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 ed the complete eradication of dysplasia and intestinal metaplasia.

4 in normal mucosa and gastric mucosa showing intestinal metaplasia.

5 atrophy, significant antral inflammation and intestinal metaplasia.

6 inflammation leads to glandular atrophy and intestinal metaplasia.

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

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

9 may induce regression or halt progression of intestinal metaplasia.

10 ere clinically similar to those with gastric intestinal metaplasia.

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

12 e, including gastric mucosal hyperplasia and intestinal metaplasia.

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

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

15 frequently than longer, visible segments of intestinal metaplasia.

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

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

18 and increased prevalence of body atrophy and intestinal metaplasia.

19 he goal of achieving complete eradication of intestinal metaplasia.

20 with and without inflammation or associated intestinal metaplasia.

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

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

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

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

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

26 for the treatment of recurrent dysplasia and intestinal metaplasia.

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

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

29 ssected targets histologically classified as intestinal metaplasia.

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

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

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

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

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

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

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

37 Loss of intestinal metaplasia after antireflux surgery is rare i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 Intestinal metaplasia, even a short length, is premalign

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

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

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

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

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

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

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

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

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

111 Both intestinal metaplasia (IM) and spasmolytic polypeptide (

112 Intestinal metaplasia (IM) and spasmolytic polypeptide-e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 Intestinal metaplasia in Barrett's esophagus is a major

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

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

134 Intestinal metaplasia in immigrant Asian populations is

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

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

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

138 Patients with intestinal metaplasia in short lengths of columnar mucos

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

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

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

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

143 Intestinal metaplasia in the esophagus is known to be a

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

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

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

147 Intestinal metaplasia in the stomach is defined by the p

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

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

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

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

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

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

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

155 Presence of specialized intestinal metaplasia is associated with increased time

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

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

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

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

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

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

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

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

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

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

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

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

168 Patients with intestinal metaplasia of the cardia were excluded.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 37 were cases of chronic atrophic gastritis, intestinal metaplasia, or dysplasia.

185 Moreover, intestinal metaplasia regressed in the majority of patie

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

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

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

189 Patients with extensive intestinal metaplasia should be offered endoscopic surve

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

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

192 All areas of intestinal metaplasia showing adherence contained sulfom

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

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

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

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

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

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

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

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

201 Intestinal metaplasia was detected in two cases, but no

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

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

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

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

206 Cardia intestinal metaplasia was more common among controls (22

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

208 Intestinal metaplasia was typed by staining with periodi

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

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

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

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

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