ライフサイエンスコーパス: intestinal metaplasia

1 normal, esophagitis, or Barrett's esophagus (intestinal metaplasia).

2 tology for 43% of patients (50 gastric and 1 intestinal metaplasia).

3 is confirmed by the histological presence of intestinal metaplasia.

4 ed the complete eradication of dysplasia and intestinal metaplasia.

5 in normal mucosa and gastric mucosa showing intestinal metaplasia.

6 he pathogenesis and malignant progression of intestinal metaplasia.

7 atrophy, significant antral inflammation and intestinal metaplasia.

8 inflammation leads to glandular atrophy and intestinal metaplasia.

9 the fundic parameters (all P < 0.03), except intestinal metaplasia.

10 may induce regression or halt progression of intestinal metaplasia.

11 ere clinically similar to those with gastric intestinal metaplasia.

12 agus, and 0 (0%) of 26 patients with gastric intestinal metaplasia.

13 e, including gastric mucosal hyperplasia and intestinal metaplasia.

14 f 468 patients with Barrett's oesophagus and intestinal metaplasia.

15 it does not reliably cause regression of the intestinal metaplasia.

16 these cancers are found adjacent to areas of intestinal metaplasia.

17 frequently than longer, visible segments of intestinal metaplasia.

18 d for inflammation, H. pylori infection, and intestinal metaplasia.

19 d EAC in patients with irregular Z line with intestinal metaplasia.

20 ight patients (8%) had a second diagnosis of intestinal metaplasia.

21 and increased prevalence of body atrophy and intestinal metaplasia.

22 with and without inflammation or associated intestinal metaplasia.

23 ith no significant change in body atrophy or intestinal metaplasia.

24 not cured showed persistence of H. pylori in intestinal metaplasia.

25 H. pylori was found in intimate contact with intestinal metaplasia.

26 cter pylori is not usually found in areas of intestinal metaplasia.

27 tute guidelines on the management of gastric intestinal metaplasia.

28 ndex lesions included atrophic gastritis and intestinal metaplasia.

29 missing baseline histologic data, or had no intestinal metaplasia.

30 he goal of achieving complete eradication of intestinal metaplasia.

31 programs for Barrett's esophagus and gastric intestinal metaplasia.

32 for the treatment of recurrent dysplasia and intestinal metaplasia.

33 that RFA is not as effective in eradicating intestinal metaplasia.

34 ssected targets histologically classified as intestinal metaplasia.

35 ri-infected p27-/- mice frequently developed intestinal metaplasia (40% at 30 weeks, 67% at 45 weeks)

36 lasia (95%) and 99 of 106 had eradication of intestinal metaplasia (93%).

37 ation of H. pylori adherence with incomplete intestinal metaplasia (a putative precursor of carcinoma

38 testinal metaplasia/dysplasia or subsquamous intestinal metaplasia, a repeat endoscopy should be perf

39 nd pathology revealed complete regression of intestinal metaplasia (absence of any sign suggestive of

40 utcomes included eradication of dysplasia or intestinal metaplasia after 2 and 3 years, durability of

41 re RFA increases the incidence of persistent intestinal metaplasia after ablation in patients with BE

42 Loss of intestinal metaplasia after antireflux surgery is rare i

43 trolled reflux is associated with persistent intestinal metaplasia after RFA.

44 hernia also were associated with persistent intestinal metaplasia after RFA.

45 d adjacent mucosa with atrophic gastritis or intestinal metaplasia (AG/IM GC+), as well as in atrophi

46 mpared with 27.9% for dysplasia and 0.0% for intestinal metaplasia among patients in the control grou

47 t CDX1 is specifically associated with early intestinal metaplasia and a later developed intestinal-t

48 e findings identify mechanisms for TF-driven intestinal metaplasia and a likely pathogenic TF hierarc

49 f complete eradication of both dysplasia and intestinal metaplasia and a reduced risk of disease prog

50 tritis to more severe pathologies, including intestinal metaplasia and adenocarcinoma.

51 tes of complete eradication of dysplasia and intestinal metaplasia and adverse events in clinical pra

52 s were complete eradication of dysplasia and intestinal metaplasia and adverse events.

53 The degree of both intestinal metaplasia and atrophy correlated inversely w

54 1) and, additionally, at 11 mpi, less severe intestinal metaplasia and dysplasia (P < 0.05).

55 w methods for the diagnosis and detection of intestinal metaplasia and dysplasia are being evaluated

56 improve targeting of biopsies to specialised intestinal metaplasia and dysplasia in Barrett's oesopha

57 a more accurate and "nonbiopsy" diagnosis of intestinal metaplasia and dysplasia.

