognostic influenc

204 der to detect high-grade dysplasia and early esophageal adenocarcinoma (EAC), the reported incidence

205 ionship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expr

206 rett's esophagus patients with dysplasia and esophageal adenocarcinoma (EAC).

207 by surgery has become a standard of care for esophageal adenocarcinoma (EAC).

208 velopment of both Barrett esophagus (BE) and esophageal adenocarcinoma (EAC).

209 their risk of high-grade dysplasia (HGD) or esophageal adenocarcinoma (EAC).

210 plification and polysomy 17 in patients with esophageal adenocarcinoma (EAC).

211 better prediction of risk for progression to esophageal adenocarcinoma (EAC).

212 ation and is believed to be the precursor of esophageal adenocarcinoma (EAC).

213 est known risk factor for the development of esophageal adenocarcinoma (EAC).

214 rtant role in imparting aggressive nature to esophageal adenocarcinoma (EAC).

215 equently undergoes loss of heterozygosity in esophageal adenocarcinoma (EAC).

216 by surgery has become a standard of care for esophageal adenocarcinoma (EAC).

217 rogression to high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC).

218 rrett's esophagus (BE) increases the risk of esophageal adenocarcinoma (EAC).

219 n progress to high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC).

220 m that predisposes individuals to developing esophageal adenocarcinoma (EAC).

221 sease that predisposes to the development of esophageal adenocarcinoma (EAC); however, the involvemen

222 nt amplification at 18q11.2 occurs in 21% of esophageal adenocarcinomas (EAC).

223 ical activity and risk of esophageal cancer (esophageal adenocarcinoma [EAC] and/or esophageal squamo

224 sophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EACA) and 100% in metastasis,

225 cell lines representing HER2 overexpressing esophageal adenocarcinomas (EACs) and EGFR overexpressin

226 rs (postmenopausal breast, kidney, pancreas, esophageal adenocarcinoma, endometrium) in CRC survivors

227 e, erosive esophagitis, Barrett's esophagus, esophageal adenocarcinoma, erosive gastritis, gastric ca

228 Barrett's esophagus and esophageal adenocarcinoma express a unique set of stroma

229 mining the role of PET CT characteristics in esophageal adenocarcinoma for patients undergoing neoadj

230 cell line HUH7, as well as in liver tumors, esophageal adenocarcinoma, glioblastoma multiforme, pros

231 .04-0.32); ovarian h(2)g = 0.30 (0.18-0.42); esophageal adenocarcinoma h(2)g = 0.24 (0.14-0.34); esop

232 mptoms to assess for Barrett's esophagus and esophageal adenocarcinoma has become a widely accepted p

233 While the role of Axl in esophageal adenocarcinoma has been addressed, there is n

234 The incidence of esophageal adenocarcinoma has increased approximately 6-

235 Although the incidence of esophageal adenocarcinoma has rapidly increased over the

236 Esophageal adenocarcinomas have mutations in tumor prote

237 Patients with esophageal adenocarcinoma histology and clinical stage T

238 95% confidence interval (CI): 4.04, 21.29), esophageal adenocarcinoma (HR = 3.70, 95% CI: 2.20, 6.22

239 Five of these patients (71%) developed an esophageal adenocarcinoma in a median time of 66 months

240 n screening; prognostication and therapy for esophageal adenocarcinoma in Barrett's esophagus have br

241 o prevent Barrett's esophagus and subsequent esophageal adenocarcinoma in humans, the reflux of an ad

242 roidal anti-inflammatory drugs might prevent esophageal adenocarcinoma in patients with Barrett's eso

243 The large increase in the incidence of esophageal adenocarcinoma in the West during the past 30

244 The rising incidence of esophageal adenocarcinoma in the Western world has led t

245 doses of aspirin and esomeprazole to prevent esophageal adenocarcinoma in these patients.

246 ence of colorectal, gastric, pancreatic, and esophageal adenocarcinomas in the digestive tract.

247 Esophageal adenocarcinoma is a cancer with rising incide

248 Esophageal adenocarcinoma is a deadly cancer with increa

249 Esophageal adenocarcinoma is a heterogeneous, chemoresis

250 Esophageal adenocarcinoma is more frequent in non-Hispan

251 The key to prevention and cure of esophageal adenocarcinoma is the detection and eradicati

252 ophagus (BE) is a premalignant condition for esophageal adenocarcinoma, its diagnosis relying initial

253 The rising incidence of esophageal adenocarcinoma led to contributions in the st

254 Patients with esophageal adenocarcinoma, long-segment Barrett's esopha

255 at affect the risk of progression from BE to esophageal adenocarcinoma might prevent its development.

