Intestinal Dysplasia Research Articles

Tu1282 Retrospective Analysis of Gastric Intestinal Metaplasia and Dysplasia in an Ethnically Diverse Urban Safety-Net Population

Tu1282 Retrospective Analysis of Gastric Intestinal Metaplasia and Dysplasia in an Ethnically Diverse Urban Safety-Net Population

Stem-cell-specific endocytic degradation defects lead to intestinal dysplasia in Drosophila.

ABSTRACTUV radiation resistance-associated gene (UVRAG) is a tumor suppressor involved in autophagy, endocytosis and DNA damage repair, but how its loss contributes to colorectal cancer is poorly understood. Here, we show that UVRAG deficiency in Drosophila intestinal stem cells leads to uncontrolled proliferation and impaired differentiation without preventing autophagy. As a result, affected animals suffer from gut dysfunction and short lifespan. Dysplasia upon loss of UVRAG is characterized by the accumulation of endocytosed ligands and sustained activation of STAT and JNK signaling, and attenuation of these pathways suppresses stem cell hyperproliferation. Importantly, the inhibition of early (dynamin-dependent) or late (Rab7-dependent) steps of endocytosis in intestinal stem cells also induces hyperproliferation and dysplasia. Our data raise the possibility that endocytic, but not autophagic, defects contribute to UVRAG-deficient colorectal cancer development in humans.

Tubular adenoma of the gallblader

Tumors of the gallbladder are rare. Adenomas of the gallbladder is mostly occur as papillary or tubular. Tubular adenomas of the gallbladder occur in middleaged and old people, and it is extremely rare in children. We present 61 year old woman in whom during an ultrasound examination of the abdomen for pain that lasts a long time discovered a chronic inflammation of the gallbladder and slightly polypoid tumor of the gallbladder. Cholecystectomy was performed based on ultrasonographic findings of polyps in the gallbladder. Macroscopic and microscopic established that it is a tubular adenoma type with intestinal epithelial dysplasia, which clearly indicates that it is adenoma with reliable signs of precancer Finding intraoperative cholangiography was normal, and the postoperative course was uneventful.

STUDY ON POINT MUTATIONS AT POSITIONS 2132 AND 2143 IN 23S RRNA GENE OF HELICOBACTER PYLORI AMONG PATIENTS WITH CHRONIC GASTRITIS

Background: Clarithromycin resistance in Helicobacter pylori has been found to be associated with point mutations at positions 2142 and 2143 in 23SrRNA gene. The aims of this study were: (1) to determine the rates of point mutations A2143G, A2142G and A2142C in 23SrRNA gene of H. pylori among patients with chronic gastritis by PCR-RFLP technique; and (2) to assessthe association between these mutations and some clinical, endoscopic and histopathological characteristics of chronic gastritis. Patients and methods: two hundreds and twenty six patients with H. pylori-positive chronic gastritis were determined A2143G, A2142G and A2142C mutations by PCR-RFLP technique with DNA extracted from endoscopic biopsy specimens of gastric mucosa. Results: The rate of point mutations at positions 2142 and 2143 in 23S rRNA gene of H. pylori was 35.4% in total, the A2143G and A2142G mutationsaccounted for 92.5% and 7.5% of all point mutations, respectively. No A2142C mutation was found. These mutations were not associated with age, gender,distribution of gastritis, and the presence of atrophic gastritis. The rate of A2143G mutation in groups with and without a history of clarithromycin treatment were 44.9% and 24.8%, respectively (p = 0,0065). The A2142G mutation was associated with intestinal metaplasia and/or dysplasia. Conclusion: The point mutations at positions 2142 and 2143 in 23S rRNA gene were found at a high rate in H. pylori strains amongpatients with chronic gastritis, with the absolute predominance of A2143G mutation. The A2143G mutation was associated with a history of clarithromycin treatment. Key words: 23S rRNA gene, Helicobacter pylori, A2143G, A2142G, A2142C mutation, clarithromycin resistance, chronic gastritis.