58 every 3 years thereafter to detect recurrent intestinal metaplasia and dysplasia.

59 involving NF-kappaB and Cdx2, which mediate intestinal metaplasia and ectopic expression of GC-C.

60 icobacter pylori; it might be a precursor to intestinal metaplasia and gastric adenocarcinoma.

61 expressed in SPEM of human and mouse and in intestinal metaplasia and gastric cancer in human beings

62 l cell nuclei in patients with gastritis and intestinal metaplasia and in human gastric organoids inf

63 of CDX2 in the gastric mucosa gives rise to intestinal metaplasia and in one model, gastric carcinom

64 troesophageal reflux causes inflammation and intestinal metaplasia and its downstream sequelum adenoc

65 ith such lineage confusion (mixed incomplete intestinal metaplasia and proliferative spasmolytic poly

66 aplastic subtype, which resembled incomplete intestinal metaplasia and shared transcriptional feature

67 ursor lesions for gastric adenocarcinoma are intestinal metaplasia and spasmolytic polypeptide expres

68 sophagus, but subsequently the importance of intestinal metaplasia and the premalignant nature of Bar

69 d CDX2 expression is associated with gastric intestinal metaplasia and tubular adenocarcinomas.

70 wing RFA, even after complete eradication of intestinal metaplasia, and caution for widespread use of

71 n in the stomach of transgenic mice promotes intestinal metaplasia, and CDX2 expression often is seen

72 with H. pylori uniformly developed atrophy, intestinal metaplasia, and dysplasia by 6 weeks and carc

73 ive gastritis, oxyntic atrophy, hyperplasia, intestinal metaplasia, and dysplasia.

74 rker for protection against gastric atrophy, intestinal metaplasia, and gastric cancer (OR for gastri

75 ults in serious sequelae, including atrophy, intestinal metaplasia, and gastric cancer.

76 re have a low risk of developing subsquamous intestinal metaplasia, and none have been reported to de

77 ium is dynamic and that microscopic areas of intestinal metaplasia are able to regress much more freq

78 the human distal esophagus, inflammation and intestinal metaplasia are associated with global alterat

79 It is now apparent that shorter lengths of intestinal metaplasia are common, and share many feature

80 e clonal architecture of gastric glands with intestinal metaplasia are important in our understanding

81 The location, extent, and severity of intestinal metaplasia are indicators of risk of developi

82 Barrett's esophagus (BE) and gastric intestinal metaplasia are related premalignant condition

83 orders, such as chronic active gastritis and intestinal metaplasia, are inversely associated with Bar

84 e ablation group had complete eradication of intestinal metaplasia, as compared with 2.3% of those in

85 er CDX1 is also uniquely associated with the intestinal metaplasia associated with putative precancer

86 to 5 years for patients with eradication of intestinal metaplasia at 2 years.

87 e developed esophageal tumors and esophageal intestinal metaplasia at 77 days.

88 at cardiac mucosa, carditis, and specialized intestinal metaplasia at an endoscopically normal-appear

89 Specialized intestinal metaplasia at the cardia was only seen in inf

90 The recent identification of specialized intestinal metaplasia at the cardia, along with the obse

91 flammation, and it is logical to assume that intestinal metaplasia at the gastroesophageal junction d

92 f Helicobacter pylori in the pathogenesis of intestinal metaplasia at the gastroesophageal junction h

93 alisation), degree of mucosal abnormalities (intestinal metaplasia, atrophy) and serological paramete

94 Esophageal tissues demonstrated specialized intestinal metaplasia (Barrett's esophagus).

95 distal esophagus, including 38 squamous, 38 intestinal metaplasia (Barrett's), and 22 gastric, obtai

96 ical ablative techniques often leave foci of intestinal metaplasia behind.

97 Both rat and human intestinal metaplasia, but not squamous epithelium, expr

98 Eradication of LGD and intestinal metaplasia can be achieved by radiofrequency

99 Complete remission of dysplasia and intestinal metaplasia can be achieved in the vast majori

100 gus segment of at least 3 cm and evidence of intestinal metaplasia can help stratify those patients a

101 hospitalization, and complete eradication of intestinal metaplasia (CEIM), were assessed using logist

102 E) with dysplasia is complete eradication of intestinal metaplasia (CEIM).

103 red epithelium (MLE, a presumed precursor in intestinal metaplasia), columnar-lined esophagus, dyspla

104 y higher MYC mRNA expression was observed in intestinal metaplasia compared to gastritis samples.