256 Cases were patients who developed esophageal adenocarcinoma more than 5 years after antire

257 encing in an independent set of pretreatment esophageal adenocarcinoma (N = 115) and nonmalignant (N

258 ium (BEACON) identified risk loci for BE and esophageal adenocarcinoma near CRTC1 and BARX1, and with

259 s likely than uninfected subjects to develop esophageal adenocarcinoma (odds ratio [OR], 0.37 [95% co

260 lso caused decreased signals of HER-2/neu in esophageal adenocarcinoma OE19 cells.

261 with Barrett's esophagus (BE) have a risk of esophageal adenocarcinoma of approximately 0.5% per year

262 otch activity will have efficacy in treating esophageal adenocarcinoma, offering a rationale to lay t

263 Reflux-induced injury promotes esophageal adenocarcinoma, one of the most rapidly incre

264 hagectomy alone for treatment of superficial esophageal adenocarcinoma or high-grade dysplasia.

265 .90) and 0.40 (0.19-0.81), respectively] and esophageal adenocarcinoma [OR (95% CI), 0.57 (0.36-0.93)

266 d the risk of gastric cardia adenocarcinoma, esophageal adenocarcinoma, or esophageal squamous cell c

267 the risk of pathologic nodal involvement in esophageal adenocarcinoma patients can be estimated by t

268 A total of 273 esophageal adenocarcinoma patients treated with surgery

269 Barrett's esophagus and esophageal adenocarcinoma patients were less likely than

270 adiation (18)F-FDG PET were derived from 217 esophageal adenocarcinoma patients who underwent chemora

271 mplified and highly expressed in a subset of esophageal adenocarcinoma patients, but this increase is

272 h poorer survival and lymph node invasion in esophageal adenocarcinoma patients.

273 Inverse correlation was also observed in 10 esophageal adenocarcinomas (Pearson's correlation -0.64,

274 ndergoing esophagectomy for locally advanced esophageal adenocarcinoma post-neoadjuvant chemoradiothe

275 Esophageal adenocarcinoma ranks sixth in cancer mortalit

276 ction for dysplasia and an esophagectomy for esophageal adenocarcinoma) received intravenous infusion

277 Esophageal adenocarcinoma risk in Barrett's esophagus (B

278 dentified another SNP associated with BE and esophageal adenocarcinoma: rs3784262, within ALDH1A2 (OR

279 ture separated nondysplastic BE samples from esophageal adenocarcinoma samples (P = .0012).

280 Risk was increased for esophageal adenocarcinoma (SIR, 1.91; 95% CI, 1.31-2.70)

281 ement of advanced and metastatic gastric and esophageal adenocarcinomas, specifically highlighting th

282 tt esophagus, low- and high-grade dysplasia, esophageal adenocarcinoma, squamous epithelium, and squa

283 In patients with esophageal adenocarcinoma, statin use after diagnosis wa

284 or Barrett esophagus, peptic strictures, and esophageal adenocarcinoma still account for a large port

285 e have been implicated in the progression to esophageal adenocarcinoma, studies investigating esophag

286 were substantially more prevalent in gastric/esophageal adenocarcinomas than colorectal tumors.

287 y the method to laser-capture-microdissected esophageal adenocarcinoma tissue, revealing a highly ane

288 capsular lymph node involvement (IC-LNI) for esophageal adenocarcinoma treated by primary surgery.

289 cal trial to evaluate the efficacy of GSI in esophageal adenocarcinoma treatment.

290 stem cell marker SOX9 was markedly higher in esophageal adenocarcinoma tumor tissues than normal tiss

291 fy all seminal contributions to the study of esophageal adenocarcinoma using the rat reflux model.

292 reported percentages of expression of CA9 in esophageal adenocarcinoma vary, and CA9 expression in pr

293 The rate of esophageal adenocarcinoma was 1 per 181 patient-years (0

294 The incidence rate of esophageal adenocarcinoma was 2.8 (95% confidence interv

295 Genomic DNA from 116 esophageal adenocarcinoma was analyzed for copy number a

296 In this study, LNM from esophageal adenocarcinoma was objectively detected using

297 lterations that contribute to development of esophageal adenocarcinoma, we know little about features

298 Patients who developed esophageal adenocarcinoma were 3 times more likely to ha

299 chemotherapy (MAGIC or FLOT) for cT3, Nx, M0 esophageal adenocarcinoma were included in the analysis.

300 ective review was performed of patients with esophageal adenocarcinoma who received CRT before esopha