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

1 g-term outcomes for clinical T1aN0 and T1bN0 esophageal adenocarcinoma.

2 reased risk for Barrett's esophagus (BE) and esophageal adenocarcinoma.

3 nd the pathogenesis of Barrett esophagus and esophageal adenocarcinoma.

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

5 esophagectomy in node-negative cT1a and cT1b esophageal adenocarcinoma.

6 s utilizing the average lipidomic profile of esophageal adenocarcinoma.

7 ly undiagnosed condition that predisposes to esophageal adenocarcinoma.

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

9 revent reflux reduces the progression toward esophageal adenocarcinoma.

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

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

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

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

14 k T2-4a, pathologically node-negative distal esophageal adenocarcinoma.

15 patients at highest risk for progression to esophageal adenocarcinoma.

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

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

18 35.7% in high grade dysplasia, and 16.7% in esophageal adenocarcinoma.

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

20 60-fold increase in the risk to evolve into esophageal adenocarcinoma.

21 a substantially decreased risk of death from esophageal adenocarcinoma.

22 ireflux surgery regarding risk of developing esophageal adenocarcinoma.

23 ients who despite antireflux surgery develop esophageal adenocarcinoma.

24 ate their abilities to reduce mortality from esophageal adenocarcinoma.

25 16q24 and extend our findings to now include esophageal adenocarcinoma.

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

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

28 sophageal strictures, Barrett esophagus, and esophageal adenocarcinoma.

29 pment sustains oncogenic lineage-survival of esophageal adenocarcinoma.

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

31 an important role in early carcinogenesis in esophageal adenocarcinoma.

32 hagus and are associated with progression to esophageal adenocarcinoma.

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

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

35 roposed as a viable treatment for submucosal esophageal adenocarcinoma.

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

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

38 well as allelic imbalances in chromosomes in esophageal adenocarcinoma.

39 t upfront, complete resection of pT1-4N1-3M0 esophageal adenocarcinoma.

40 patients with completely resected pT2-4aN0M0 esophageal adenocarcinoma.

41 ove identification of individuals at risk of esophageal adenocarcinoma.

42 nited States, and is a major risk factor for esophageal adenocarcinoma.

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

44 00/CBP and Notch has a synergistic effect in esophageal adenocarcinoma.

45 s representative of the genomic landscape of esophageal adenocarcinoma.

46 sophageal strictures, Barrett esophagus, and esophageal adenocarcinoma.

47 small proportion of patients, development of esophageal adenocarcinoma.

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

49 insights into the molecular pathogenesis of esophageal adenocarcinomas.

50 71% of patients had high-grade dysplasia or esophageal adenocarcinoma, 15% had low-grade dysplasia,

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

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

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

54 ho were tested for genetic susceptibility to esophageal adenocarcinoma (a polygenic risk score based

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

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

57 upfront, complete resection of node-positive esophageal adenocarcinoma, AC was associated with improv

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

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

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

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

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

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

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

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

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

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

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

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

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

71 Importance: Esophageal adenocarcinoma and its precursor lesion Barre

72 es (LNR) is an indicator of cancer burden in esophageal adenocarcinoma and may identify patients who

73 ng adjuvant therapy for patients with distal esophageal adenocarcinoma and no pathologic evidence of

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

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

76 emometrics to assess the phospholipidomes of esophageal adenocarcinoma and relevant control tissues.

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

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

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

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

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

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

83 uent type of somatic structural variation in esophageal adenocarcinoma, and the second most frequent

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

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

86 Esophageal adenocarcinoma arises from Barrett's esophagu

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

88 ing intervals: for baseline diagnosis of HGD/esophageal adenocarcinoma: at 3, 6, and 12 months and an

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

90 t identified individuals who later developed esophageal adenocarcinoma (based on age, sex, body mass

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

92 Patients with cN+ esophageal adenocarcinoma benefit significantly from neo

93 ent trimodality therapy for locally advanced esophageal adenocarcinoma between 1995 and 2017.

94 In esophageal adenocarcinoma, Bmi-1 amplification was detec

95 of 117 patients were highly discriminant for esophageal adenocarcinoma both in discovery (AUC = 0.97)

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

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

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

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

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

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

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

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

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

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

106 Notably, esophageal adenocarcinoma cases harboring RPS6KB1-VMP1 f

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

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

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

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

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

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

113 tically, silencing the carbon switch ACLY in esophageal adenocarcinoma cells shortened glycerophospho

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

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

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

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

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

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

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

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

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

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

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

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

126 Esophageal adenocarcinoma develops through a cascade of

127 Survival duration of esophageal adenocarcinoma did not significantly differ b

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

129 Esophageal adenocarcinoma (EA) and its premalignant lesi

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

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

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

133 Esophageal adenocarcinoma (EA) is a rapidly fatal cancer

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

135 1980s, an alarming rise in the incidence of esophageal adenocarcinoma (EA) led to screening of patie

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

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

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

139 progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA).

140 risk factor for Barrett's esophagus (BE) and esophageal adenocarcinoma (EA).