105 ccurred in 92.6% for dysplasia and 88.2% for intestinal metaplasia compared with 27.9% for dysplasia

106 surveillance for Barrett's oesophagus (with intestinal metaplasia confirmed by TFF3 and a minimum Ba

107 FA) in the randomized controlled Ablation of Intestinal Metaplasia Containing Dysplasia (AIM) trial.

108 Complete resolution of intestinal metaplasia (CRIM) was achieved in 30 patients

109 Complete remission of intestinal metaplasia (CRIM) was defined as eradication

110 ients in whom it was present before surgery, intestinal metaplasia disappeared in 14% of patients, an

111 remalignant conditions, but no inflammation, intestinal metaplasia, dysplasia, or cancer up to 1 year

112 from the neosquamous epithelium demonstrate intestinal metaplasia/dysplasia or subsquamous intestina

113 i-related cardia inflammation (P = 0.01) and intestinal metaplasia elsewhere in the stomach, indicati

114 ents drive CDX1 expression and contribute to intestinal metaplasia, epithelial dedifferentiation, and

115 Intestinal metaplasia, even a short length, is premalign

116 h rat and human squamous epithelium, but not intestinal metaplasia, expressed squamous transcription

117 l junction than it has been in patients with intestinal metaplasia extending up into the distal esoph

118 ial gastritis, 18 atrophic gastritis, and 18 intestinal metaplasia from cancer-free individuals of No

119 th suspected gastric atrophy with or without intestinal metaplasia, gastric biopsies should be obtain

120 Atrophic gastritis (AG) and gastric intestinal metaplasia (GIM) are well defined intermediat

121 Gastric intestinal metaplasia (GIM) is a precursor to gastric ad

122 of precancerous conditions, such as gastric intestinal metaplasia (GIM).

123 ori infection, chronic active gastritis, and intestinal metaplasia had similar epidemiologic patterns

124 e eradication (endoscopic and histologic) of intestinal metaplasia has been achieved with BET, survei

125 Thus, the development of intestinal metaplasia has been viewed as a mechanism by

126 with H. heilmannii was seen associated with intestinal metaplasia, however this need further confirm

127 rmal/chronic gastritis (CG) mucosa (0.09) to intestinal metaplasia (IM) (0.16), flat dysplasias (0.40

128 there have been concerns about recurrence of intestinal metaplasia (IM) after ablation.

129 Gastric intestinal metaplasia (IM) and gastric cancer are associ

130 Both intestinal metaplasia (IM) and spasmolytic polypeptide (

131 Intestinal metaplasia (IM) and spasmolytic polypeptide-e

132 nant conditions, atrophic gastritis (AG) and intestinal metaplasia (IM) are characterized by an incre

133 ori (H. pylori)-infected gastric mucosa with intestinal metaplasia (IM) changes.

134 Intestinal metaplasia (IM) extending above the EGJ was d

135 f MSI in gastric carcinogenesis by examining intestinal metaplasia (IM) from patients with and withou

136 The development of intestinal metaplasia (IM) has been purported to be a cr

137 s of multifocal atrophic gastritis (MAG) and intestinal metaplasia (IM) have occurred.

138 remalignant lesions gastric atrophy (GA) and intestinal metaplasia (IM) influence gastric cancer risk

139 Intestinal metaplasia (IM) is a pre-malignant condition

140 Intestinal metaplasia (IM) is considered a key pivot poi

141 Intestinal metaplasia (IM) is defined by the presence of

142 tests excluded, 52/314 patients (16.6%) had intestinal metaplasia (IM) on endoscopic biopsies, which

143 aseline diagnosis and to estimate GC risk by intestinal metaplasia (IM) subtype and anatomic location

144 sustained complete remission of neoplasia or intestinal metaplasia (IM), IM in gastric cardia, or bur

145 s conditions, i.e., atrophic mucosa (AM) and intestinal metaplasia (IM), in patients with chronic gas

146 s the most important risk factor for gastric intestinal metaplasia (IM).

147 olypeptide-expressing metaplasia (SPEM), and intestinal metaplasia (IM).

148 atients with chronic gastritis (CG, N = 37), intestinal metaplasia (IM, N = 21) or gastric cancer (GC

149 remained eradicated in >85% of patients and intestinal metaplasia in >75%, without maintenance RFA.

150 a seen in 87-96% and complete eradication of intestinal metaplasia in 57-96% of treated patients.

