Canadian Journal of Gastroenterology and Hepatology最新文献

{"title":"Navigating the Terrain of Post-Polypectomy Surveillance: Charting the Complex Landscape of Guidelines and Recurrence Risks.","authors":"Xiaojin Tao, Jun Yao","doi":"10.1155/cjgh/2782582","DOIUrl":"10.1155/cjgh/2782582","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a leading cause of global cancer-related morbidity and mortality. The majority of CRC cases arise through two well-established pathways: the conventional adenoma-carcinoma sequence and the serrated neoplasia pathway. Colonoscopic polypectomy significantly reduces the incidence of CRC, yet postoperative recurrence rates remain substantial, underscoring the critical role of post-polypectomy colonoscopic surveillance (PPCS). Recent updates to PPCS guidelines by major gastroenterological societies-including the US Multisociety Task Force (USMSTF), European Society of Gastrointestinal Endoscopy (ESGE), British Society of Gastroenterology/Association of Coloproctology of Great Britain and Ireland/Public Health England (BSG/ACPGBI/PHE), and the Asia-Pacific Task Force-reflect evolving strategies for risk stratification and surveillance intervals. While all guidelines prioritize colonoscopy resources for high-risk populations and reduce burden for low-risk individuals, significant variations persist in definitions of high-risk adenomas (HRA), recommendations for surveillance intervals, and management of specific histological subtypes such as villous architecture. This review comprehensively compares these updated guidelines, highlighting consensus and discordance in clinical recommendations. Furthermore, it synthesizes evidence on multifactorial recurrence risks, encompassing baseline adenoma characteristics, patient-specific factors, and the quality of endoscopic procedures. Regarding the association with the same risk factor, traditional adenomas and serrated polyps may demonstrate heterogeneity. Understanding these elements is essential for optimizing personalized surveillance strategies and reducing recurrent adenoma burden. Finally, we hope that this review will provide decision-making support for countries lacking standalone guidelines and help clinicians navigate complex and contradictory guideline recommendations.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e2782582"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Retrospective Analysis of 581 Cases of Esophagogastric Variceal Bleeding Complicated by Portal Vein Thrombosis at a Single Center.","authors":"Jiayi Zhang, Yingying He, Shanshan Wu, Derun Kong","doi":"10.1155/cjgh/8185878","DOIUrl":"10.1155/cjgh/8185878","url":null,"abstract":"<p><strong>Background: </strong>Esophagogastric variceal bleeding (EGVB) and portal vein thrombosis (PVT) are common complications of liver cirrhosis and frequently coexist, with reported prevalence rate up to 32.5%. Their coexistence complicates clinical management and is associated with adverse outcomes. Early identification of PVT may improve patient management and prognosis.</p><p><strong>Objective: </strong>To investigate the prevalence, clinical characteristics, and risk factors of PVT in patients with EGVB and to develop a nomogram for the early identification of PVT.</p><p><strong>Methods: </strong>This retrospective case-control study included 581 consecutive cirrhotic patients with EGVB treated at a single center. Patients were classified into PVT and non-PVT groups according to imaging findings. The demographic characteristics, clinical manifestations, laboratory parameters, and treatment histories were compared between the two groups. Risk factors associated with PVT were identified using logistic regression analysis, and a predictive nomogram was subsequently developed to estimate the probability of PVT occurrence.</p><p><strong>Results: </strong>Among the 581 patients, 201 patients (34.6%) had concomitant PVT. The median age was 55 years (interquartile range, 48.0-64.0 years), and 384 (66.1%) were male. Compared with the non-PVT group, patients with PVT more frequently presented with abdominal pain (15.9% vs. 10.3%, p = 0.048) and hepatic hydrothorax (18.9% vs. 12.4%, p = 0.034) than the non-PVT group. Multivariable analysis identified previous splenectomy (OR = 4.615, 95% CI: 2.418-8.806; p < 0.001) and endoscopic treatment (OR = 2.414; 95% CI 1.644-3.545; p < 0.001) were as independent risk factors for PVT. Patients with Yerdel Grade IV had a significantly higher prevalence of splenectomy than those with Yerdel Grade I (59.1% vs. 23.4%). Similarly, the prevalence of PVT was significantly higher among patients with a history of endoscopic treatment than among those without (46.9% vs. 26.6%, p < 0.001). D-dimer and fibrin degradation product (FDP) levels were significantly elevated in the PVT group. Receiver operating characteristic analysis identified optimal cutoff values of 0.995 μg/mL for D-dimer and 2.665 μg/mL for FDP. A nomogram incorporating significant predictors demonstrated moderate discrimination for identifying PVT (AUC = 0.751).