Browse
Submit Data
Databases
API
Help

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Simultaneous Recognition of Atrophic Gastritis and Intestinal Metaplasia on White Light Endoscopic Images Based on Convolutional Neural Networks: A Multicenter Study.

ABSTRACT:

Introduction

Patients with atrophic gastritis (AG) or gastric intestinal metaplasia (GIM) have elevated risk of gastric adenocarcinoma. Endoscopic screening and surveillance have been implemented in high incidence countries. The study aimed to evaluate the accuracy of a deep convolutional neural network (CNN) for simultaneous recognition of AG and GIM.

Methods

Archived endoscopic white light images with corresponding gastric biopsies were collected from 14 hospitals located in different regions of China. Corresponding images by anatomic sites containing AG, GIM, and chronic non-AG were categorized using pathology reports. The participants were randomly assigned (8:1:1) to the training cohort for developing the CNN model (TResNet), the validation cohort for fine-tuning, and the test cohort for evaluating the diagnostic accuracy. The area under the curve (AUC), sensitivity, specificity, and accuracy with 95% confidence interval (CI) were calculated.

Results

A total of 7,037 endoscopic images from 2,741 participants were used to develop the CNN for recognition of AG and/or GIM. The AUC for recognizing AG was 0.98 (95% CI 0.97-0.99) with sensitivity, specificity, and accuracy of 96.2% (95% CI 94.2%-97.6%), 96.4% (95% CI 94.8%-97.9%), and 96.4% (95% CI 94.4%-97.8%), respectively. The AUC for recognizing GIM was 0.99 (95% CI 0.98-1.00) with sensitivity, specificity, and accuracy of 97.9% (95% CI 96.2%-98.9%), 97.5% (95% CI 95.8%-98.6%), and 97.6% (95% CI 95.8%-98.6%), respectively.

Discussion

CNN using endoscopic white light images achieved high diagnostic accuracy in recognizing AG and GIM.

SUBMITTER: Lin N

PROVIDER: S-EPMC8337066 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Expression data from gastric tissues with non-atrophic gastritis, intestinal metaplasia, and gastric cancer

Project description:We identified several hub genes and key pathways associated with GC and IM initiation and progression by analyzing the DEGs, which provided a detailed molecular mechanism underlying GC and IM occurrence and progression.

2022-12-30 | GSE191275 | GEO

Prediction of Gastric Cancer in Intestinal Metaplasia and Atrophic Gastritis

Project description:The primary objectives of this study are: * To identify clinical or histological factors associated with gastric cancer development in patients with IM and AG * To establish a machine learning algorithm for prediction of future gastric cancer risks and individual risk stratification in patient with IM and AG

| 2373934 | ecrin-mdr-crc

Chronic atrophic gastritis and intestinal metaplasia surrounding diffuse-type gastric cancer: Are they just bystanders in the process of carcinogenesis?

Project description:BackgroundGastric cancer (GC) is categorized as diffuse- and intestinal-type adenocarcinoma. Intestinal-type GC is associated with chronic gastritis, atrophic gastritis (AG), and intestinal metaplasia (IM), precursors of dysplastic changes. Diffuse-type GC is generally known to undergo de novo carcinogenesis and is not associated with chronic mucosal changes. However, clinically, AG and IM are frequently observed surrounding diffuse-type GC. This study aimed to evaluate the role of AG and IM in diffuse-type GC.MethodsWe retrospectively reviewed the data of patients undergoing surgery for early GC. We divided patients with diffuse-type GC into two groups according to the presence of AG and IM based on Kyoto classification of gastritis. The clinicopathological characteristics were compared between the groups.ResultsAmong patients with diffuse-type GC, 52.5% patients had AG and 18.4% had severe AG. With regard to IM, 42.1% patients had IM and 17.1% had severe IM. Diffuse-type GC combined with severe AG or IM showed larger tumor size and higher submucosal invasion rate than that without severe AG or IM. However, the lymph node metastasis (LNM) rate was not significantly different between the two groups. In multivariate analysis, severe AG or IM was not an independent risk factor for LNM.ConclusionsSevere AG or IM surrounding diffuse-type gastric cancer suggests a collapse of normal mucosal barriers and leads to the spread of cancer cells. Although the association between chronic mucosal changes and LNM is unclear, more caution is needed during endoscopy especially for complete resection of diffuse-type GC with these features.

| S-EPMC6919620 | biostudies-literature

Comparative proteomics analysis of chronic atrophic gastritis: changes of protein expression in chronic atrophic gastritis without Helicobacter pylori infection.

