Journal of Gastroenterology最新文献

{"title":"The risk stratification and predictive performance of a new combined polygenic risk score for hepatocellular carcinoma.","authors":"Chengxiao Yu, Yuchen Tang, Maojie Liu, Xin Xu, Xinyuan Ge, Hongxia Ma, Guangfu Jin, Hongbing Shen, Ci Song, Zhibin Hu","doi":"10.1007/s00535-024-02144-5","DOIUrl":"10.1007/s00535-024-02144-5","url":null,"abstract":"<p><strong>Background: </strong>Recent genome-wide association studies (GWASs) in liver diseases have generated some polygenic risk scores (PRSs), but their predictive effectiveness on hepatocellular carcinoma (HCC) risk assessment remains unclear.</p><p><strong>Methods: </strong>Here, we constructed a novel combined polygenic risk score and evaluated its increment to the well-established risk model. We used 15 HCC-associated genetic loci from two PRSs and FinnGen GWAS data to calculate a PRS-combined score and to fit the related PRS model in the UK Biobank cohort (N = 436,162). The PRS-combined score was further assessed for risk stratification for HCC integrating with the recommended clinical risk scores.</p><p><strong>Results: </strong>The PRS-combined model achieved a better AUC (0.657) than that of PRS-HFC (0.637) and PRS-cirrhosis (0.645). The top 20% of the PRS-combined distribution had a 3.25 increased risk of HCC vs. the middle decile (45-55%). At the population level, the addition of PRS-combined to the CLivD score significantly increased the C-statistic (from 0.716 to 0.746) and provided a remarkable improvement in reclassification (NRI = 0.088) at the 10-year risk threshold of 0.2%. In clinic, additional assessment of PRS-combined would reclassify 34,647 intermediate-risk participants as high genetic risk, corresponding to an increase of 63.92% (62/97) of the HCC events classified at high risk using the Fibrosis-4 alone.</p><p><strong>Conclusions: </strong>The PRS may enhance HCC risk prediction effectiveness in the general population and refine risk stratification of the conventional clinical indicator.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1011-1020"},"PeriodicalIF":6.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141912927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a novel oncolytic adenovirus controlled by CDX2 promoter for esophageal adenocarcinoma therapy.","authors":"Naohiko Nakamura, Shuhei Shinoda, Mizuho Sato-Dahlman, Brett Roach, Kari Jacobsen, Masato Yamamoto","doi":"10.1007/s00535-024-02147-2","DOIUrl":"10.1007/s00535-024-02147-2","url":null,"abstract":"<p><strong>Background: </strong>Prognosis of esophageal adenocarcinoma (EAC) is still poor. Therefore, the development of novel therapeutic modalities is necessary to improve therapeutic outcomes in EAC. Here, we report a novel promoter-controlled oncolytic adenovirus targeting CDX2 (Ad5/3-pCDX2) and its specific anticancer effect for EAC.</p><p><strong>Methods: </strong>We used OE19, OE33, HT29, MKN28, RH30, and HEL299 cell lines. To establish CDX2 overexpressing OE19 cells, pCMV-GLI1 plasmid was transfected to OE19 (OE19 + GLI1). The virus replication and cytocidal effect of replication competent Ad5/3-pCDX2 were analyzed in vitro. Antitumor effect of Ad5/3-pCDX2 was assessed in xenograft mouse models by intratumoral injection of the viruses. Finally, efficacy of combination therapy with Ad5/3-pCDX2 and 5FU was evaluated.</p><p><strong>Results: </strong>EAC cells and HT29 showed high mRNA levels of CDX2, but not MKN28, RH30, and HEL299. We confirmed that deoxycholic acid (DCA) exposure enhanced CDX2 expression in EAC cells and OE19 + GLI1 had persistent CDX2 overexpression without DCA. Ad5/3-pCDX2 showed stronger cytocidal effect in OE19 + GLI1 than OE19, whereas Ad5/3-pCDX2 did not kill CDX2-negative cells. Ad5/3-pCDX2 was significantly replicated in EAC cells and the virus replication was higher in OE19 + GLI1 and OE19 with DCA compared to OE19 without DCA exposure. In vivo, Ad5/3-pCDX2 significantly suppressed OE19 tumor growth and the antitumor effect was enhanced in OE19 + GLI1 tumor. In contrast, Ad5/3-pCDX2 did not show significant antitumor effect in MKN28 tumor. Moreover, Ad5/3-pCDX2 significantly increased the efficacy of 5FU in vitro and in vivo.</p><p><strong>Conclusions: </strong>Ad5/3-pCDX2 showed specific anticancer effect for EAC, which was enhanced by bile acid exposure. Ad5/3-pCDX2 has promising potential for EAC therapy in the clinical setting.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"986-999"},"PeriodicalIF":6.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11495994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corynoline protects chronic pancreatitis via binding to PSMA2 and alleviating pancreatic fibrosis.","authors":"Pengyuan Wang, Bangwei Huang, Yu Liu, Xin Tan, Libo Liu, Baoru Zhang, Zhaoshen Li, Le Kang, Lianghao Hu","doi":"10.1007/s00535-024-02145-4","DOIUrl":"10.1007/s00535-024-02145-4","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic fibrosis is the main pathological feature of chronic pancreatitis. There is a lack of medications that effectively alleviate or reverse pancreatic fibrosis and thus cure chronic pancreatitis.