</p><p><strong>Conclusion: </strong>PVT was present in approximately one-third of cirrhotic with EGVB. Previous splenectomy and endoscopic intervention were independently associated with PVT, while abdominal pain and hepatic hydrothorax were more common clinical manifestations. The nomogram showed moderate diagnostic performance and may facilitate early identification of PVT; however, external validation is required before routine clinical application.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e8185878"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GPR39 Suppresses Ferroptosis via the Nrf2/SLC7A11 Axis and Reduces the Sensitivity of Colorectal Cancer to Anti-PD-1 Immunotherapy.","authors":"Cong Zhou, Xiaoling Fang, Jiaying Lin, Xiang Jiang, Huihui Li, Jiaoe Chen, Qiang Chen","doi":"10.1155/cjgh/5689742","DOIUrl":"10.1155/cjgh/5689742","url":null,"abstract":"<p><strong>Background: </strong>PD-1 blockade has yet to achieve broad clinical success in colorectal cancer (CRC), with microsatellite-stable tumors proving especially resistant. At the same time, ferroptosis has emerged as a mechanistic link between redox control in tumor cells and the antitumor immune response. GPR39 is overexpressed in CRC, but its functional role in ferroptosis and immunotherapy resistance is currently unclear.</p><p><strong>Methods: </strong>GPR39 expression was analyzed in human and mouse CRC cell lines. GPR39 knockdown, with or without the ferroptosis inhibitor liproxstatin-1, was performed to determine whether GPR39 regulates CRC cell proliferation and migration through ferroptosis. Ferroptosis was evaluated by measuring lipid peroxidation, glutathione (GSH) levels, ferrous iron (Fe²⁺) accumulation, and reactive oxygen species (ROS). Mechanistic involvement of the nuclear factor erythroid 2-related factor 2 (Nrf2)/solute carrier family 7 member 11 (SLC7A11) signaling axis was examined using Nrf2 overexpression. Subcutaneous implantation of MC38 cells with stable GPR39 knockdown was performed to evaluate whether GPR39 regulates tumor sensitivity to anti-PD-1 treatment in vivo in a ferroptosis-dependent manner.</p><p><strong>Results: </strong>GPR39 was markedly upregulated in CRC cell lines. GPR39 knockdown induced ferroptosis, characterized by increased lipid peroxidation, Fe²⁺ accumulation, and oxidative stress and accompanied by suppression of the Nrf2/SLC7A11 pathway. Nrf2 overexpression reversed these changes. Functionally, silencing GPR39 inhibited the proliferative and migratory capacities of CRC cells, effects that were largely rescued by liproxstatin-1. In vivo, GPR39 knockdown significantly potentiated the antitumor activity of PD-1 blockade, as evidenced by suppressed tumor progression accompanied by enhanced infiltration of CD8⁺ T cells, whereas ferroptosis inhibition abrogated these effects.</p><p><strong>Conclusion: </strong>GPR39 suppresses ferroptosis in CRC via the Nrf2/SLC7A11 axis, thereby limiting PD-1 immunotherapy efficacy.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e5689742"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148702667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and Validation of the Chinese Physicians' Reactions to Uncertainty Scale for Endoscopy: A Mixed-Methods Approach.","authors":"Yingnan Deng, Hanyue Ding, Wen Shi, Weiyang Zheng, Xiaowei Tang, Zhuo Yang, Hui Ding, Yunlu Feng, Aiming Yang, Dong Wu","doi":"10.1155/cjgh/2337892","DOIUrl":"10.1155/cjgh/2337892","url":null,"abstract":"<p><strong>Objectives: </strong>To develop and validate a Chinese Physicians' Reactions to Uncertainty Scale for Endoscopy for assessing endoscopists' reactions to uncertainty in clinical practice.</p><p><strong>Methods: </strong>Using a mixed-methods design, we translated the original Physicians' Reactions to Uncertainty scale and generated endoscopy-specific items through focus-group interviews. The draft scale was refined through Delphi consultation and then evaluated in an online survey of 360 digestive endoscopists from 204 hospitals in China. Item reduction was based on dispersion, critical ratio, and item-total correlation analyses. Construct validity was assessed using exploratory factor analysis and confirmatory factor analysis. Content validity was evaluated using item-level and scale-level content validity indices, and reliability was examined using Cronbach's alpha and split-half reliability.