ライフサイエンスコーパス: metaplasia

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

2 hich have chronically inflamed stomachs with metaplasia.

3 e points, showed reduced acinar-to-duct cell metaplasia.

4 ys associated with IL-13-induced goblet cell metaplasia.

5 sal IL-33 and TSLP was sufficient for mucous metaplasia.

6 quired for maximum ILC2 expansion and mucous metaplasia.

7 oblet cells) and thereby reproduce Barrett's metaplasia.

8 nts with Barrett's oesophagus and intestinal metaplasia.

9 decreased along with increasing goblet cell metaplasia.

10 on, TH2 cytokine production, and mucous cell metaplasia.

11 tients with irregular Z line with intestinal metaplasia.

12 recruitment, IgA secretion, and mucous cell metaplasia.

13 iven effects on lung function or goblet cell metaplasia.

14 seline histologic data, or had no intestinal metaplasia.

15 achieving complete eradication of intestinal metaplasia.

16 o retinal detachment-induced lens epithelial metaplasia.

17 gonism in the progenitor niche that promotes metaplasia.

18 ifferentiation and leads to acinar to ductal metaplasia.

19 the molecular phenotype of postesophagectomy metaplasia.

20 induces cellular injury, and provokes acinar metaplasia.

21 L-17A significantly attenuated AHR and mucus metaplasia.

22 ial cells, and augmentation of acinar-ductal metaplasia.

23 velopment of SPEM, as well as progression of metaplasia.

24 gulated in and required for acinar-to-ductal metaplasia.

25 -17, eotaxin, and eosinophils and more mucus metaplasia.

26 eligible patients, 45 (36%) had evidence of metaplasia.

27 ment alleviates inflammation and goblet cell metaplasia.

28 gastrokine1 and mucin5ac, indicating gastric metaplasia.

29 , eosinophilic inflammation, and goblet cell metaplasia.

30 size, decrease in cell density, and squamous metaplasia.

31 female mice developing keratinizing squamous metaplasia.

32 stic phenotype that ultimately progressed to metaplasia.

33 xpression of SPDEF and Bcl-2 and mucous cell metaplasia.

34 w level inflammation as a driver for colonic metaplasia.

35 ion in the asthmatic airway with goblet cell metaplasia.

36 disorders accompanied by chronic goblet cell metaplasia.

37 y contribute to the development of Barrett's metaplasia.

38 chemokines, IgE production, and mucous cell metaplasia.

39 r Barrett's esophagus and gastric intestinal metaplasia.

40 nt acini, as well as in pancreatitis-induced metaplasia.

41 pre-metaplastic cell type that progresses to metaplasia.

42 ronchoalveolar lavage eosinophils and mucous metaplasia.

43 role of the niche has not been delineated in metaplasia.

44 ed for baseline gastritis and progression to metaplasia.

45 ich perpetuate type 2 inflammation and mucus metaplasia.

46 d by the histological presence of intestinal metaplasia.

47 ronchial airway inflammation and goblet cell metaplasia.

48 ion, which precedes acinar proliferation and metaplasia.

49 well-defined histological stages, including metaplasia.

50 esis and malignant progression of intestinal metaplasia.

51 amycin also reverted established goblet cell metaplasia.

52 anced airway hyperreactivity and mucous cell metaplasia.

53 y for non-Hodgkin lymphoma (48%) and myeloid metaplasia (31%).

54 uamous mucosa tissues, 3.7% in columnar cell metaplasia, 5.8% in Barrett's esophagus, 19.0% in low gr

55 Importantly, acinar-to-ductal metaplasia, a crucial step for initiation of PDAC, was f

56 Goblet cell metaplasia, a disabling hallmark of chronic lung disease

57 would also revert IL-17-induced goblet cell metaplasia, a prediction confirmed by our experiments.