</p><p><strong>Methods: </strong>We screened drugs that could alleviate pancreatic fibrosis from 80 traditional Chinese medicine monomers and verified their efficacy and mechanisms.</p><p><strong>Results: </strong>We preliminarily identified corynoline as an antifibrotic candidate by drug screening among 80 compounds. In vitro, corynoline dose-dependently reduces collagen I synthesis in pancreatic stellate cells induced by TGF-β1 and inhibits its activation. Furthermore, we found that corynoline could alleviate the morphological disruption, such as acinar cell atrophy, collagen deposition etc., as well as reduced pancreatic weight in mice with chronic pancreatitis. We further validated the antifibrotic effect of corynoline in mRNA and protein levels. We also found that corynoline could inhibit NF-κB signaling pathway in vitro and in vivo. Next, we identified PSMA2 as the binding protein of corynoline by Lip-SMap and validated it using DARTS. Moreover, the siRNA of PSMA2 disrupts the anti-fibrotic effect of corynoline.</p><p><strong>Conclusion: </strong>In conclusion, corynoline is a promising agent for the treatment of pancreatic fibrosis and chronic pancreatitis.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1037-1051"},"PeriodicalIF":6.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141982471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-molecule sequencing of the whole HCV genome revealed envelope deletions in decompensated cirrhosis associated with NS2 and NS5A mutations.","authors":"Kozue Yamauchi, Shinya Maekawa, Leona Osawa, Yasuyuki Komiyama, Natsuko Nakakuki, Hitomi Takada, Masaru Muraoka, Yuichiro Suzuki, Mitsuaki Sato, Shinichi Takano, Nobuyuki Enomoto","doi":"10.1007/s00535-024-02146-3","DOIUrl":"10.1007/s00535-024-02146-3","url":null,"abstract":"<p><strong>Background: </strong>Defective hepatitis C virus (HCV) genomes with deletion of the envelope region have been occasionally reported by short-read sequencing analyses. However, the clinical and virological details of such deletion HCV have not been fully elucidated.</p><p><strong>Methods: </strong>We developed a highly accurate single-molecule sequencing system for full-length HCV genes by combining the third-generation nanopore sequencing with rolling circle amplification (RCA) and investigated the characteristics of deletion HCV through the analysis of 21 patients chronically infected with genotype-1b HCV.</p><p><strong>Result: </strong>In 5 of the 21 patients, a defective HCV genome with approximately 2000 bp deletion from the E1 to NS2 region was detected, with the read frequencies of 34-77%, suggesting the trans-complementation of the co-infecting complete HCV. Deletion HCV was found exclusively in decompensated cirrhosis (5/12 patients), and no deletion HCV was observed in nine compensated patients. Comparing the amino acid substitutions between the deletion and complete HCV (DAS, deletion-associated substitutions), the deletion HCV showed higher amino acid mutations in the ISDR (interferon sensitivity-determining region) in NS5A, and also in the TMS (transmembrane segment) 3 to H (helix) 2 region of NS2.</p><p><strong>Conclusions: </strong>Defective HCV genome with deletion of envelope genes is associated with decompensated cirrhosis. The deletion HCV seems susceptible to innate immunity, such as endogenous interferon with NS5A mutations, escaping from acquired immunity with deletion of envelope proteins with potential modulation of replication capabilities with NS2 mutations. The relationship between these mutations and liver damage caused by HCV deletion is worth investigating.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1021-1036"},"PeriodicalIF":6.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential of an artificial intelligence for diagnosing MRI images in rectal cancer: multicenter collaborative trial.","authors":"Atsushi Hamabe, Ichiro Takemasa, Masayuki Ishii, Koichi Okuya, Koya Hida, Daisuke Nishizaki, Atsuhiko Sumii, Shigeki Arizono, Shigeshi Kohno, Koji Tokunaga, Hirotsugu Nakai, Yoshiharu Sakai, Masahiko Watanabe","doi":"10.1007/s00535-024-02133-8","DOIUrl":"10.1007/s00535-024-02133-8","url":null,"abstract":"<p><strong>Background: </strong>An artificial intelligence-based algorithm we developed, mrAI, satisfactorily segmented the rectal tumor, rectum, and mesorectum from MRI data of rectal cancer patients in an initial study. Herein, we aimed to validate mrAI using an independent dataset.