Project description:Chronic atrophic gastritis (CAG) is a very common gastritis and one of the major precursor lesions of gastric cancer, one of the most common cancers worldwide. The molecular mechanism underlying CAG is unclear, but its elucidation is essential for the prevention and early detection of gastric cancer and appropriate intervention. A combination of two-dimensional gel electrophoresis and mass spectrometry was used in the present study to analyze the differentially expressed proteins. Samples from 21 patients (9 females and 12 males; mean age: 61.8 years) were used. We identified 18 differentially expressed proteins in CAG compared with matched normal mucosa. Eight proteins were up-regulated and 10 down-regulated in CAG when compared with the same amounts of proteins in individually matched normal gastric mucosa. Two novel proteins, proteasome activator subunit 1 (PSME1), which was down-regulated in CAG, and ribosomal protein S12 (RPS12), which was up-regulated in CAG, were further investigated. Their expression was validated by Western blot and RT-PCR in 15 CAG samples matched with normal mucosa. The expression level of RPS12 was significantly higher in CAG than in matched normal gastric mucosa (P < 0.05). In contrast, the expression level of PSME1 in CAG was significantly lower than in matched normal gastric mucosa (P < 0.05). This study clearly demonstrated that there are some changes in protein expression between CAG and normal mucosa. In these changes, down-regulation of PSME1 and up-regulation of RPS12 could be involved in the development of CAG. Thus, the differentially expressed proteins might play important roles in CAG as functional molecules.

| S-EPMC3854201 | biostudies-literature

Training Effect on the Inter-observer Agreement in Endoscopic Diagnosis and Grading of Atrophic Gastritis according to Level of Endoscopic Experience.

Project description:Endoscopic diagnosis of atrophic gastritis can contribute to risk stratification and thereby tailored screening for gastric cancer. We aimed to evaluate the effect of training on inter-observer agreement in diagnosis and grading of endoscopic atrophic gastritis (EAG) according to the level of endoscopists' experience.Twelve endoscopists (six less-experienced and six experienced) participated in this prospective study. The training session consisted of 1) four interventions with two-week intervals, and 2) a follow-up period (two follow-up assessments without feedback). EAG was categorized as C1 to O3 according to the Kimura-Takemoto classification. Kappa statistics were used to calculate inter-observer agreement.At baseline, kappa indexes were 0.18 in the less-experienced group and 0.32 in the experienced group, respectively. After four interventions with feedback, the kappa index improved in both groups and was sustained during the follow-up period. Overall diagnostic yields of EAG were 43.1% ± 10.7% in pre-intervention and 46.8% ± 5.9% in post-intervention. Variability in the rate of diagnosis of EAG significantly decreased in the less-experienced group (r = 0.04, P = 0.003).Irrespective of experience level, inter-observer agreement for diagnosis and grading of EAG improved after training and remained stable after intervention.

| S-EPMC5890086 | biostudies-other

Endoscopic atrophic classification before and after H. pylori eradication is closely associated with histological atrophy and intestinal metaplasia.

Project description:BACKGROUND AND STUDY AIMS: The relationship between endoscopic atrophy classification (EAC) and histological gastric atrophy and intestinal metaplasia (IM) was examined before and after Helicobacter pylori (H. pylori) eradication in order to evaluate the usefulness of EAC for detecting the risk of gastric cancer following eradication. PATIENTS AND METHODS: A total of 230 patients (137 males, 93 females; mean age: 58.0 ± 11.8 y) with successful eradication were enrolled. EAC score was defined as follows: C0(none): 0, C1: 1, C2: 2, C3: 3, O1: 4, O2: 5, and O3(severe): 6. Histological atrophy and IM score (0 to 3) from the antrum and the corpus were evaluated with updated Sydney system for histological atrophy and IM. RESULTS: The mean EAC scores were 3.46 before eradication and 3.20 after eradication (P = 0.026). The mean atrophy scores before and after eradication were 1.45 and 0.92 at the antrum (P < 0.001) and 0.50 and 0.07 at the corpus (P < 0.001), respectively. The mean IM scores before and after eradication were 0.55 and 0.47 at the antrum (P = 0.154), and 0.09 and 0.05 at the corpus (P = 0.096), respectively. The histological atrophy scores showed significant improvement after eradication, while IM showed no significant change. The Mantel-Haenszel test for trend indicated there was a significant correlation between EAC and histological atrophy and IM, except antral atrophy after eradication. CONCLUSIONS: EAC exhibited a significant correlation between histological atrophy and IM, and represents a noninvasive classification method. EAC may be beneficial in evaluating the risk of gastric cancer after H. pylori eradication.

| S-EPMC4554494 | biostudies-other

Identification of Gastritis Subtypes by Convolutional Neuronal Networks on Histological Images of Antrum and Corpus Biopsies.