</p><p><strong>Results: </strong>The final scale comprised 16 items across four dimensions: concerns about uncertainty and bad outcomes, disclosing uncertainty to patients, disclosing mistakes to physicians, and endoscopy-specific uncertainty responses and self-efficacy. In exploratory factor analysis, four factors explained 73.474% of the total variance. Confirmatory factor analysis supported an acceptable four-factor model fit (χ²/df = 2.778, RMSEA = 0.098, IFI = 0.908, TLI = 0.931). Cronbach's alpha was 0.818 for the overall scale and 0.801-0.932 for the subscales. Split-half reliability was 0.919. Item-level content validity indices ranged from 0.86 to 1.00, and the scale-level content validity index was 0.96.</p><p><strong>Conclusions: </strong>The Chinese Physicians' Reactions to Uncertainty Scale for Endoscopy is a reliable and valid instrument for assessing endoscopists' reactions to uncertainty in China.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e2337892"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148867443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Smoking Cessation Attempts on Outcomes in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Large Propensity Score-Matched Cohort Study.","authors":"Mohammad Alabbas, Osama Hamid, Barbara Balog, Umesh Bhagat, Omar Saab, Rama Nanah, Omar T Sims, Jamak Modaresi Esfeh","doi":"10.1155/cjgh/5902236","DOIUrl":"10.1155/cjgh/5902236","url":null,"abstract":"<p><strong>Background and aims: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent, and smoking is associated with greater disease severity. We investigated whether documented smoking cessation attempts among adults with MASLD were associated with liver-related outcomes, cardiovascular outcomes, and all-cause mortality.</p><p><strong>Methods: </strong>We performed a retrospective cohort study using the TriNetX Research Network. Adults (≥ 18 years) with MASLD and documented smoking history were included. A smoking cessation attempt was defined by cessation counseling and/or cessation pharmacotherapy; comparators had no documented cessation attempt. Patients with depressive disorders and competing liver etiologies were excluded. Cohorts were matched 1:1 using propensity scores, and outcomes were analyzed using Cox proportional hazards models. Sensitivity analyses were performed at fixed follow-up horizons of 6 months, 1 year, and 2 years.</p><p><strong>Results: </strong>Among 418,784 eligible patients, 85,639 had a documented cessation attempt and 333,145 did not; after matching, 83,315 patients remained in each cohort. In the matched cohort, cessation attempt was associated with lower hazards of cirrhosis progression (1.7% vs. 2.1%; HR 0.87, 95% CI 0.81-0.93), hepatocellular carcinoma (0.2% vs. 0.3%; HR 0.58, 95% CI 0.48-0.70), portal hypertension (0.8% vs. 1.1%; HR 0.77, 95% CI 0.70-0.86), and MASH progression (2.2% vs. 2.9%; HR 0.76, 95% CI 0.71-0.81). The cessation attempt was also associated with higher hazards of MACE (13.6% vs. 11.4%; HR 1.24, 95% CI 1.20-1.28), peripheral artery disease (4.1% vs. 3.2%; HR 1.33, 95% CI 1.26-1.40), and all-cause mortality (8.5% vs. 7.3%; HR 1.23, 95% CI 1.18-1.27). Fixed-horizon analyses showed similar patterns over time.</p><p><strong>Conclusions: </strong>In adults with MASLD and smoking history, documented smoking cessation attempts were associated with lower hazards of several liver outcomes but higher cardiovascular event rates and mortality, findings likely influenced by residual confounding and clinical risk clustering in patients receiving cessation interventions.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e5902236"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the Link Between Smoking and Fatty Liver via Ultrasound Elastography: A Cross-Sectional Analysis Study.","authors":"Yue Feng, Zhengqing Mu, Changsong Xu, Fan Zhou","doi":"10.1155/cjgh/4584914","DOIUrl":"10.1155/cjgh/4584914","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the link between smoking and fatty liver, particularly the influence of different smoking patterns on its prevalence, aiming to provide insights for public health policies.</p><p><strong>Patients and methods: </strong>We conducted a cross-sectional analysis of data from 6140 adults participating in the NHANES between 2017 and 2020. Participants were categorized into nonsmoking, secondhand smoke exposure, and active smoking groups based on serum cotinine levels. Multivariable regression models were used to assess the associations between smoking status and fatty liver, controlling for potential confounders.