151 stoperative biopsies showed complete loss of intestinal metaplasia in 73% of the patients with CIM co

152 ustained complete remission of neoplasia and intestinal metaplasia in 90% of patients; neoplasia recu

153 he findings of cardiac mucosa, carditis, and intestinal metaplasia in an endoscopically normal-appear

154 Intestinal metaplasia in Barrett's esophagus is a major

155 sive procedure, has been used for diagnosing intestinal metaplasia in Barrett's.

156 uate the frequency of H. pylori adherence to intestinal metaplasia in different populations.

157 ri and signs of chronic active gastritis and intestinal metaplasia in gastric biopsy samples were inv

158 Intestinal metaplasia in immigrant Asian populations is

159 nflammation, H. pylori infection, and cardia intestinal metaplasia in patients with and without GERD.

160 y ablation (RFA) can eradicate dysplasia and intestinal metaplasia in patients with dysplastic Barret

161 standard endoscopy can enhance the yield of intestinal metaplasia in patients with suspected short-s

162 Patients with intestinal metaplasia in short lengths of columnar mucos

163 The origin of intestinal metaplasia in short segments of columnar muco

164 plasia, and CDX2 expression often is seen in intestinal metaplasia in stomach and esophagus.

165 metaplasia, with almost complete absence of intestinal metaplasia in subjects infected with i2-type

166 by gastroesophageal reflux disease, whereas intestinal metaplasia in the distal stomach is often a c

167 Intestinal metaplasia in the esophagus is known to be a

168 everity of chronic GERD; and the presence of intestinal metaplasia in the gap defines Barrett esophag

169 hagus) appear to be distinct from those with intestinal metaplasia in the gastric cardia.

170 that CDX2 is important for the initiation of intestinal metaplasia in the gastric mucosa, but the rol

171 Intestinal metaplasia in the stomach is defined by the p

172 collected data on BE recurrence (defined as intestinal metaplasia in the tubular esophagus) and dysp

173 veillance guidelines for gastric atrophy and intestinal metaplasia in the Western world, future asses

174 y, aberrant CDX2 expression is often seen in intestinal metaplasias in the stomach and esophagus and

175 In primary colorectal cancers and intestinal metaplasias in the stomach, CDX2 and LI-cadhe

176 bacter pylori from gastritis to precancerous intestinal metaplasia, in human gastric organoids, and i

177 osa containing goblet cells--the hallmark of intestinal metaplasia--in 10% to 15% of patients who are

178 various histological classifications of BE (intestinal metaplasia, "indefinite for dysplasia", low g

179 Cardia intestinal metaplasia is associated with H. pylori-relat

180 Presence of specialized intestinal metaplasia is associated with increased time

181 Barrett's esophagus (BE), or specialized intestinal metaplasia, is a premalignant heterogeneous e

182 s of gastric folds, and, if with concomitant intestinal metaplasia, light blue crests and white opaqu

183 Less is known about the potential for intestinal metaplasia limited to the cardia (CIM) to reg

184 rgery is more effective in producing loss of intestinal metaplasia located only at the gastroesophage

185 l adhesion characteristics, or their type of intestinal metaplasia may have biochemical properties th

186 epithelium occurred earlier than specialized intestinal metaplasia (median 4.8 vs 8.1 yr; P = 0.025).

187 pc(Min/+) mice and are increased in Multiple Intestinal Metaplasia (Min) polyps.

188 IM GC+), as well as in atrophic gastritis or intestinal metaplasia mucosa of patients without GC (AG/

189 nt Barrett's esophagus (n = 43), and gastric intestinal metaplasia (n = 26) were immunostained for CK

190 scopic mucosal biopsy specimens of Barrett's intestinal metaplasia (n = 30), Barrett's dysplasia (n =

191 nosed between 1993 and 2005 with specialized intestinal metaplasia (n = 3167).

192 GC, i.e., in atrophic mucosal glands without intestinal metaplasia (non-IM) and intestinal metaplasti

193 In the case of Barrett's oesophagus, intestinal metaplasia occurs at the gastro-oesophageal j

194 the diagnosis of atrophic gastritis because intestinal metaplasia occurs in underlying atrophic muco

195 cardiac mucosa might be the precursor of the intestinal metaplasia of BE.

