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1 43% of patients (50 gastric and 1 intestinal metaplasia).
2 ys associated with IL-13-induced goblet cell metaplasia.
3 eligible patients, 45 (36%) had evidence of metaplasia.
4 gastrokine1 and mucin5ac, indicating gastric metaplasia.
5 , eosinophilic inflammation, and goblet cell metaplasia.
6 size, decrease in cell density, and squamous metaplasia.
7 female mice developing keratinizing squamous metaplasia.
8 sal IL-33 and TSLP was sufficient for mucous metaplasia.
9 quired for maximum ILC2 expansion and mucous metaplasia.
10 xpression of SPDEF and Bcl-2 and mucous cell metaplasia.
11 w level inflammation as a driver for colonic metaplasia.
12 ion in the asthmatic airway with goblet cell metaplasia.
13 oblet cells) and thereby reproduce Barrett's metaplasia.
14 disorders accompanied by chronic goblet cell metaplasia.
15 y contribute to the development of Barrett's metaplasia.
16 chemokines, IgE production, and mucous cell metaplasia.
17 r Barrett's esophagus and gastric intestinal metaplasia.
18 nts with Barrett's oesophagus and intestinal metaplasia.
19 nt acini, as well as in pancreatitis-induced metaplasia.
20 OVA-specific IgE production and goblet cell metaplasia.
21 decreased along with increasing goblet cell metaplasia.
22 ar cell dedifferentiation, regeneration, and metaplasia.
23 poor differentiation, distant metastasis and metaplasia.
24 en-induced lung inflammation and goblet cell metaplasia.
25 ar cell differentiation and viability during metaplasia.
26 on, TH2 cytokine production, and mucous cell metaplasia.
27 atment of recurrent dysplasia and intestinal metaplasia.
28 size, decrease in cell density, and squamous metaplasia.
29 ration, collagen deposition, and goblet cell metaplasia.
30 tients with irregular Z line with intestinal metaplasia.
31 R null mice failed to show RV-induced mucous metaplasia.
32 t protected from IL-13-induced AHR and mucus metaplasia.
33 recruitment, IgA secretion, and mucous cell metaplasia.
34 seline histologic data, or had no intestinal metaplasia.
35 achieving complete eradication of intestinal metaplasia.
36 o retinal detachment-induced lens epithelial metaplasia.
37 e points, showed reduced acinar-to-duct cell metaplasia.
38 ifferentiation and leads to acinar to ductal metaplasia.
39 the molecular phenotype of postesophagectomy metaplasia.
40 induces cellular injury, and provokes acinar metaplasia.
41 L-17A significantly attenuated AHR and mucus metaplasia.
42 ial cells, and augmentation of acinar-ductal metaplasia.
43 velopment of SPEM, as well as progression of metaplasia.
44 gulated in and required for acinar-to-ductal metaplasia.
45 -17, eotaxin, and eosinophils and more mucus metaplasia.
46 0.47] x 10(-3) mm(2)/sec; n = 13), apocrine metaplasia ([2.01 +/- 0.38] x 10(-3) mm(2)/sec; n = 13),
48 from squamous epithelium (7%), columnar cell metaplasia (22%), Barrett's esophagus (22%), to low- (45
50 uamous mucosa tissues, 3.7% in columnar cell metaplasia, 5.8% in Barrett's esophagus, 19.0% in low gr
52 tic acinar cells, resulting in acinar-ductal metaplasia, a dedifferentiated state that is poised for
53 ere incapable of undergoing acinar to ductal metaplasia, a process associated with development of pre
55 y increased airway eosinophilia, goblet cell metaplasia, accumulation of ILC2s and TH2 cells, type 2
57 cini, and particularly high in acinar ductal metaplasia (ADM) and PanIN lesions, where IER3 colocaliz
58 e pancreas that have undergone acinar-ductal metaplasia (ADM) can transform into premalignant cells t
60 t that pancreatitis-induced acinar-to-ductal metaplasia (ADM) is a key event for pancreatic ductal ad
65 inar cell state can lead to acinar-to-ductal metaplasia (ADM), a precursor lesion to the development
66 roenvironment to pancreatic acinar-to-ductal metaplasia (ADM), a preneoplastic transition in oncogeni
67 ve mechanisms that initiate acinar-to-ductal metaplasia (ADM), a process that replaces damaged acinar
68 ic acinar cells can undergo acinar-to-ductal metaplasia (ADM), a reprogramming event that induces tra
69 ucts, chronic pancreatitis, acinar to ductal metaplasia (ADM), and mucinous metaplasia that resembles
70 ocrine pancreas can undergo acinar-to-ductal metaplasia (ADM), as in the case of pancreatitis where p
72 for oncogenic Kras-mediated acinar-to-ductal metaplasia (ADM), pancreatic intraepithelial neoplasias
73 cell reprogramming known as acinar-to-ductal metaplasia (ADM)-a precursor of pancreatic intraepitheli
77 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 toxicity and IL-13 and IL-17A inducing mucus metaplasia, airway fibrosis, and vascular remodeling.