58 taplasia/dysplasia or subsquamous intestinal metaplasia, a repeat endoscopy should be performed and v

59 Goblet cell metaplasia accompanies common pulmonary disorders that a

60 y increased airway eosinophilia, goblet cell metaplasia, accumulation of ILC2s and TH2 cells, type 2

61 e, had uterine neoplasms comprising squamous metaplasia, adenofibroma and adenomyoma.

62 DC is required for KRAS-driven acinar-ductal metaplasia (ADM) and its progression to pancreatic intra

63 cini, and particularly high in acinar ductal metaplasia (ADM) and PanIN lesions, where IER3 colocaliz

64 e pancreas that have undergone acinar-ductal metaplasia (ADM) can transform into premalignant cells t

65 paB-Ras deficiency promotes acinar-to-ductal metaplasia (ADM) during tumour initiation as well as tum

66 Acinar-to-ductal metaplasia (ADM) has been identified as a key tumor init

67 t that pancreatitis-induced acinar-to-ductal metaplasia (ADM) is a key event for pancreatic ductal ad

68 inar cell state can lead to acinar-to-ductal metaplasia (ADM), a precursor lesion to the development

69 roenvironment to pancreatic acinar-to-ductal metaplasia (ADM), a preneoplastic transition in oncogeni

70 ve mechanisms that initiate acinar-to-ductal metaplasia (ADM), a process that replaces damaged acinar

71 Mst1r overexpression increased acinar-ductal metaplasia (ADM), accelerated the progression of pancrea

72 es, the ductal phenotype of acinar-to-ductal metaplasia (ADM), and dysplasia with Dice coefficients o

73 ucts, chronic pancreatitis, acinar to ductal metaplasia (ADM), and mucinous metaplasia that resembles

74 e phenotypes during pancreatic acinar ductal metaplasia (ADM), pancreatic acini from wild type and KO

75 for oncogenic Kras-mediated acinar-to-ductal metaplasia (ADM), pancreatic intraepithelial neoplasias

76 cell reprogramming known as acinar-to-ductal metaplasia (ADM)-a precursor of pancreatic intraepitheli

77 press KrasG12D by promoting acinar-to-ductal metaplasia (ADM).

78 floxed mice that facilitate acinar-to-ductal metaplasia (ADM).

79 ells to a ductal phenotype (acinar-to-ductal metaplasia, ADM) occurs after injury or inflammation of

80 mucosa with atrophic gastritis or intestinal metaplasia (AG/IM GC+), as well as in atrophic gastritis

81 proliferated near airways and induced mucus metaplasia, airway hyperresponsiveness, and airway eosin

82 rease in pulmonary inflammation, mucous cell metaplasia, airway hyperresponsiveness, and OVA-specific

83 ology characterized by increased goblet cell metaplasia, airway hyperresponsiveness, and Th2-mediated

84 isorder characterized by inflammation, mucus metaplasia, airway remodeling, and hyperresponsiveness.

85 ecific overexpression of SOX17 led to ductal metaplasia along with inflammation and collagen depositi

86 27.9% for dysplasia and 0.0% for intestinal metaplasia among patients in the control group (P < .001

87 lete eradication of dysplasia and intestinal metaplasia and adverse events in clinical practice.

88 lete eradication of dysplasia and intestinal metaplasia and adverse events.

89 old mice, but not mature mice, causes mucous metaplasia and airway hyperresponsiveness that are assoc

90 ion of 6-day-old immature mice causes mucous metaplasia and airway hyperresponsiveness which is assoc

91 IL-13-producing ILC2s; and exaggerated mucus metaplasia and airway hyperresponsiveness.

92 e 2 response, which causes persistent mucous metaplasia and airways hyperresponsiveness.

93 organized masses resembling acinar to ductal metaplasia and chronic pancreatitis.

94 In the stomach, chronic inflammation causes metaplasia and creates a favorable environment for the e

95 The cellular and molecular basis of metaplasia and declining neurogenesis in the aging olfac

96 A combination of hyperplasia and dysplasia, metaplasia and dysplasia, and hyperplasia, metaplasia, a

97 the incidence of postesophagectomy columnar metaplasia and dysplasia, and the timescale over which i

98 rs thereafter to detect recurrent intestinal metaplasia and dysplasia.