</p><p><strong>Results: </strong>Active smokers showed a significantly higher prevalence of fatty liver compared to nonsmokers, especially among obese subgroups. In obese populations, both active smoking and secondhand smoke exposure remarkably increased the risk of fatty liver (OR = 2.51, p = 0.014). In contrast, a negative but statistically nonsignificant association was found between smoking and fatty liver in nonobese individuals.</p><p><strong>Conclusion: </strong>Therefore, smoking, particularly among obese individuals, is a significant contributor to fatty liver. Raising public awareness of the risks associated with smoking could help enhance liver health and overall quality of life.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e4584914"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13382998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148521564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Cirrhosis Etiology and Intensive Care Accessibility on Upper Gastrointestinal Bleeding: A Prospective Observational Study.","authors":"Mariana Barros Marcondes, Clara Fantinelli Moreno, Cíntia Mitsue Pereira Suzuki, Maxwell Antonio Garcia Rodrigues, Alecsandro Moreira, Xingshun Qi, Fernando Gomes Romeiro","doi":"10.1155/cjgh/1409025","DOIUrl":"10.1155/cjgh/1409025","url":null,"abstract":"<p><strong>Background: </strong>Upper gastrointestinal bleeding (UGIB) is a significant cause of cirrhosis decompensation; however, there is still controversy on risk factors for poor outcomes. This study aims to explore the impact of additional variables, such as liver disease etiology and intensive care unit (ICU) accessibility, on mortality, rebleeding, and infection rates.</p><p><strong>Methods: </strong>Cox regression analysis was employed to identify predictors associated with mortality and rebleeding, while Poisson regression analysis was utilized to assess associations with infections.</p><p><strong>Results: </strong>A total of 228 patients were included, with the majority classified as Child-Pugh B and C. Among them, 96 patients (42.1%) had alcohol-associated liver disease (ALD), of which 45 (46.9%) were in alcohol abstinence. One hundred and ninety-five patients (85.5%) survived, while 33 (14.5%) died. Intubation was required for 31 patients (13.6%), and 28 were transferred to the ICU. Antibiotic prophylaxis was administered to 219 patients (96%), and 55 (24.1%) developed infections. Both orotracheal intubation and transfusions were associated with high mortality, whereas ALD was linked to a lower risk of death (p < 0.001, 0.029, and 0.005, respectively). Intubation was also correlated with an increased risk of rebleeding, while transfer to ICU reduced this complication (p = 0.012 and 0.045, respectively). The Child-Pugh score and length of hospitalization were associated with the occurrence of infections (p = 0.037 and < 0.001, respectively).</p><p><strong>Conclusions: </strong>Intubation, transfusions, liver disease etiology, and ICU accessibility are critical predictors following UGIB in cirrhosis. Additionally, the Child-Pugh score and duration of hospitalization are directly proportional to the risk of infections in this context.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov identifier: NCT04662918.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e1409025"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148101971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic Value and Related Molecular Mechanisms of miR-5003-3p in Hepatocellular Carcinoma.","authors":"Hao Yan, Wei Shan, Qian Xia, Wanting Fang","doi":"10.1155/cjgh/1318790","DOIUrl":"10.1155/cjgh/1318790","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is a malignant tumor worldwide with a high mortality rate and recurrence rate. Numerous miRNAs are being applied to the healing and prognosis of HCC. A prior investigation predicted that miR-5003-3p was linked to HCC, but the relevant molecular mechanisms were not clear.</p><p><strong>Aim: </strong>To discover the prognostic value and molecular mechanisms concerned of miR-5003-3p in HCC.</p><p><strong>Methods: </strong>A total of 125 tumor specimens from HCC patients were obtained in this study, along with corresponding adjacent noncancerous tissue samples collected as a control. The levels of miR-500-3p and MAL2 in tumor tissues and cells were detected by RT-qPCR. The prognostic value of miR-500-3p was evaluated using Kaplan-Meier curve and COX regression model. The effects of miR-500-3p on cellular malignant phenotypes were assessed via CCK-8 and Transwell assays. The target sites of miR-500-3p were identified using bioinformatics analysis. The dual-luciferase reporter assay validated the target relationship between them.