82 ly characteristic of asthma, including mucus metaplasia, airway hyperreactivity (AHR), and airway inf
83 rease in pulmonary inflammation, mucous cell metaplasia, airway hyperresponsiveness, and OVA-specific
84 ology characterized by increased goblet cell metaplasia, airway hyperresponsiveness, and Th2-mediated
85 D19(+), and NK1.1(+) cells; emphysema; mucus metaplasia; airway fibrosis; vascular remodeling; and ri
86 ecific overexpression of SOX17 led to ductal metaplasia along with inflammation and collagen depositi
87 27.9% for dysplasia and 0.0% for intestinal metaplasia among patients in the control group (P < .001
88 tion in lung diseases associated with mucous metaplasia and a mechanism by which patients with florid
91 old mice, but not mature mice, causes mucous metaplasia and airway hyperresponsiveness that are assoc
94 stent pulmonary inflammation and goblet cell metaplasia and contribute to significant morbidity and m
95 A combination of hyperplasia and dysplasia, metaplasia and dysplasia, and hyperplasia, metaplasia, a
96 the incidence of postesophagectomy columnar metaplasia and dysplasia, and the timescale over which i
100 rrays revealed the presence of tuft cells in metaplasia and early-stage tumors, along with SOX17 expr
103 tor of pancreatitis, during acinar-to-ductal metaplasia and in early pancreatic intraepithelial neopl
104 lation of inflammatory cells and goblet cell metaplasia and increased levels of Pim1 kinase and T(H)2
105 oxin forms induced more severe and extensive metaplasia and inflammation in the mouse stomach than st
106 f epithelium is a hotspot for pre-neoplastic metaplasia and malignancy, but the cells of origin for t
107 neutralizing Ab attenuated RV-induced mucous metaplasia and methacholine responses, and IL-4R null mi
108 ohistochemical staining revealed mucous cell metaplasia and muc5AC expression in RV1B- but not sham-i
110 ed at investigating whether goblet cell (GC) metaplasia and mucus production are differentially regul
111 might be less sensitive to IL-13-induced GC metaplasia and mucus production through lower expression
112 tely and chronically OVA-challenged mice, GC metaplasia and mucus production were observed in proxima
113 ll as a significant depletion of goblet cell metaplasia and mucus secretion markers after HDM exposur
114 development and is required for goblet cell metaplasia and normal Th2 inflammatory responses to HDM
115 hat Hh signaling is reactivated in Barrett's metaplasia and overexpression of Sonic hedgehog (SHH) in
116 rance of Kras(G12D)-induced acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasias, wh
119 (mucin-producing goblet cell hyperplasia and metaplasia and smooth muscle hypertrophy and fibrosis);
120 ght into the cell of origin of squamous cell metaplasia and squamous cell carcinoma of the colon.
123 ver new biomarkers for stomach preneoplastic metaplasias and neoplastic lesions by generating proteom
125 of inflammation, necrosis, acinar-to-ductal metaplasia, and acinar-cell hypertrophy; this led to tis
126 and neutrophilia, tissue inflammation, mucus metaplasia, and AHR that were partially reversible with
128 exacerbated airway inflammation, goblet cell metaplasia, and airway remodeling, but all of these feat
129 of the airway, subepithelial fibrosis, mucus metaplasia, and airway-hyperreactivity were also attenua
131 ven after complete eradication of intestinal metaplasia, and caution for widespread use of ablation,
132 ilia, elevated mucin expression, goblet cell metaplasia, and distal airspace enlargement, but had no
134 , metaplasia and dysplasia, and hyperplasia, metaplasia, and dysplasia was found in 3.4%, 6.3%, and 4
136 hymal lung inflammation, alveolar epithelial metaplasia, and epithelial endoplasmic reticulum stress
137 s to persistent airways inflammation, mucous metaplasia, and hyperresponsiveness, which are mediated,
139 cells, led to formation of acinar to ductal metaplasia, and induced focal inflammatory changes compa
144 the exocrine compartment, accelerated fatty metaplasia, and persistent ADM after acute caerulein-ind
145 s involves transient phases of inflammation, metaplasia, and redifferentiation, driven by cell-cell i
146 s characterized by eosinophilia, goblet cell metaplasia, and T helper T(H)2 cytokine production, whic
147 ion with increased eosinophilia, goblet cell metaplasia, and TH2 cytokine production in WT mice, whic
148 ronchioles, causing squamous and goblet cell metaplasia, and the loss of Clara and ciliated cells.