99 a lower staining index of WNT3A in Barrett's metaplasia and EAC, than in squamous epithelium specimen

100 nd primary specimens of squamous epithelium, metaplasia and EAC.

101 rrays revealed the presence of tuft cells in metaplasia and early-stage tumors, along with SOX17 expr

102 Foxa3 induced goblet cell metaplasia and enhanced expression of a network of genes

103 ylori; it might be a precursor to intestinal metaplasia and gastric adenocarcinoma.

104 tor of pancreatitis, during acinar-to-ductal metaplasia and in early pancreatic intraepithelial neopl

105 ei in patients with gastritis and intestinal metaplasia and in human gastric organoids infected with

106 ronic atrophic gastritis can lead to gastric metaplasia and increase risk of gastric adenocarcinoma.

107 oxin forms induced more severe and extensive metaplasia and inflammation in the mouse stomach than st

108 f epithelium is a hotspot for pre-neoplastic metaplasia and malignancy, but the cells of origin for t

109 ed at investigating whether goblet cell (GC) metaplasia and mucus production are differentially regul

110 might be less sensitive to IL-13-induced GC metaplasia and mucus production through lower expression

111 tely and chronically OVA-challenged mice, GC metaplasia and mucus production were observed in proxima

112 ll as a significant depletion of goblet cell metaplasia and mucus secretion markers after HDM exposur

113 development and is required for goblet cell metaplasia and normal Th2 inflammatory responses to HDM

114 hat Hh signaling is reactivated in Barrett's metaplasia and overexpression of Sonic hedgehog (SHH) in

115 rance of Kras(G12D)-induced acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasias, wh

116 on factor FOXA3 in regulation of goblet cell metaplasia and pulmonary innate immunity.

117 Mechanisms regulating both goblet cell metaplasia and susceptibility to viral infection associa

118 IL33 promotes metaplasia and the sequelae of eosinophil-dependent down

119 s revealed expression of SOX17 in pancreatic metaplasia and tumors.

120 tment, and increased cytokeratin 19-positive metaplasias and immune cell infiltration.

121 ees of extramedullary hematopoiesis (myeloid metaplasia) and splenomegaly.

122 of inflammation, necrosis, acinar-to-ductal metaplasia, and acinar-cell hypertrophy; this led to tis

123 and neutrophilia, tissue inflammation, mucus metaplasia, and AHR that were partially reversible with

124 ophilia, type 2 cytokine levels, goblet cell metaplasia, and airway hyperresponsiveness.

125 gob5 mRNA expression, ILC2 expansion, mucus metaplasia, and airway hyperresponsiveness.

126 exacerbated airway inflammation, goblet cell metaplasia, and airway remodeling, but all of these feat

127 icient for eosinophilic inflammation, mucous metaplasia, and airways hyperresponsiveness.

128 ilia, elevated mucin expression, goblet cell metaplasia, and distal airspace enlargement, but had no

129 Hyperplasia, metaplasia, and dysplasia alone were found in 11.7%, 24.

130 , metaplasia and dysplasia, and hyperplasia, metaplasia, and dysplasia was found in 3.4%, 6.3%, and 4

131 hymal lung inflammation, alveolar epithelial metaplasia, and epithelial endoplasmic reticulum stress

132 ry cells, submucosal thickening, goblet cell metaplasia, and increased collagen content.

133 cells, led to formation of acinar to ductal metaplasia, and induced focal inflammatory changes compa

134 parietal cell loss, mucinous epithelial cell metaplasia, and massive eosinophilic inflammation.

135 response, induce goblet cell hyperplasia and metaplasia, and mucus hypersecretion in the airways.

136 the exocrine compartment, accelerated fatty metaplasia, and persistent ADM after acute caerulein-ind

137 s involves transient phases of inflammation, metaplasia, and redifferentiation, driven by cell-cell i

138 ues and attenuated airway eosinophils, mucus metaplasia, and subepithelial collagen.