Gastric atrophy: use of OLGA staging system in practice.

This study used the OLGA system to characterize the histology pattern of gastritis in dyspeptic outpatients with a mean age of 45 years from regions with different gastric cancer risks. Several classification systems have been purposed for understanding the status of the gastric mucosa. Currently, the Sydney system is the most widely employed. Nevertheless, the applicability of the Sydney system in therapeutic and prognostic areas is a matter of debate. Given this shortcoming an international group of gastroenterologists and pathologists developed a new system named Operative Link on Gastritis Assessment (OLGA). In this cross-sectional comparative study the OLGA system was used to characterize the histology pattern of gastritis in 685 dyspeptic patients referring to the department of gastroenterology of a training hospital. No significant correlation was found between active inflammation and total OLGA score (P > 0.05). Also, no statistically significant correlation was found between activity and intestinal metaplasia, dysplasia, atrophy, and cancer (P > 0.05). Even though, there is a positive correlation between mild chronic inflammation and total OLGA score, no correlation has been identified between chronicity and dysplasia or cancer (P > 0.05). Nearly, In all cases withno dysplasia OLGA scorewaszero but all patients with gastric cancer OLGA score was more than two. Generally, the activity is not a useful factor in predicting prognosis and its loss of relation with total OLGA score does not make OLGA score any less predictable.

Helicobacter pylori and Gastric Cancer: Timing and Impact of Preventive Measures.

Helicobacter pylori (H. pylori) is a Gram negative spiraliform bacterium that is commonly found in the stomach. H. pylori infection is still one of the world's most frequent infections, present in the stomachs of approximately one-half of the world's people. H. pylori infection is etiologically linked to histologic chronic active gastritis, peptic ulcer disease, and primary B-cell gastric lymphoma (gastric MALT lymphoma) and represents the major risk factor for the development of sporadic non-cardia gastric cancer (GC) of both intestinal and diffuse type. Studies that have examined the impact of GC prevention through H. pylori eradication have shown mixed results, but recent data suggest that prevention is only efficacious in patients without intestinal metaplasia or dysplasia. This indicates that, like in Barrett's esophagus, we need better clinical risk markers to indicate which patients are at greatest risk of developing cancer to guide clinical strategies. Furthermore, recent epidemiological data have suggested a possible contribution of H. pylori in modifying the risk of developing other gastrointestinal malignancies (including esophageal, pancreatic, hepatocellular, and colorectal cancer), although mechanistically these associations remain unexplained. We review clinically relevant aspects of H. pylori infection in the context of GC development as well as studies that have examined the impact of eradication on GC development and, lastly, discuss these recent epidemiological studies connecting H. pylori infection to extragastric gastrointestinal malignancies.

Cytoplasmic Drosha Is Aberrant in Precancerous Lesions of Gastric Carcinoma and Its Loss Predicts Worse Outcome for Gastric Cancer Patients.

The nuclear localization of Drosha is critical for its function as a microRNA maturation regulator. Dephosphorylation of Drosha at serine 300 and serine 302 disrupts its nuclear localization, and aberrant distribution of Drosha has been detected in some tumors. The purpose of the present study was to assess cytoplasmic/nuclear Drosha expression in gastric cancer carcinogenesis and progression. Drosha expression and its subcellular location was investigated by immunohistochemical staining of a set of tissue microarrays composed of normal adjacent tissues (374), chronic gastritis (137), precancerous lesions (94), and gastric adenocarcinoma (829) samples, and in gastric cancer cell lines with varying differentiation by immunofluorescence and western blot assay. Gradual loss of cytoplasmic Drosha was accompanied by tumor progression in both gastric cancer tissues and cell lines, and was inversely associated with tumor volume (P = 0.002), tumor grade (P < 0.001), tumor stage (P = 0.018), and distant metastasis (P = 0.026). Aberrant high levels of cytoplasmic Drosha were apparent in intestinal metaplasia and dysplasia tissues. The levels of nuclear Drosha were sharply decreased in chronic gastritis and maintained through precancerous lesions to gastric cancer. High levels of cytoplasmic Drosha predicted longer survival (LR = 7.088, P = 0.008) in gastric cancer patients. Our data provide novel insights into gastric cancer that cytoplasmic Drosha potentially plays a role in preventing carcinogenesis and tumor progression, and may be an independent predictor of patient outcome.

