gastric intestinal metaplasia
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2022 ◽  
Vol 73 ◽  
pp. 103476
Author(s):  
Pak Kin Wong ◽  
Liang Yao ◽  
Tao Yan ◽  
I. Cheong Choi ◽  
Hon Ho Yu ◽  
...  

Author(s):  
Eugene Kligman ◽  
Hiba Ali ◽  
Ellie Chen ◽  
Frederick Peng ◽  
David Szafron ◽  
...  

2021 ◽  
Author(s):  
Harshabad Singh ◽  
Davide Seruggia ◽  
Shariq Madha ◽  
Madhurima Saxena ◽  
Ankur K. Nagaraja ◽  
...  

Barrett's esophagus (BE) and gastric intestinal metaplasia are related premalignant conditions in which areas of human stomach epithelium express mixed gastric and intestinal features. Intestinal transcription factors (TFs) are expressed in both conditions, with unclear causal roles and cis-regulatory mechanisms. Ectopic CDX2 reprogrammed isogenic mouse stomach organoid lines to a hybrid stomach–intestinal state transcriptionally similar to clinical metaplasia; squamous esophageal organoids resisted this CDX2-mediated effect. Reprogramming was associated with induced activity at thousands of previously inaccessible intestine-restricted enhancers, where CDX2 occupied DNA directly. HNF4A, a TF recently implicated in BE pathogenesis, induced weaker intestinalization by binding a novel shadow Cdx2 enhancer and hence activating Cdx2 expression. CRISPR/Cas9-mediated germline deletion of that cis-element demonstrated its requirement in Cdx2 induction and in the resulting activation of intestinal genes in stomach cells. dCas9-conjugated KRAB repression mapped this activity to the shadow enhancer's HNF4A binding site. Altogether, we show extensive but selective recruitment of intestinal enhancers by CDX2 in gastric cells and that HNF4A-mediated ectopic CDX2 expression in the stomach occurs through a conserved shadow cis-element. These findings identify mechanisms for TF-driven intestinal metaplasia and a likely pathogenic TF hierarchy.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Mimi C. Tan ◽  
Taher Jamali ◽  
Theresa H. Nguyen ◽  
Amy Galvan ◽  
Robert J. Sealock ◽  
...  

2021 ◽  
Author(s):  
Julia M. Lerch ◽  
Rish K. Pai ◽  
Ian Brown ◽  
Anthony J. Gill ◽  
Dhanpat Jain ◽  
...  

AbstractThe extent of gastric intestinal metaplasia (GIM) can be used to determine the risk of gastric cancer. Eleven international gastrointestinal expert pathologists estimated the extent of GIM on haematoxylin and eosin (H&E)- and Alcian blue-Periodic acid Schiff (AB-PAS)-stained slides of 46 antrum biopsies in 5% increments. Interobserver agreement was tested with the intraclass correlation coefficient (ICC). Correlation between standard deviation and extent of GIM was evaluated with the Spearman correlation. The interobserver agreement was very good (ICC = 0.983, 95% confidence interval (CI) 0.975–0.990). The use of AB-PAS did not increase the agreement (ICC = 0.975, 95% CI 0.961–0.985). Cases with a higher amount of metaplastic epithelium demonstrated a higher standard deviation (rs = 0.644; p < 0.01), suggesting lower diagnostic accuracy in cases with extensive GIM. In conclusion, estimating the extent of GIM on H&E-stained slides in patients with chronic atrophic gastritis can be achieved satisfactorily with high interobserver agreement, at least among international expert gastrointestinal pathologists.


Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6242
Author(s):  
Darina Kohoutova ◽  
Matthew Banks ◽  
Jan Bures