139 prevent spontaneous gastric inflammation and metaplasia, and suggest that glucocorticoid deficiency m

140 ion with increased eosinophilia, goblet cell metaplasia, and TH2 cytokine production in WT mice, whic

141 -33-induced eosinophilic inflammation, mucus metaplasia, and type 2 inflammatory responses.

142 downstream eosinophilic inflammation, mucus metaplasia, and type 2 inflammatory responses.

143 odeling fails, and signs of acinar-to-ductal metaplasia appear.

144 location, extent, and severity of intestinal metaplasia are indicators of risk of developing gastric

145 e mechanism(s) by which inflammation induces metaplasia are poorly understood.

146 We discuss the concept of metaplasia as a wound-healing response, and how cardiac

147 chemokines, IgE production, and mucous cell metaplasia, as compared with the adoptive transfer of HD

148 eases in HDM-induced inflammation and mucous metaplasia, as well as reduced IL-4, IL-25, CD68, Gob5,

149 s increased mucous cell density (mucous cell metaplasia) associated with mucus obstruction.

150 rmore, aged miR-32 transgenic mice exhibited metaplasia-associated prostatic intraepithelial neoplasi

151 a pre-metaplastic pattern, which lacked the metaplasia-associated transcripts.

152 ectopic lumenal KRT14(+) cells, and signs of metaplasia (attenuated E-cadherin staining).

153 of samples of 7 tissue types (columnar cell metaplasia, Barrett esophagus, low- and high-grade dyspl

154 rom 20 EAC-associated genes was performed on metaplasia biopsies using Ion AmpliSeq DNA sequencing.

155 -oesophageal reflux disease (GORD)-Barrett's metaplasia (BM)-oesophageal adenocarcinoma (OAC) model.

156 pes have been proposed as the source of this metaplasia but in all cases the evidence is inconclusive

157 of at least 3 cm and evidence of intestinal metaplasia can help stratify those patients at highest r

158 Metaplasia can result when injury reactivates latent dev

159 ophagus is a squamous-to-columnar epithelial metaplasia caused by reflux esophagitis.

160 tion, and complete eradication of intestinal metaplasia (CEIM), were assessed using logistic regressi

161 plasia is complete eradication of intestinal metaplasia (CEIM).

162 determine whether Paneth cell hyperplasia or metaplasia characteristically occurs in the colons of ch

163 s with chronic atrophic gastritis, can cause metaplasia, characterized by gastric cell expression of

164 GD), Barrett's esophagus (BE), columnar cell metaplasia (CM), squamous cell carcinoma (SCC), and squa

165 in the CCR specifically prevents age-related metaplasia, commensal dysbiosis and functional decline i

166 92.6% for dysplasia and 88.2% for intestinal metaplasia compared with 27.9% for dysplasia and 0.0% fo

167 mice also demonstrated increased goblet cell metaplasia compared with Pten(+/-) mice.

168 randomized controlled Ablation of Intestinal Metaplasia Containing Dysplasia (AIM) trial.

169 ophageal squamous epithelium (EPC-1, EPC-2), metaplasia (CP-A) and dysplasia (CP-B) to esophageal ade

170 Complete resolution of intestinal metaplasia (CRIM) was achieved in 30 patients (83%) at a

171 were frequently found in areas of pancreatic metaplasia, decreased throughout tumor progression, and

172 hat HSP90 inhibitors will revert goblet cell metaplasia, despite active upstream inflammatory signali

173 Lineage tracing studies confirmed that the metaplasia developed directly from Kras (G12D)-induced c

174 Preneoplastic ductal metaplasia developed in mice lacking pancreatic p110alph

175 opment and progression of esophageal mucosal metaplasia, dysplasia and carcinoma.

176 mples revealed FOXA2 expression in Barrett's metaplasia, dysplasia, and adenocarcinoma but not in eso

177 the importance of aberrant chromatin in the metaplasia-dysplasia sequence.