Gastric Intestinal Metaplasia in a U.S. Tertiary Care Population

Introduction: Gastric cancer is the fifth most common cancer worldwide, though the prevalence in the U.S. remains low. Gastric intestinal metaplasia (GIM) is known to be a precancerous condition and significantly increases a patient's risk of gastric cancer. GIM in the U.S. has not been well studied, however, and consensus guidelines for screening and surveillance are lacking. Methods: This was a retrospective analysis of patients with gastric intestinal metaplasia, dysplasia and cancer in a large, tertiary care center between November, 1993 and August, 2014. IRB approval was obtained prior to the initiation of the study. Results: 64,570 upper endoscopies were performed in our health system between 11/93 and 8/14. Of these, roughly 2,810 (4.4%) had biopsies with gastric intestinal metaplasia, gastric dysplasia or gastric cancer. Charts were reviewed for 1,233 patients. Of these, 1,151 had intestinal metaplasia, 52 had gastric cancer, 17 had low-grade dysplasia and 13 had high-grade dysplasia. Of the patients with intestinal metaplasia, 573 were male and 578 were female. The age range was 17 to 106 (median 62). The most common racial group was Caucasian (43%), followed by Asian (22%). The most common indications for EGD were abdominal pain (21%), GERD (20%) and anemia (12%). 43 patients (3.7%) had EGD performed for either GIM screening or surveillance. 336 (29%) had biopsies positive for H Pylori. 196 patients had surveillance recommended for IM. Of these, 83 (42%) had the surveillance procedure performed. Conclusion: Gastric intestinal metaplasia may be more prevalent than previously recognized in certain groups of patients in the U.S. In our study, 22% of the patients with intestinal metaplasia were of Asian descent, though only 6.7% of all endoscopies over the study period were performed on Asian patients. Further study is needed to assess the prevalence of intestinal metaplasia and risk of progression to gastric cancer in this group. Furthermore, adherence to recommended surveillance was 42%, suggesting further patient and provider education and outreach are needed.

Identification of CEACAM5 as a Biomarker for Prewarning and Prognosis in Gastric Cancer.

MGd1, a monoclonal antibody raised against gastric cancer cells, possesses a high degree of specificity for gastric cancer (GC). Here we identified that the antigen of MGd1 is CEACAM5, and used MGd1 to investigate the expression of CEACAM5 in non-GC and GC tissues (N=643), as a biomarker for prewarning and prognosis. The expression of CEACAM5 was detected by immunohistochemistry in numerous tissues; its clinicopathological correlation was statistically analyzed. CEACAM5 expression was increased progressively from normal gastric mucosa to chronic atrophic gastritis, intestinal metaplasia, dysplasia and finally to GC (p<0.05). In gastric precancerous lesions (intestinal metaplasia and dysplasia), CEACAM5-positive patients had a higher risk of developing GC as compared with CEACAM5-negative patients (OR = 12.68, p<0.001). Besides, CEACAM5 was found positively correlated with invasion depth of gastric adenocarcinoma (p<0.001). In survival analysis, CEACAM5 was demonstrated to be an independent prognostic predictor for patients with GC of clinical stage IIIA/IV (p=0.033). Our results demonstrate that CEACAM5 is a promising biomarker for GC prewarning and prognostic evaluation.