196 that hTERT, MYC, and TP53 are deregulated in intestinal metaplasia of individuals from Northern Brazi

197 Patients with intestinal metaplasia of the cardia were excluded.

198 gment BE (SSBE), and microscopic specialized intestinal metaplasia of the esophagogastric junction (S

199 Themes and concepts pertaining to intestinal metaplasia of the esophagus and cardia are de

200 Sixty patients with intestinal metaplasia of the esophagus or cardia had ant

201 Barrett's esophagus, a condition of intestinal metaplasia of the esophagus, is associated wi

202 Cardiac mucosa is the precursor of intestinal metaplasia of the esophagus.

203 BEST PRACTICE ADVICE 11: Intestinal metaplasia of the gastric cardia (without res

204 In addition, ngn3(-/-) mice display intestinal metaplasia of the gastric epithelium.

205 selectively expressed in epithelial cells in intestinal metaplasia of the human stomach and esophagus

206 Its aberrant expression in intestinal metaplasia of the upper gastrointestinal trac

207 n residents newly diagnosed with specialized intestinal metaplasia on at least 1 of 4 esophageal biop

208 oviders should be aware that the presence of intestinal metaplasia on gastric histology almost invari

209 ould recognize, however, that a diagnosis of intestinal metaplasia on gastric histopathology implies

210 Wild-type mice developed intestinal metaplasia only after 75 weeks of infection;

211 ssected targets histologically classified as intestinal metaplasia or "indefinite for dysplasia" span

212 taplasia to specialized columnar epithelium (intestinal metaplasia or Barrett's esophagus), which can

213 es from patients whose disease progressed to intestinal metaplasia or dysplasia, compared with patien

214 is not clear if dysplasias are derived from intestinal metaplasia or how dysplasias expand.

215 explain the transient expression of CDX1 in intestinal metaplasia or the molecular inactivation mech

216 37 were cases of chronic atrophic gastritis, intestinal metaplasia, or dysplasia.

217 ns can undergo a cell fate switch leading to intestinal metaplasia, predisposing to malignancy.

218 Moreover, intestinal metaplasia regressed in the majority of patie

219 ondysplastic Barrett's in 7 of 16 (44%), and intestinal metaplasia regressed to cardiac mucosa in 9 o

220 olytic polypeptide-expressing metaplasia and intestinal metaplasia, respectively.

221 hTERT, MYC, and p53 immunoreactivity only in intestinal metaplasia samples.

222 Patients with extensive intestinal metaplasia should be offered endoscopic surve

223 ts who have achieved complete eradication of intestinal metaplasia should undergo surveillance every

224 ho have not achieved complete eradication of intestinal metaplasia should undergo surveillance every

225 All areas of intestinal metaplasia showing adherence contained sulfom

226 pecificity of OCT for diagnosing specialized intestinal metaplasia (SIM).

227 asing, the earliest lesion being specialized intestinal metaplasia (SIM).

228 Loss of TP53 was also only detected in intestinal metaplasia specimens.

229 ls, and that fission is a mechanism by which intestinal metaplasia spreads.

230 ews reports on the prevalence of subsquamous intestinal metaplasia (SSIM) in patients with Barrett's

231 with a transitional, CDX2(+)/MIST1(-) hybrid-intestinal metaplasia stage.

232 igher scores for gastric mucosal atrophy and intestinal metaplasia than those with fewer repeat regio

233 hageal junction appear to arise from foci of intestinal metaplasia that develop either in the distal

234 Intestinal metaplasia was detected in two cases, but no

235 splasia was eradicated in 50 of 54 (93%) and intestinal metaplasia was eradicated in 48 of 54 (89%).

236 splasia was eradicated in 51 of 52 (98%) and intestinal metaplasia was eradicated in 51 of 52 (98%);

237 eradicated in 55 of 56 of subjects (98%) and intestinal metaplasia was eradicated in 51 of 56 (91%).

238 assified as complete responders (CRs) if all intestinal metaplasia was eradicated in fewer than 3 abl

239 Cardia intestinal metaplasia was more common among controls (22

240 Intestinal metaplasia was observed in 3(3%)(p = 1.0) of

241 Intestinal metaplasia was typed by staining with periodi

242 Overall PPVs for atrophic gastritis and intestinal metaplasia were 12.4% and 18.9%, respectively

243 We observed that individuals with intestinal metaplasia were all infected with H. pylori s

244 of gastric disease, peaking in tissues with intestinal metaplasia, whereas pEGFR, pEGFR-ERBB2, and p

245 iseases and gastric atrophy, with or without intestinal metaplasia, which predisposes to gastric canc

246 rates of complete remission of dysplasia and intestinal metaplasia with overall survival comparable t

247 le was strongly associated with precancerous intestinal metaplasia, with almost complete absence of i

248 hese findings associate VZV with specialized intestinal metaplasia within the esophagus and suggest a