178 eosquamous epithelium demonstrate intestinal metaplasia/dysplasia or subsquamous intestinal metaplasi

179 -1beta limits type 2 inflammation and mucous metaplasia following RV infection by suppressing epithel

180 duct, pancreatic duct, and tumor-associated metaplasias from the mice were analyzed for tuft cell an

181 Bronchial epithelial goblet cell metaplasia (GCM) with hyperplasia is a prominent feature

182 on (endoscopic and histologic) of intestinal metaplasia has been achieved with BET, surveillance endo

183 k factors that induce progression to gastric metaplasia have not been identified.

184 autonomic dysfunction, and cervical squamous metaplasia (HPV-related).

185 Muc5ac and Gob5 mRNA, markers of goblet cell metaplasia/hyperplasia.

186 RV-induced mucous metaplasia, ILC2 expansion, airway hyperresponsiveness,

187 ions, atrophic gastritis (AG) and intestinal metaplasia (IM) are characterized by an increase of prol

188 ori)-infected gastric mucosa with intestinal metaplasia (IM) changes.

189 ocal atrophic gastritis (MAG) and intestinal metaplasia (IM) have occurred.

190 lesions gastric atrophy (GA) and intestinal metaplasia (IM) influence gastric cancer risk.

191 Intestinal metaplasia (IM) is a pre-malignant condition of the gast

192 Intestinal metaplasia (IM) is defined by the presence of goblet cel

193 gnosis and to estimate GC risk by intestinal metaplasia (IM) subtype and anatomic location.

194 s, i.e., atrophic mucosa (AM) and intestinal metaplasia (IM), in patients with chronic gastritis who

195 important risk factor for gastric intestinal metaplasia (IM).

196 expressing metaplasia (SPEM), and intestinal metaplasia (IM).

197 h chronic gastritis (CG, N = 37), intestinal metaplasia (IM, N = 21) or gastric cancer (GC, N = 16) f

198 tone patients, hyperplasia was found in 32%, metaplasia in 47.8%, dysplasia in 15.7%, and carcinoma i

199 siveness (AHR), lung inflammation, and mucus metaplasia in a dual Th2/Th17 model of asthma.

200 ROCK2, to AHR, inflammation and goblet cell metaplasia in a mast cell-dependent model of allergic ai

201 ly partially mediates inflammation and mucus metaplasia in a mixed Th2/Th17 model of steroid-resistan

202 Jagged inhibition also reversed goblet cell metaplasia in a preclinical asthma model, providing a th

203 data suggest that IL-13 drives AHR and mucus metaplasia in a STAT6-dependent manner, without directly

204 perreactivity, eosinophilia, and goblet cell metaplasia in allergen-sensitized mice.

205 , IL-4 and IL-13 production, and goblet cell metaplasia in an Aspergillus fumigatus-induced asthma mo

206 of emphysema and large areas of goblet cell metaplasia in bronchial and bronchiolar epithelium.

207 The generation of mucous metaplasia in immature RV-infected mice involves a compl

208 FOXA3 induces goblet cell metaplasia in response to infection or Th2 stimulation.

209 se hepatocytes can undergo reversible ductal metaplasia in response to injury, expand as ducts, and s

210 , with almost complete absence of intestinal metaplasia in subjects infected with i2-type strains, ev

211 y patients with a < 1 cm segment of columnar metaplasia in the distal esophagus, also called an irreg

212 y patients with a < 1 cm segment of columnar metaplasia in the distal esophagus, also called an irreg

213 Metaplasia in the esophageal remnant after esophagectomy

214 transduction, airway inflammation, and mucus metaplasia in the lungs.

215 olymorphic forms of VacA on inflammation and metaplasia in the mouse stomach.

216 ted increase in the incidence of goblet cell metaplasia in the prostate epithelium.

217 nhibition of MEK might reverse preneoplastic metaplasia in the stomach.