Prevalence of gastric precancerous lesions among chronic dyspeptic patients and related common risk factors.

Gastric cancer is one of the leading causes of cancer-related deaths worldwide. Progression of gastric cancer follows several steps from gastritis to atrophy, intestinal metaplasia, dysplasia, and finally cancer. The aim of this study was to determine the prevalence of gastric precancerous lesions and related common risk factors in a group of chronic dyspeptic patients. A total of 688 chronic dyspeptic patients older than 40 years of age were consecutively enrolled. The exclusion criteria were pregnancy, and a history of gastric cancer and gastric surgery. A questionnaire including demographic and clinical data, smoking habits, alcohol use, NSAIDs, and regular aspirin use was completed for all patients. Upper endoscopy and gastric biopsy were performed for all of the participants according to the standard protocols. Upper endoscopy was performed for all of the participants and biopsies were taken according to the biopsy protocol. The specimens were examined in a blinded manner by two expert gastrointestinal pathologists. The mean age of the participants was 57.87±9.10 years; there were 361 (52.5%) women. The prevalence of intestinal metaplasia, gastric atrophy, dysplasia, and positive Helicobacter pylori infection was 19.8, 12.8, 3.2%, and 64.5%, respectively. Age and H. pylori infection showed a significant association with pathological findings (odds ratio=3.10, 95% confidence interval: 1.91-4.72 and odds ratio=3.56, 95% confidence interval: 2.30-5.53, respectively). According to the high prevalence of precancerous lesions in patients with chronic dyspepsia who were older than 40 years of age, upper endoscopy and gastric mapping sampling for the detection of these lesions is recommended in intermediate-risk to high-risk areas.

Haemocytes control stem cell activity in the Drosophila intestine.

SUMMARYCoordination of stem cell activity with inflammatory responses is critical for regeneration and homeostasis of barrier epithelia. The temporal sequence of cell interactions during injury-induced regeneration is only beginning to be understood. Here we show that intestinal stem cells (ISCs) are regulated by macrophage-like hemocytes during the early phase of regenerative responses of the Drosophila intestinal epithelium. Upon tissue damage, hemocytes are recruited to the intestine and secrete the TGFβ/BMP homologue Dpp, inducing ISC proliferation by activating the Type I receptor Saxophone and the Smad homologue Smox. Activated ISCs then switch their response to Dpp by inducing expression of Thickveins, a second Type I receptor that has previously been shown to re-establish ISC quiescence by activating Mad. The interaction between hemocytes and ISCs promotes infection resistance, but also contributes to the development of intestinal dysplasia in aging flies. We propose that similar interactions influence pathologies like inflammatory bowel disease and colorectal cancer in humans.

345 Transepithelial Brush Biopsy With Computer-Assisted Tissue Analysis Increases Detection of Residual or Recurrent Intestinal Metaplasia and Dysplasia Following Endoscopic Ablation of Barrett's Esophagus

Radiofrequency ablation (RFA) and liquid nitrogen spray cryotherapy (SCT) are ablative techniques used to eradicate Barrett's esophagus (BE). Residual or recurrent intestinal metaplasia (IM) can be present without endoscopically visible disease. Post-ablation surveillance using forceps biopsies (FB) leaves significant mucosa unsampled, which creates a risk of missing IM or dysplasia. Wide Area Transepithelial Sampling with Computer-Assisted 3-Dimensional Tissue Analysis (WATS3D) has been shown to increase detection of metaplasia and dysplasia when used in addition to FB.