149 onic inflammation, hyperplasia, and mucinous metaplasia, and, later in life, of pseudointestinal meta
150 location, extent, and severity of intestinal metaplasia are indicators of risk of developing gastric
151 chemokines, IgE production, and mucous cell metaplasia, as compared with the adoptive transfer of HD
152 eases in HDM-induced inflammation and mucous metaplasia, as well as reduced IL-4, IL-25, CD68, Gob5,
153 rmore, aged miR-32 transgenic mice exhibited metaplasia-associated prostatic intraepithelial neoplasi
154 of samples of 7 tissue types (columnar cell metaplasia, Barrett esophagus, low- and high-grade dyspl
155 sion pattern of a modest number of miRNAs in metaplasia biopsies could identify the BE patients at hi
156 rom 20 EAC-associated genes was performed on metaplasia biopsies using Ion AmpliSeq DNA sequencing.
157 pes have been proposed as the source of this metaplasia but in all cases the evidence is inconclusive
158 of at least 3 cm and evidence of intestinal metaplasia can help stratify those patients at highest r
162 tion, and complete eradication of intestinal metaplasia (CEIM), were assessed using logistic regressi
164 determine whether Paneth cell hyperplasia or metaplasia characteristically occurs in the colons of ch
165 GD), Barrett's esophagus (BE), columnar cell metaplasia (CM), squamous cell carcinoma (SCC), and squa
166 in the CCR specifically prevents age-related metaplasia, commensal dysbiosis and functional decline i
167 92.6% for dysplasia and 88.2% for intestinal metaplasia compared with 27.9% for dysplasia and 0.0% fo
171 were frequently found in areas of pancreatic metaplasia, decreased throughout tumor progression, and
172 Lineage tracing studies confirmed that the metaplasia developed directly from Kras (G12D)-induced c
175 mples revealed FOXA2 expression in Barrett's metaplasia, dysplasia, and adenocarcinoma but not in eso
176 erplasia, spasmolytic polypeptide-expressing metaplasia, dysplasia, and ultimately gastric intraepith
178 ed by epithelial cells during the esophageal metaplasia-dysplasia-carcinoma sequence influence dendri
179 ic cells are recruited during the esophageal metaplasia-dysplasia-carcinoma sequence, through the act
181 CDX1 expression and contribute to intestinal metaplasia, epithelial dedifferentiation, and carcinogen
182 I include: bone marrow edema, sclerosis, fat metaplasia, formation of syndesmophytes, and ankylosis.
183 is, 18 atrophic gastritis, and 18 intestinal metaplasia from cancer-free individuals of Northern Braz
184 duct, pancreatic duct, and tumor-associated metaplasias from the mice were analyzed for tuft cell an
186 her lung leukocyte counts, more airway mucus metaplasia, greater lung levels of some Th2 cytokines, a
192 ions, atrophic gastritis (AG) and intestinal metaplasia (IM) are characterized by an increase of prol
199 omplete remission of neoplasia or intestinal metaplasia (IM), IM in gastric cardia, or buried glands
200 s, i.e., atrophic mucosa (AM) and intestinal metaplasia (IM), in patients with chronic gastritis who
204 tone patients, hyperplasia was found in 32%, metaplasia in 47.8%, dysplasia in 15.7%, and carcinoma i
205 mplete remission of neoplasia and intestinal metaplasia in 90% of patients; neoplasia recurred in 3 p
207 ROCK2, to AHR, inflammation and goblet cell metaplasia in a mast cell-dependent model of allergic ai
208 ly partially mediates inflammation and mucus metaplasia in a mixed Th2/Th17 model of steroid-resistan
209 Jagged inhibition also reversed goblet cell metaplasia in a preclinical asthma model, providing a th
210 data suggest that IL-13 drives AHR and mucus metaplasia in a STAT6-dependent manner, without directly
211 , IL-4 and IL-13 production, and goblet cell metaplasia in an Aspergillus fumigatus-induced asthma mo
218 se hepatocytes can undergo reversible ductal metaplasia in response to injury, expand as ducts, and s
219 , with almost complete absence of intestinal metaplasia in subjects infected with i2-type strains, ev
220 y patients with a < 1 cm segment of columnar metaplasia in the distal esophagus, also called an irreg
221 y patients with a < 1 cm segment of columnar metaplasia in the distal esophagus, also called an irreg