218 data on BE recurrence (defined as intestinal metaplasia in the tubular esophagus) and dysplastic BE r

219 uidelines for gastric atrophy and intestinal metaplasia in the Western world, future assessment of th

220 in descending colon and rectum; Paneth cell metaplasia in this region and aberrant lysozyme producti

221 hibitors prevented IL-13-induced goblet cell metaplasia in vitro and in vivo.

222 ced pronounced airway inflammation and mucus metaplasia in WT mice, which was nearly completely abrog

223 ri from gastritis to precancerous intestinal metaplasia, in human gastric organoids, and in patients

224 After metaplasia-inducing injury, ZCs can become SPEM cells, a

225 );Braf(LSL-V600E/+) mice resulted in gastric metaplasia, inflammation, and adenoma development, chara

226 Metaplasia is a precancerous lesion associated with an i

227 Presence of specialized intestinal metaplasia is associated with increased time from surger

228 Columnar metaplasia is common following esophagectomy, but the ab

229 I lectin (spasmolytic polypeptide-expressing metaplasia marker) were increased only by WT H. pylori I

230 es characterized by cilial loss and squamous metaplasia may alter PAR-2 polarization.

231 epithelial responses, including mucous cell metaplasia (MCM), but their roles in mucoinflammatory ai

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

233 ck cells and chief cells as they progress to metaplasia mice with chronic gastritis.

234 ) adenomas, including loss of LRIG1, gastric metaplasia (MUCIN5AC and MUCIN6), and increased amphireg

235 well as in atrophic gastritis or intestinal metaplasia mucosa of patients without GC (AG/IM GC-) and

236 N = 33) and 129 controls including Barrett's metaplasia (N = 16), benign upper gastrointestinal disea

237 ed pathology akin to the mucous and squamous metaplasia, neutrophilic inflammation, and fibrosis seen

238 sence of goblet cells whereas nongoblet cell metaplasia (NGM) lacks goblet cells.

239 n atrophic mucosal glands without intestinal metaplasia (non-IM) and intestinal metaplastic glands (I

240 the case of Barrett's oesophagus, intestinal metaplasia occurs at the gastro-oesophageal junction, wh

241 genetic airway diseases, including the mucus metaplasia of asthma, chloride channel dysfunction of cy

242 osa might be the precursor of the intestinal metaplasia of BE.

243 the epithelium with migration and subsequent metaplasia of epithelial cells, resulting in excessive t

244 mplex and SOX9 also characterises the ductal metaplasia of submucosal glands that occurs during the d

245 Squamous metaplasia of the bronchial epithelium was increased in

246 BEST PRACTICE ADVICE 11: Intestinal metaplasia of the gastric cardia (without residual colum

247 AK/Stat signaling in the aging gut induces a metaplasia of the gastric epithelium, CCR decline, and s

248 ormations within the eye: adipose or osseous metaplasia of the lens and adipose tissue in the vitreou

249 opathology were targeted to the IP, columnar metaplasia of the lower esophagus, gastric corpus and an

250 tructures in the duct epithelium with cystic metaplasia of the PDG, which resembled human IPMN; these

251 option for airway diseases with goblet cell metaplasia of unknown mechanism.

252 Metaplasias often have characteristics of developmentall

253 ients whose disease progressed to intestinal metaplasia or dysplasia, compared with patients whose di

254 type (SASP) that attenuates acinar-to-ductal metaplasia, pancreatic intraepithelial neoplasia (PanIN)

255 Paneth cell metaplasia (PCM) is well described in adults but little

256 on of 6-day-old BALB/c mice induces a mucous metaplasia phenotype that is dependent on type 2 innate

257 one is sufficient to induce acinar-to-ductal metaplasia, potentiate inflammation, and induce a KRAS-p

258 oid inflammatory cells decreased goblet cell metaplasia, reduced lung inflammation, and decreased air

259 lls as an indicator, we tested if pancreatic metaplasia represents transdifferentiation to a biliary

260 s suggest that persistent airway goblet cell metaplasia requires HSP90 activity and that HSP90 inhibi

261 gr5.p65fl/fl mice had lower inflammation and metaplasia scores than pL2.Lgr5.N2IC mice.