</p><p><strong>Results: </strong>miR-5003-3p levels were remarkably elevated in HCC tissues, and late TNM stage (I + II) was dramatically higher versus early TNM stage (III + IV). Lymph node metastasis, TNM stage, and differentiated degree were linked notably to miR-5003-3p expression. Upregulated miR-5003-3p was an independent risk factor for HCC. In vitro, downregulated miR-5003-3p could induce apoptosis and restrain proliferation, migration, and invasion, which could be rescued by depressed MAL2.</p><p><strong>Conclusion: </strong>miR-5003-3p may be an independent prognostic factor for HCC. Mechanistically, miR-5003-3p negatively regulates MAL2 to promote cellular processes. These findings highlight the potential of miR-5003-3p as a novel prognostic biomarker and a promising therapeutic target for HCC.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e1318790"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147624336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Independent Prognosis Prediction of Hepatocellular Carcinoma Using MicroRNA-Based Single and Combined Biomarkers.","authors":"Long-Bin Jeng, Wen-Ling Chan, Chiao-Fang Teng","doi":"10.1155/cjgh/1491679","DOIUrl":"10.1155/cjgh/1491679","url":null,"abstract":"<p><p>Although there are various treatment modalities available for hepatocellular carcinoma (HCC), HCC is still among the most common causes of cancer-related death globally. Identifying independent biomarkers of poor prognosis in HCC patients remains a critical goal to allow timely intervention and ameliorate patient survival. MicroRNAs (miRNAs), the most widely investigated small noncoding RNAs to date, play a crucial role in regulating the initiation and progression of HCC. The expression of numerous miRNAs is altered in tumor tissues and blood specimens of HCC patients, underscoring their potential as promising prognostic biomarkers. This review offers an exhaustive overview of the current literature examining tissue- and circulation-derived miRNAs as single or combined independent prognostic biomarkers in HCC patients.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e1491679"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13310390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148340636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FUT2-Mediated Fucosylation of OLFM4 Promotes Colon Cancer Cell Differentiation.","authors":"Caihan Duan, Keyi Zhang, Lingzhi Hou, Jiawei Chen, Jun Liu, Huiying Shi, Chaoqun Han","doi":"10.1155/cjgh/7502916","DOIUrl":"10.1155/cjgh/7502916","url":null,"abstract":"<p><strong>Background: </strong>Fucosyltransferase 2 (FUT2) deficiency exacerbates inflammation, a known risk factor for colon cancer. However, the precise role and underlying mechanism of FUT2 in regulating colon cancer cell differentiation remain unclear. Although olfactomedin-4 (OLFM4) has been known to have a tumor-suppressive effect, its functional interaction with FUT2 in colon cancer remains unexplored.</p><p><strong>Methods: </strong>FUT2 expression levels were assessed using TCGA and cBioPortal databases and in different colon cancer cell lines. ALP assays were performed to evaluate the effect of FUT2 on cancer cell differentiation. Transwell invasion assays, scratch assays, and tumor sphere formation assays were used to investigate the functional effects of FUT2 on colon cancer cells. N-glycosylation proteomics and UEA-I chromatography were used to identify the regulatory effect of FUT2 on OLFM4 fucosylation.</p><p><strong>Results: </strong>FUT2 expression was associated with the differentiation degree of colon cancer cell lines. Based on their endogenous FUT2 expression, we overexpressed FUT2 in SW480 cells (low baseline) and knocked it down in HT29 cells (high baseline). Overexpressing FUT2 promoted the differentiation of SW480 cells and inhibited their migration, invasion, EMT, and stemness. Conversely, knockdown of FUT2 in HT29 cells reduced its degree of differentiation and increased its malignancy. N-glycosylation proteomics analysis and UEA-I chromatography indicated OLFM4 as a downstream target of FUT2. FUT2-mediated fucosylation of OLFM4 is positively correlated with the degree of cancer cell differentiation. Knockdown of OLFM4 attenuated differentiation in FUT2-overexpressing SW480 cells, while overexpression of OLFM4 produced opposite effects.</p><p><strong>Conclusion: </strong>FUT2 promotes colon cancer cell differentiation by mediating OLFM4 fucosylation, suggesting that FUT2 may serve as a therapeutic target for colon cancer.</p>","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"2026 1","pages":"e7502916"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13317148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148354230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}