223 chronic GERD; and the presence of intestinal metaplasia in the gap defines Barrett esophagus and canc
227 data on BE recurrence (defined as intestinal metaplasia in the tubular esophagus) and dysplastic BE r
228 uidelines for gastric atrophy and intestinal metaplasia in the Western world, future assessment of th
229 );Braf(LSL-V600E/+) mice resulted in gastric metaplasia, inflammation, and adenoma development, chara
234 chanism by which patients with florid mucous metaplasia may tolerate microbial burdens that are usual
237 ) adenomas, including loss of LRIG1, gastric metaplasia (MUCIN5AC and MUCIN6), and increased amphireg
238 well as in atrophic gastritis or intestinal metaplasia mucosa of patients without GC (AG/IM GC-) and
240 N = 33) and 129 controls including Barrett's metaplasia (N = 16), benign upper gastrointestinal disea
243 the case of Barrett's oesophagus, intestinal metaplasia occurs at the gastro-oesophageal junction, wh
244 the epithelium with migration and subsequent metaplasia of epithelial cells, resulting in excessive t
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
251 tructures in the duct epithelium with cystic metaplasia of the PDG, which resembled human IPMN; these
252 ared capable of provoking widespread fibrous metaplasia of the pigment epithelium that was mainly res
254 gets histologically classified as intestinal metaplasia or "indefinite for dysplasia" spanned a range
255 ients whose disease progressed to intestinal metaplasia or dysplasia, compared with patients whose di
258 type (SASP) that attenuates acinar-to-ductal metaplasia, pancreatic intraepithelial neoplasia (PanIN)
260 one is sufficient to induce acinar-to-ductal metaplasia, potentiate inflammation, and induce a KRAS-p
262 oid inflammatory cells decreased goblet cell metaplasia, reduced lung inflammation, and decreased air
263 However, central airway resistance and mucus metaplasia remained elevated in CC10-IkappaBalphaSR tran
264 lls as an indicator, we tested if pancreatic metaplasia represents transdifferentiation to a biliary
267 achieved complete eradication of intestinal metaplasia should undergo surveillance every 6 months fo
268 achieved complete eradication of intestinal metaplasia should undergo surveillance every year for 2
269 omal hyperplasia was admixed with epithelial metaplasia, sometimes with keratin pearls, consistent wi
274 on the prevalence of subsquamous intestinal metaplasia (SSIM) in patients with Barrett's esophagus,
275 BC) and/or goblet cell hyperplasia, squamous metaplasia, structural and functional abnormalities of c
276 epithelial mucus hypersecretion, goblet cell metaplasia, subepithelial fibrosis and enhanced airway h
278 ated with the severity of airway goblet cell metaplasia, suggesting that PVs can influence the inflam
279 d 53bp1 (Trp53bp1) in areas of acinar ductal metaplasia, suggesting that rpS6 phosphorylation attenua
280 mmation, airway hyperreactivity, goblet cell metaplasia, Th2/Th17 cytokines, dendritic cells, activat
282 lug attenuated TGF-alpha-induced acinar cell metaplasia to ductal structures and TGF-alpha-induced ex
289 We observed that individuals with intestinal metaplasia were all infected with H. pylori strains cont
290 activation of Dicer and pancreatitis-induced metaplasia were associated with repression of acinar dif
292 l determinant of pancreatic inflammation and metaplasia, whereas a number of developmental signals an
294 disease, peaking in tissues with intestinal metaplasia, whereas pEGFR, pEGFR-ERBB2, and pERBB2 were
295 The primary focus was epithelial injury and metaplasia, which are cardinal features of asthma and in
297 mplete remission of dysplasia and intestinal metaplasia with overall survival comparable to patients
298 2D) and SOX17 in mice induces development of metaplasias with a biliary phenotype containing tuft cel
299 ngly associated with precancerous intestinal metaplasia, with almost complete absence of intestinal m
300 on, smooth muscle thickening and goblet cell metaplasia without changes in IgE and Th1, Th2 and Th17
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