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

142 ce of head and neck cancer (HNC; n = 2,453), esophageal adenocarcinoma (EA; n = 855), esophageal squa

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

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

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

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

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

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

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

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

151 gnostic prediction of the clinical course in esophageal adenocarcinoma (EAC) are still not implemente

152 Esophageal adenocarcinoma (EAC) arises from Barrett esop

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

154 ), metaplasia (CP-A) and dysplasia (CP-B) to esophageal adenocarcinoma (EAC) cell lines (OE33, OE19)

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

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

157 gastroesophageal reflux disease (GERD), yet esophageal adenocarcinoma (EAC) disproportionately affec

158 Esophageal adenocarcinoma (EAC) has a dismal prognosis,

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

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

161 n and biological role of ITGAV expression in esophageal adenocarcinoma (EAC) has not been analyzed so

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

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

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

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

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

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

168 Esophageal adenocarcinoma (EAC) is a growing problem wit

169 Esophageal adenocarcinoma (EAC) is a highly aggressive d

170 Esophageal adenocarcinoma (EAC) is a highly lethal cance

171 Esophageal adenocarcinoma (EAC) is a poor-prognosis canc

172 Esophageal adenocarcinoma (EAC) is an aggressive maligna

173 Esophageal adenocarcinoma (EAC) is characterized by resi

174 A key barrier to controlling esophageal adenocarcinoma (EAC) is identifying those mos

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

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

177 Esophageal adenocarcinoma (EAC) is one of the most frequ

178 Esophageal adenocarcinoma (EAC) is rapidly increasing in

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

180 Esophageal adenocarcinoma (EAC) is resistant to standard

181 Esophageal adenocarcinoma (EAC) is the most prevalent es

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

183 The poor outcomes in esophageal adenocarcinoma (EAC) prompted us to interroga

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

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

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

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

188 d survival in patients with locally advanced esophageal adenocarcinoma (EAC) treated with neoadjuvant

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

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

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

192 a predisposing factor for the development of esophageal adenocarcinoma (EAC), a particularly lethal c

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

194 esophagus (BE) can progress to dysplasia and esophageal adenocarcinoma (EAC), accompanied by mutation

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

196 patients with high-grade dysplasia (HGD) or esophageal adenocarcinoma (EAC), from 1992 through 2015,

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

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

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

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

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

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

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

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

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

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

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

208 sophagus (BE) is the only known precursor to esophageal adenocarcinoma (EAC).

209 which Barrett's esophagus (BE) progresses to esophageal adenocarcinoma (EAC).

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

211 reflux and is implicated the development of esophageal adenocarcinoma (EAC).

212 ) predisposes for the malignant condition of esophageal adenocarcinoma (EAC).

213 unstable and heterogeneous cancers, such as esophageal adenocarcinoma (EAC).

214 Barrett's esophagus (BE) is a precursor to esophageal adenocarcinoma (EAC).

215 ine kinases are co-overexpressed in a subset esophageal adenocarcinoma (EAC).

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

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

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

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

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

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

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

223 Esophageal adenocarcinomas (EACs) are heterogeneous and

224 Approximately 15% to 43% of esophageal adenocarcinomas (EACs) are human epidermal gr

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

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

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

228 , DESI-MSI can objectively identify invasive esophageal adenocarcinoma from a number of premalignant

229 r, colon cancer, non-small cell lung cancer, esophageal adenocarcinoma, glioblastoma multiforme, ovar

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

233 Esophageal adenocarcinomas have mutations in tumor prote

234 Patients with esophageal adenocarcinoma histology and clinical stage T

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

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

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

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

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

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

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

242 esected, pathologically node-negative distal esophageal adenocarcinoma, independent of presence of hi

243 Esophageal adenocarcinoma is a cancer with rising incide

244 Esophageal adenocarcinoma is a deadly cancer with increa

245 Esophageal adenocarcinoma is a heterogeneous, chemoresis

246 n the management of subsets of clinical T1N0 esophageal adenocarcinoma is controversial.

247 whether MSI can objectively identify primary esophageal adenocarcinoma is currently unknown and repre

248 Esophageal adenocarcinoma is more frequent in non-Hispan

249 The incidence of esophageal adenocarcinoma is rising, survival remains po

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

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

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

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

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

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

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

257 nction, a site where Barrett's esophagus and esophageal adenocarcinoma often arise clinically.

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

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

260 cleotide variants previously associated with esophageal adenocarcinoma or squamous cell carcinoma.

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

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

263 A total of 273 esophageal adenocarcinoma patients treated with surgery

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

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

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

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

268 Esophageal adenocarcinoma ranks sixth in cancer mortalit

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

270 identification of individuals who developed esophageal adenocarcinoma remained at 0.80.

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

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

273 Among many other changes, esophageal adenocarcinoma samples were markedly enriched

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

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

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

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

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

279 ) and those with other main risk factors for esophageal adenocarcinoma, such as older age, male sex,

280 phagectomy for BE patients with intramucosal esophageal adenocarcinoma (T1a).

281 to esophagectomy in patients with submucosal esophageal adenocarcinoma (T1b) with low-risk features (

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

283 inical T1aN0 (n = 2545) and T1bN0 (n = 1281) esophageal adenocarcinoma that received either ER (cT1a,

284 s, these methods were applied for a model of esophageal adenocarcinoma that was previously calibrated

285 Testing for genetic variants associated with esophageal adenocarcinoma therefore seems unlikely to im

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

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

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

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

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

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

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

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

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

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

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

297 itive disease in patients with cT1a and cT1b esophageal adenocarcinoma were 4% and 15%, respectively.

298 585 patients with esophageal adenocarcinoma were analyzed immunohistochemi

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

300 d to identify adult patients with pT2-4aN0M0 esophageal adenocarcinoma who underwent definitive surge