</p><p><strong>Methods: </strong>We utilized MRI images collected in another nationwide research project, \"Open versus Laparoscopic Surgery for Advanced Low Rectal Cancer Patients\". MRIs from 467 cases with upfront surgery were utilized; six radiologists centralized the MRI evaluations. The diagnostic accuracies of mrAI and the radiologists for tumor depth were compared using pathologic diagnosis as a reference.</p><p><strong>Results: </strong>For all cases, centralized diagnosis demonstrated 84.2% sensitivity, 37.7% specificity, and 73.7% accuracy; mrAI exhibited 70.6% sensitivity, 61.3% specificity, and 68.5% accuracy. After limiting MRIs to those acquired by a Philips scanner, with an inter-slice spacing of ≤ 6 mm-both conditions similar to those used in the development of mrAI-the performance of mrAI improved to 76.8% sensitivity, 76.7% specificity, and 76.7% accuracy, while the centralized diagnosis showed 81.8% sensitivity, 36.7% specificity, and 71.3% accuracy. Regarding relapse-free survival, the prognosis for tumors staged ≥ T3 was significantly worse than for tumors staged ≤ T2 (P = 0.0484) in the pathologic diagnosis. While no significant difference was observed between ≥ T3 and ≤ T2 tumors in the centralized diagnosis (P = 0.1510), the prognosis for ≥ T3 was significantly worse in the mrAI diagnosis (P = 0.0318).</p><p><strong>Conclusion: </strong>Proper imaging conditions for MRI can enhance the accuracy of mrAI, which has the potential to provide feedback to radiologists without overestimating tumor stage.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"896-904"},"PeriodicalIF":6.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11415406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141860047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A culprit for carcinogenesis hiding in daylight: normal-weight obesity.","authors":"Osman Cagin Buldukoglu, Serkan Ocal, Ayhan Hilmi Cekin","doi":"10.1007/s00535-024-02142-7","DOIUrl":"10.1007/s00535-024-02142-7","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"958-959"},"PeriodicalIF":6.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Profile of plasma microRNAs as a potential biomarker of Wilson's disease.","authors":"Ana Sánchez-Monteagudo, Edna Ripollés, Oihana Murillo, Sofia Domènech, María Álvarez-Sauco, Eva Girona, Isabel Sastre-Bataller, Ariadna Bono, Luis García-Villarreal, Antonio Tugores, Francisco García-García, Gloria González-Aseguinolaza, Marina Berenguer, Carmen Espinós","doi":"10.1007/s00535-024-02135-6","DOIUrl":"10.1007/s00535-024-02135-6","url":null,"abstract":"<p><strong>Background: </strong>Wilson's disease (WD) is a rare condition resulting from autosomal recessive mutations in ATP7B, a copper transporter, manifesting with hepatic, neurological, and psychiatric symptoms. Timely diagnosis and appropriate treatment yield a positive prognosis, while delayed identification and/or insufficient therapy lead to a poor outcome. Our aim was to establish a prognostic method for WD by characterising biomarkers based on circulating microRNAs.</p><p><strong>Methods: </strong>We conducted investigations across three cohorts: discovery, validation (comprising unrelated patients), and follow-up (revisiting the discovery cohort 3 years later). All groups were compared to age- and gender-matched controls. Plasma microRNAs were analysed via RNA sequencing in the discovery cohort and subsequently validated using quantitative PCR in all three cohorts. To assess disease progression, we examined the microRNA profile in Atp7b^-/- mice, analysing serum samples from 6 to 44 weeks of age and liver samples at three time points: 20, 30, and 40 weeks of age.</p><p><strong>Results: </strong>In patients, elevated levels of the signature microRNAs (miR-122-5p, miR-192-5p, and miR-885-5p) correlated with serum activities of aspartate transaminase, alanine aminotransferase and gamma-glutamyl transferase. In Atp7b^-/- mice, levels of miR-122-5p and miR-192-5p (miR-885-5p lacking a murine orthologue) increased from 12 weeks of age in serum, while exhibiting fluctuations in the liver, possibly attributable to hepatocyte regenerative capacity post-injury and the release of hepatic microRNAs into the bloodstream.</p><p><strong>Conclusions: </strong>The upregulation of the signature miR-122-5p, miR-192-5p, and miR-885-5p in patients and their correlation with liver disease progression in WD mice support their potential as biomarkers of WD.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"921-931"},"PeriodicalIF":6.