262 Patients with extensive intestinal metaplasia should be offered endoscopic surveillance.

263 achieved complete eradication of intestinal metaplasia should undergo surveillance every 6 months fo

264 achieved complete eradication of intestinal metaplasia should undergo surveillance every year for 2

265 omal hyperplasia was admixed with epithelial metaplasia, sometimes with keratin pearls, consistent wi

266 is a specific marker of mouse gastric corpus metaplasia (spasmolytic polypeptide expressing metaplasi

267 re called spasmolytic polypeptide-expressing metaplasia (SPEM) cells.

268 Spasmolytic polypeptide-expressing metaplasia (SPEM) develops in patients with chronic atro

269 ates with spasmolytic polypeptide-expressing metaplasia (SPEM) in mice.

270 tinalized spasmolytic polypeptide-expressing metaplasia (SPEM) was detected in SAMP stomachs, which w

271 ophy, and spasmolytic polypeptide-expressing metaplasia (SPEM), a putative precursor of gastric cance

272 ell loss, spasmolytic polypeptide-expressing metaplasia (SPEM), and intestinal metaplasia (IM).

273 known as spasmolytic polypeptide-expressing metaplasia (SPEM), increases the risk for progression to

274 taplasia (spasmolytic polypeptide expressing metaplasia, SPEM).

275 IL22 promotes acinar to ductal metaplasia, stem cell features, and increased expression

276 epithelial mucus hypersecretion, goblet cell metaplasia, subepithelial fibrosis and enhanced airway h

277 CS-exposed NHPs developed robust mucus metaplasia, submucosal gland hypertrophy and hyperplasia

278 ated with the severity of airway goblet cell metaplasia, suggesting that PVs can influence the inflam

279 etween chronic gastritis and intestinalizing metaplasia that may serve as a potential therapeutic tar

280 nar to ductal metaplasia (ADM), and mucinous metaplasia that resembles PanIN1a.

281 reased their expression of markers of ductal metaplasia; these effects of IL22 were prevented with in

282 lug attenuated TGF-alpha-induced acinar cell metaplasia to ductal structures and TGF-alpha-induced ex

283 umans, we expanded the definition of gastric metaplasia to include Gkn3 mRNA and GKN3-positive cells

284 Histological suspicion of metaplasia was confirmed centrally.

285 Intestinal metaplasia was detected in two cases, but no neoplasia.

286 Dissection of immune pathways leading to metaplasia was evaluated, including eosinophil depletion

287 fy novel therapeutic targets for goblet cell metaplasia, we studied the transcriptional response prof

288 We observed that individuals with intestinal metaplasia were all infected with H. pylori strains cont

289 6) signaling, airway inflammation, and mucus metaplasia were assessed.

290 s airway hyperresponsiveness and goblet cell metaplasia were evaluated.

291 l determinant of pancreatic inflammation and metaplasia, whereas a number of developmental signals an

292 Bcl-2 sustains mucous cell metaplasia, whereas p53(-/-) mice display chronically in

293 disease, peaking in tissues with intestinal metaplasia, whereas pEGFR, pEGFR-ERBB2, and pERBB2 were

294 effect, decreasing IL-25, IL-33, and mucous metaplasia while increasing IL-17 expression.

295 ine immune responses, ILC2 number, and mucus metaplasia, while decreasing IL-17 mRNA expression.

296 d a focus of mineralised fibro-cartilaginous metaplasia with endochondral ossification in the last ca

297 2D) and SOX17 in mice induces development of metaplasias with a biliary phenotype containing tuft cel

298 ngly associated with precancerous intestinal metaplasia, with almost complete absence of intestinal m

299 on, smooth muscle thickening and goblet cell metaplasia without changes in IgE and Th1, Th2 and Th17

300 airway hyperresponsiveness, and goblet cell metaplasia, without any synergistic effects.