Project description:Gastritis is a prevalent disease and commonly classified into autoimmune (A), bacterial (B), and chemical (C) type gastritis. While the former two subtypes are associated with an increased risk of developing gastric intestinal adenocarcinoma, the latter subtype is not. In this study, we evaluated the capability to classify common gastritis subtypes using convolutional neuronal networks on a small dataset of antrum and corpus biopsies. 1230 representative 500 × 500 µm images of 135 patients with type A, type B, and type C gastritis were extracted from scanned histological slides. Patients were allocated randomly into a training set (60%), a validation set (20%), and a test set (20%). One classifier for antrum and one classifier for corpus were trained and optimized. After optimization, the test set was analyzed using a joint result from both classifiers. Overall accuracy in the test set was 84% and was particularly high for type B gastritis with a sensitivity of 100% and a specificity of 93%. Classification of gastritis subtypes is possible using convolutional neural networks on a small dataset of histopathological images of antrum and corpus biopsies. Deep learning strategies to support routine diagnostic pathology merit further evaluation.

| S-EPMC7555568 | biostudies-literature

Urine metabolomics of rats with chronic atrophic gastritis.

Project description:Background/aimTo use liquid chromatography-mass spectrometry (LC-MS) to identify endogenous differential metabolites in the urine of rats with chronic atrophic gastritis (CAG).Materials and methodsMethylnitronitrosoguanidine (MNNG) was used to produce a CAG model in Wistar rats, and HE staining was used to determine the pathological model. LC-MS was used to detect the differential metabolic profiles in rat urine. Diversified analysis was performed by the statistical method.ResultsCompared with the control group, the model group had 68 differential metabolites, 25 that were upregulated and 43 that were downregulated. The main metabolic pathways were D-glutamine and D-glutamic acid metabolism, histidine metabolism and purine metabolism.ConclusionBy searching for differential metabolites and metabolic pathways in the urine of CAG rats, this study provides effective experimental data for the pathogenesis and clinical diagnosis of CAG.

| S-EPMC7657567 | biostudies-literature

Next Generation Sequencing Facilitates Quantitative Analysis of atrophic gastritis and atrophic gastritis receivng PEEPA-P5 antrum epithelial Transcriptomes

Project description:We had one goal to perform this study: Atrophic gastritis and atrophic gastritis receivng PEEPA-P5 antrum epithelial Transcriptomes

2023-05-27 | GSE205006 | GEO

Inflammation-Associated Senescence Promotes Helicobacter pylori-Induced Atrophic Gastritis.

Project description:Background & aimsThe association between cellular senescence and Helicobacter pylori-induced atrophic gastritis is not clear. Here, we explore the role of cellular senescence in H pylori-induced atrophic gastritis and the underlying mechanism.MethodsC57BL/6J mice were infected with H pylori for biological and mechanistic studies in vivo. Gastric precancerous lesions from patients and mouse models were collected and analyzed using senescence-associated beta-galactosidase, Sudan Black B, and immunohistochemical staining to analyze senescent cells, signaling pathways, and H pylori infection. Chromatin immunoprecipitation, luciferase reporter assays, and other techniques were used to explore the underlying mechanism in vitro.ResultsGastric mucosa atrophy was highly associated with cellular senescence. H pylori promoted gastric epithelial cell senescence in vitro and in vivo in a manner that depended on C-X-C motif chemokine receptor 2 (CXCR2) signaling. Interestingly, H pylori infection not only up-regulated the expression of CXCR2 ligands, C-X-C motif chemokine ligands 1 and 8, but also transcriptionally up-regulated the expression of CXCR2 via the nuclear factor-?B subunit 1 directly. In addition, CXCR2 formed a positive feedback loop with p53 to continually enhance senescence. Pharmaceutical inhibition of CXCR2 in an H pylori-infected mouse model attenuated mucosal senescence and atrophy, and delayed further precancerous lesion progression.ConclusionsOur study showed a new mechanism of H pylori-induced atrophic gastritis through CXCR2-mediated cellular senescence. Inhibition of CXCR2 signaling is suggested as a potential preventive therapy for targeting H pylori-induced atrophic gastritis. GEO data set accession numbers: GSE47797 and GSE3556.

| S-EPMC7859172 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data