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11415402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141766245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nrf2/ASPM axis regulated vasculogenic mimicry formation in hepatocellular carcinoma under hypoxia.","authors":"Yueyao Zhang, Na Che, Song Wang, Jie Meng, Nan Zhao, Jiyuan Han, Xueyi Dong, Yanlei Li, Jing Mo, Xiulan Zhao, Tieju Liu","doi":"10.1007/s00535-024-02140-9","DOIUrl":"10.1007/s00535-024-02140-9","url":null,"abstract":"<p><strong>Background: </strong>Hypoxic microenvironment is a common feature of most solid tumors including hepatocellular carcinoma (HCC). Vasculogenic mimicry (VM) formation by tumor cells could provide blood supply to tumor cells under hypoxia. NFE2 like basic leucine zipper (bZIP) transcription factor 2 (Nrf2), a regulator of cellular homeostasis, may promote tumor progression in the hypoxic conditions. However, the role and regulatory mechanisms of Nrf2 in HCC are not fully elucidated.</p><p><strong>Methods: </strong>Nrf2 and assembly factor for spindle microtubules (ASPM) expression modulations were conducted by lentiviral transfections. Western blot, immunofluorescence, ChIP-qPCR, dual-luciferase reporter gene assay, flow cytometry, RNA sequencing, multiple bioinformatics databases analysis, cell function assays in vitro, mouse model in vivo and human HCC tissues were employed to assess the effect of Nrf2/ASPM axis on HCC progression under hypoxia.</p><p><strong>Results: </strong>Nrf2 and ASPM expression facilitated epithelial-mesenchymal transition (EMT), cancer stem cells (CSCs) feature, and VM formation of HCC cells under hypoxia. Furthermore, Nrf2-regulated ASPM expression, via binding directly to the promoter region of ASPM and transcriptionally promoting ASPM expression. ASPM re-expression in Nrf2 knockdown cells or ASPM knockdown in Nrf2 overexpression cells reversed the cellular function caused by Nrf2. Meantime, retinol metabolism pathway was disrupted following abnormal ASPM expression. Nrf2/ASPM axis in murine models accelerated tumor growth and VM, corroborating in vitro findings. All-trans retinoic acid treatment reversed stemness and VM of HCC cells in vitro and in vivo. Clinically, Nrf2 and ASPM expressions were related to poor prognosis of HCC patients.</p><p><strong>Conclusions: </strong>Nrf2 drives EMT, CSCs characteristics and VM in HCC under hypoxia through the modulation of ASPM. Retinol metabolism pathway was dysregulated in HCC cells with ASPM overexpression. Nrf2/ASPM axis and related pathway provided potential therapeutic target for HCC.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"941-957"},"PeriodicalIF":6.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141889418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to the letter by Buldukoglu et al. regarding our manuscript \"Body mass index and survival among patients with advanced biliary tract cancer: a single-institutional study with nationwide data-based validation\".","authors":"Shinya Takaoka, Tsuyoshi Hamada, Yousuke Nakai, Hideo Yasunaga, Mitsuhiro Fujishiro","doi":"10.1007/s00535-024-02143-6","DOIUrl":"10.1007/s00535-024-02143-6","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"960-961"},"PeriodicalIF":6.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resistant starch reduces glycolysis by HK2 and suppresses high-fructose corn syrup-induced colon tumorigenesis.","authors":"Ying Zhang, Weiyi Shen, Zhehang Chen, Jiamin He, Lijun Feng, Lan Wang, Shujie Chen","doi":"10.1007/s00535-024-02138-3","DOIUrl":"10.1007/s00535-024-02138-3","url":null,"abstract":"<p><strong>Background: </strong>The intake of high-fructose corn syrup (HFCS) may increase the risk of colorectal cancer (CRC). This study aimed to explore the potential effects and mechanisms of resistant starch (RS) in HFCS-induced colon tumorigenesis.</p><p><strong>Methods: </strong>The azoxymethane/dextran sodium sulfate (AOM/DSS) and Apc^Min/+ mice models were used to investigate the roles of HFCS and RS in CRC in vivo. An immunohistochemistry (IHC) staining analysis was used to detect the expression of proliferation-related proteins in tissues. 16S rRNA sequencing for microbial community, gas chromatography for short-chain fatty acids (SCFAs), and mass spectrometry analysis for glycolysis products in the intestines were performed. Furthermore, lactic acid assay kit was used to detect the glycolysis levels in vitro.</p><p><strong>Results: </strong>RS suppressed HFCS-induced colon tumorigenesis through reshaping the microbial community. Mechanistically, the alteration of the microbial community after RS supplement increased the levels of intestinal SCFAs, especially butyrate, leading to the suppression of glycolysis and CRC cell proliferation by downregulating HK2.</p><p><strong>Conclusions: </strong>Our study identified RS as a candidate of protective factors in CRC and may provide a potential target for HFCS-related CRC treatment.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"905-920"},"PeriodicalIF":6.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11415400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}