Mo1185 Clinical Outcome of Patients With Neuronal Intestinal Dysplasia Type B: Results of Different Therapeutic Options

Mo1185 Clinical Outcome of Patients With Neuronal Intestinal Dysplasia Type B: Results of Different Therapeutic Options

P19 Evidence for histological lesions precursor to intestinal-type sinonasal adenocarcinoma

Background Intestinal-type sinonasal adenocarcinomas (ITAC) are rare tumors, related to occupational exposure to wood and leather dust. Clinical symptoms are often indistinguishable from symptoms of patients with benign sinonasal disease, and as a consequence, patients frequently present with advanced-stage tumors. Multistep carcinogenesis through various histological changes accompanied by accumulating genetic alterations has not been demonstrated for ITAC. The aim of this study was to identify histological changes precursor to ITAC that may be useful for early detection for tumors in individuals at risk. Material and methods H&E stained paraffin sections from mucosa adjacent to primary tumor or recurrence of 136 patients with ITAC were evaluated for the presence of respiratory or olfactory epithelium, dysplasia, cuboid metaplasia, squamous metaplasia, and cylindrocellular hyperplasia. Protein expression of differentiation markers CK7, CK20, CDX2, B-III tubulin, Lysozyme, MUC2 and MUC5, and cancer-related genes B-catenin, p53, p16 and Cox2 were analyzed by immunohistochemistry. Results Our preliminary data revealed cuboid metaplasia in more than half of the cases, while intestinal metaplasia and dysplasia, accompanied by a switch to CK7−/CK20+/CDX2+ and in some cases p53/Cox2 expression, occurred in approximately 10–15%. Discussion Possible lesions precursor to ITAC were found infrequently however it may be speculated that these lesions often become destroyed by the growth of the ITAC tumor mass. Therefore we suggest that histological evaluation aided by CK20 and perhaps other biomarkers may be used for screening individuals at risk.

Helicobacter pylori eradication cannot reduce the risk of gastric cancer in patients with intestinal metaplasia and dysplasia: evidence from a meta-analysis.

The effect of Helicobacter pylori (H. pylori) eradication on gastric cancer (GC) prevention is controversial. Intestinal metaplasia (IM) seems to be a "point of no return" in the precancerous cascade. We performed a meta-analysis of randomized controlled trials (RCTs) to illustrate this issue. The MEDLINE, EMBASE, Cochrane Library were searched for relevant RCTs that were published in any language up to March 2014. By dividing participants into subgroups based on their baseline diagnoses as group <IM (normal, non-atrophic gastritis, atrophic gastritis) and group ≥ IM(intestinal metaplasia, dysplasia), the relative risk (RR) of GC in each study compared treatment group with control group were pooled using Mantel-Haenszel fixed-effect model and publication bias analyses were performed. Ten studies from eight RCTs were included in this analysis, for a total of 7,955 participants. H. pylori treatment compared with control significantly reduced the risk of GC, with a pooled RR of 0.64 (95% CI, 0.48-0.85). Subgroup analysis for patients with non-atrophic gastritis, atrophic gastritis (<IM) yielded a similar results (RR = 0.25, 95% CI, 0.08-0.81). But this difference was not observed in patients with intestinal metaplasia, dysplasia (≥ IM) (RR = 0.88; 95% CI, 0.59-1.31). Our results suggested that patients with Intestinal metaplasia or dysplasia could not benefit from the H. pylori treatment on the risk of GC.

Detection of Intestinal Cancer by Local, Topical Application of a Quenched Fluorescence Probe for Cysteine Cathepsins

Early detection of colonic polyps can prevent up to 90% of colorectal cancer deaths. Conventional colonoscopy readily detects the majority of premalignant lesions, which exhibit raised morphology. However, lesions that are flat and depressed are often undetected using this method. Therefore, there is a need for molecular-based contrast agents to improve detection rates over conventional colonoscopy. We evaluated a quenched fluorescent activity-based probe (qABP; BMV109) that targets multiple cysteine cathepsins that are overexpressed in intestinal dysplasia in a genetic model of spontaneous intestinal polyp formation and in a chemically induced model of colorectal carcinoma. We found that the qABP selectively targets cysteine cathepsins, resulting in high sensitivity and specificity for intestinal tumors in mice and humans. Additionally, the qABP can be administered by either intravenous injection or by local delivery to the colon, making it a highly valuable tool for improved detection of colorectal lesions using fluorescence-guided colonoscopy.