The mortality rates of gastric carcinoma remain high, despite the progress in research and development in disease mechanisms and treatment. Therefore, recognition of gastric precancerous lesions and early neoplasia is crucial. Two subtypes of sporadic gastric cancer have been recognized: cardia subtype and non-cardia (distal) subtype, the latter being more frequent and largely associated with infection of Helicobacter pylori, a class I carcinogen. Helicobacter pylori initiates the widely accepted Correa cascade, describing a stepwise progression through precursor lesions from chronic inflammation to gastric atrophy, gastric intestinal metaplasia and neoplasia. Our knowledge on He-licobacter pylori is still limited, and multiple questions in the context of its contribution to the pathogenesis of gastric neoplasia are yet to be answered. Awareness and recognition of gastric atrophy and intestinal metaplasia on high-definition white-light endoscopy, image-enhanced endoscopy and magnification endoscopy, in combination with histology from the biopsies taken accurately according to the protocol, are crucial to guiding the management. Standard indications for endoscopic resections (endoscopic mucosal resection and endoscopic submucosal dissection) of gastric dysplasia and intestinal type of gastric carcinoma have been recommended by multiple societies. Endoscopic evaluation and surveillance should be offered to individuals with an inherited predisposition to gastric carcinoma.


Author(s):  
Diogo Libânio ◽  
Raquel Ortigão ◽  
Pedro Pimentel-Nunes ◽  
Mário Dinis-Ribeiro

Gastric cancer is the third leading cause of cancer-related death. In Western countries, its lower prevalence and the absence of mass screening programmes contribute to late diagnosis and a slower implementation of minimally invasive treatments. A secondary prevention strategy through endoscopic surveillance of patients at high risk of intestinal-type gastric adenocarcinoma or by screening gastric cancer within colorectal screening programmes is cost-effective in intermediate-risk countries, though the identification of these patients remains challenging. Virtual chromoendoscopy with narrow-band imaging improves the accuracy of endoscopic diagnosis, significantly increasing the sensitivity for intestinal metaplasia while preserving specificity. Endoscopic grading of gastric intestinal metaplasia is feasible, correlates well with histological staging systems and also with gastric neoplasia risk and can be used to stratify risk. Endoscopic submucosal dissection (ESD) in the West achieves efficacy and safety outcomes similar to those reported for Eastern countries, and the long-term disease-specific survival is higher than 95%. A prospective comparative study with gastrectomy confirms its higher safety and its benefits concerning health-related quality of life. However, ESD is associated with a 5% risk of postprocedural bleeding and a 20% risk of non-curative resection. The knowledge of risk factors for adverse events and non-curative resection can improve patient selection. The risk of metachronous lesions after ESD is high (3–5% per year), and endoscopic surveillance is needed. The management of patients with non-curative resection can be optimized using risk scoring systems for lymph node metastasis.


2021 ◽  
Vol 46 ◽  
pp. S717
Author(s):  
M. Pimenta ◽  
M. Carriço ◽  
C. Sousa Guerreiro ◽  
A. Araújo ◽  
P. Fidalgo

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0260019
Author(s):  
Hudson M. Holmes ◽  
Andre G. Jove ◽  
Mimi C. Tan ◽  
Hashem B. El-Serag ◽  
Aaron P. Thrift

Background Chronic alcohol use is a risk factor for non-cardia gastric adenocarcinoma. However, it is less well understood whether alcohol use is a risk factor for premalignant mucosal changes, namely gastric intestinal metaplasia. We examined the association between various parameters of alcohol use and risk of gastric intestinal metaplasia. Methods We used data from 2084 participants (including 403 with gastric intestinal metaplasia) recruited between February 2008-August 2013 into a cross-sectional study at the Michael E. DeBakey Veterans Affairs Medical Center in Houston, Texas. All participants underwent a study upper endoscopy with systematic gastric mapping biopsies. Cases had intestinal metaplasia on any non-cardia gastric biopsy. Participants self-reported lifetime history of alcohol consumption, along with other lifestyle risk factors, through a study survey. We calculated odds ratios (OR) and 95% confidence intervals (95% CI) for categories of average alcohol consumption using multivariable logistic regression, and restricted cubic spline regression to explore the potential shape of a dose-response relationship. Results Compared to lifelong non-drinkers, individuals who consumed on average ≥28 drinks per week had no elevated risk for gastric intestinal metaplasia (adjusted OR, 1.27; 95% CI, 0.74–2.19). Based on a spline regression curve and its 95% CI, there was also no demonstrable association between cumulative lifetime alcohol consumption and risk of gastric intestinal metaplasia. Similarly, we found no association between beverage type (beer, wine, liquor/spirits) and risk for gastric intestinal metaplasia. Conclusions Neither amount of alcohol consumed nor specific beverage type was associated with risk of gastric intestinal metaplasia.


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