Пороки развития кишечника у недоношенных, протекающие под маской некротического энтероколита

Some congenital malformations of the gastrointestinal tract in premature infants are difficult to diagnose due to a lack of specific clinical picture. As a rule, they are masked under necrotizing enterocolitis resulting in the improper management of such patients. The article describes two clinical cases of Hirschsprung's disease and neuronal intestinal dysplasia in newborns. Both cases were regarded as necrotizing enterocolitis of newborns resulting in tactical treatment errors. We made a conclusion that the surgical tactics for patients with congenital disorders of both the enteric nervous system and muscular intestinal wall tissue, which manifest themselves as enterocolitis or perforation, should be determined only when you are fully confident in the functional usefulness of all parts of the intestine.

Differentiation reprogramming in gastric intestinal metaplasia and dysplasia: role of SOX2 and CDX2.

Intestinal metaplasia (IM), which results from de-novo expression of CDX2, and dysplasia are precursor lesions of gastric cancer that are associated with an increased risk for cancer development. There is much evidence suggesting a role for the transcription factor SOX2 in gastric differentiation. The aim of this study was to attempt to establish the relationship of SOX2 with CDX2 and with the differentiation reprogramming that characterizes gastric carcinogenesis, to assess their involvement in IM and dysplasia. Characterization of gastric (SOX2, MUC5AC, and MUC6) and intestinal (CDX2 and MUC2) markers in normal gastric mucosa, in 55 foci of IM and in 26 foci of dysplasia, was performed by immunohistochemistry. SOX2 was expressed in the normal gastric mucosa, in the presumptive stem cell compartment, and was maintained in 7% of the complete (MUC5AC-negative) and 85% of the incomplete (MUC5AC-positive) IM subtypes. Twelve per cent of the dysplastic lesions expressed SOX2, and the association with MUC5AC was lost. CDX2 was present in all IMs and dysplastic lesions. SOX2 is associated with gastric differentiation in incomplete IM and is lost in the progression to dysplasia, whereas CDX2 is acquired denovo in IM and maintained in dysplasia. This suggests that the balance between gastric and intestinal differentiation programmes impacts on the gastric carcinogenesis cascade progression.

Abstract A27: BLM overexpression promotes tumorigenicity in an azoxymethane/dextran sulfate (AOM/DSS) murine model of intestinal cancer

Abstract The role of genomic instability in colorectal cancer susceptibility is well established by studies of hereditary non-polyposis colon cancer (HNPCC), its associated disruption of DNA mismatch repair, and other DNA repair deficiencies that predispose to colon cancer. DNA repair deficiency that results in loss of capacity to maintain the genome leads to increased mutation or chromosome instability that in turn increases tumor formation. In some recent experiments using mouse models of cancer, deletion of genomic housekeeping genes promoted tumorigenesis. The Blm gene encodes a RecQ helicase that represses aberrant homologous recombination. Previous experiments using ApcMin/+ mice showed that a heterozygous Blm mutation increased intestinal tumor formation and tumor dysplasia. Conversely, mice over-expressing BLM displayed more than a 50% reduction of intestinal tumor number compared to wild-type controls. In order to isolate the effect of a Blm mutation on tumorigenicity, we used C57Bl/6 mice treated with azoxymethane and dextran sulfate to induce polyp formation. We predicted that mice with homozygous deletion of Blm would show an increase in tumor formation compared to wild-type mice, and transgenic mice over-expressing BLM would display fewer polyps. After treating our mice for 12 weeks and sacrificing them between 155 and 165 days of age, we found that mice with a complete deletion of Blm displayed a decrease in polyp formation compared to wild-type controls (3.0 polyps v. 5.5 polyps, p = 0.004). Transgenic mice over-expressing BLM in this model showed an increase in median polyp formation compared to wild-type controls (8.5 polyps v. 5.5 polyps, p = 0.01). Ongoing experiments will clarify the mechanism by which Blm promotes tumorigenesis in this mouse model of colon cancer. Citation Format: Kenechi Ebede, Michael McIlhatton, William Hankey, Joanna Groden. BLM overexpression promotes tumorigenicity in an azoxymethane/dextran sulfate (AOM/DSS) murine model of intestinal cancer. [abstract]. In: Proceedings of the AACR Special Conference: The Translational Impact of Model Organisms in Cancer; Nov 5-8, 2013; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2014;12(11 Suppl):Abstract nr A27.

Gastric ulcer patients are more susceptible to developing gastric cancer compared with concomitant gastric and duodenal ulcer patients

Intestinal metaplasia (IM) and dysplasia are precancerous lesions of gastric cancer (GC); however, the prevalence of IM and dysplasia in patients exhibiting single gastric ulcer (GU) and concomitant gastric and duodenal ulcer (CGDU) varies. In the present study consecutive patients who had undergone esophagogastroduodenal endoscopy were retrospectively screened, and those presenting with GU or CGDU were further evaluated for IM and dysplasia. Patients diagnosed with GC or lymphoma and patients with a history of anti-Helicobacter pylori, non-steroidal anti-inflammatory medicine (NSAIM), H2-receptor antagonist or proton pump inhibitor therapy, were excluded from the present study. Of the 204,073 consecutively screened cases, 8,855 (4.3%) and 2,397 (1.2%) were diagnosed with GU and CGDU, respectively. A total of 1,722 GU and 233 CGDU patients were excluded; thus, 7,133 and 2,164 cases of GU and CGDU, respectively (n=9,297), were included in the present study. IM and dysplasia were observed in 1,348 (14.5%) and 210 (2.3%) patients, respectively. IM was more frequently identified in GU patients compared with CGDU patients (16.4 vs. 8.3%; odds ratio [OR], 2.158; 95% confidence interval [CI], 1.830–2.545; χ2=86.932; P<0.001); furthermore, GU patients exhibited significantly more frequent IM compared with CGDU patients at the gastric antrum (14.2 vs. 5.5%; OR, 2.818; 95% CI, 2.199–3.610; χ2=72.299; P<0.001), gastric incisura (24.0 vs. 14.1%; OR, 1.922; 95% CI, 1.502–2.432; χ2=30.402; P<0.001) and gastric corpus (12.6 vs. 3.3%; OR, 4.259; 95% CI, 1.030–17.609; χ2=4.736; P=0.026). Dysplasia was significantly more frequently identified in GU patients compared with CGDU patients (2.7 vs. 0.7%; OR, 4.027; 95% CI, 2.376–6.823; χ2=31.315; P<0.001), with GU patients exhibiting significantly more severe dysplasia at the gastric antrum (2.4 vs. 0.7%; OR, 3.339; 95% CI, 1.735–6.425; χ2=14.652; P<0.001) and the gastric incisura (2.9 vs. 0.7%; OR, 4.255; 95% CI, 1.694–10.689; χ2=11.229; P<0.001). Additionally, mild IM was more frequently identified in GU patients compared with CGDU patients (15.2 vs. 7.1%; OR, 2.353; 95% CI, 1.972–2.807; χ2=94.798; P<0.001) and dysplasia of a mild (1.7 vs. 0.6%; OR, 2.807; 95% CI, 1.580–4.987; χ2=13.519; P<0.001) or moderate/severe grade (1.1 vs. 0.09%; OR, 11.642; 95% CI, 2.857–47.439; χ2=18.896; P<0.001) was more frequent in GU patients compared with CGDU patients. IM and dysplasia were more frequently observed in GU compared with CGDU patients in the present study, which may be associated with an increased probability of developing GC.