Maya Magdy Abdelwahab, Ahmad S Ghattas, Ahmed Tawheed
{"title":"Implications of gut microbiota in hepatic and pancreatic diseases: Gut-liver-pancreas axis.","authors":"Maya Magdy Abdelwahab, Ahmad S Ghattas, Ahmed Tawheed","doi":"10.4254/wjh.v17.i9.109965","DOIUrl":"10.4254/wjh.v17.i9.109965","url":null,"abstract":"<p><p>The gut-liver-pancreas axis (GLPA) is a critical network shaped by gut microbiota (GM) and their metabolites, essential for maintaining metabolic and immune balance. Disruption of this microbial equilibrium, known as dysbiosis, contributes to the development and progression of various hepatic and pancreatic diseases. Through mechanisms such as increased intestinal permeability and exposure to microbial products-including lipopolysaccharide, trimethylamine-N-oxide, and secondary bile acids-dysbiosis promotes inflammation, oxidative stress, insulin resistance, and carcinogenesis. These changes are linked to conditions including metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cirrhosis, hepatocellular carcinoma, pancreatitis, pancreatic ductal adenocarcinoma, and diabetes. Emerging tools like stool metagenomics and serum metabolomics help identify microbial biomarkers for diagnosis and risk stratification. While interventions such as probiotics, dietary changes, and fecal microbiota transplantation aim to restore microbial balance, their success remains inconsistent. This work aims to highlight the pathogenic role of GM across the GLPA, with special emphasis on the underexplored gut-pancreas connection. Advancing our understanding of the GLPA can unlock novel microbiota-targeted approaches for early diagnosis and treatment of hepatopancreatic diseases.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"109965"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Leandro Sierra, Arjun Chatterjee, Renan Prado, Akash Khurana, Roma Patel, Stephen Firkins, Roberto Simons-Linares
{"title":"Impact of metabolic endoscopy on fibrosis regression in steatotic liver disease.","authors":"Leandro Sierra, Arjun Chatterjee, Renan Prado, Akash Khurana, Roma Patel, Stephen Firkins, Roberto Simons-Linares","doi":"10.4254/wjh.v17.i9.108144","DOIUrl":"10.4254/wjh.v17.i9.108144","url":null,"abstract":"<p><p>Metabolic endoscopy represents a promising alternative in the management of steatotic liver disease, particularly metabolic dysfunction-associated steatohepatitis (MASH), a progressive form of metabolic dysfunction-associated steatotic liver disease (MASLD). With the rising global prevalence of MASLD-affecting over one-third of the adult population-and its close association with obesity, insulin resistance, and metabolic syndrome, there is an urgent need for innovative, minimally invasive therapies that can reverse liver fibrosis and prevent progression to cirrhosis and hepatocellular carcinoma. Traditional management of MASLD relies on lifestyle modifications and bariatric surgery, yet these approaches are hampered by issues of adherence, invasiveness, and accessibility. This review examines endoscopic bariatric metabolic therapies including endoscopic sleeve gastroplasty (ESG), intragastric balloons (IGB), duodenal mucosal resurfacing (DMR), and duodeno-jejunal bypass liners (DJBL), as well as revisional procedures like endoscopic revisional gastroplasty (ERG) and transoral outlet reduction (TORe). Clinical studies and meta-analyses indicate that metabolic endoscopy is safe and effective for liver fibrosis in MASH. ESG appears to offer the greatest fibrosis reduction, while IGB and DJBL yield modest improvements, and DMR shows no significant effect. Among revisional therapies, ERG has demonstrated fibrosis reduction, although the benefits of TORe remain to be fully evaluated.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"108144"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Stratification and selection of therapies to improve survival in severe alcoholic hepatitis.","authors":"Ajay Kumar Mishra, Amit Goel","doi":"10.4254/wjh.v17.i9.109118","DOIUrl":"10.4254/wjh.v17.i9.109118","url":null,"abstract":"<p><p>Severe alcoholic hepatitis (SAH) is associated with high short-term mortality. The SAH population exhibits extreme heterogeneity in disease severity, clinical presentation, decompensations, and outcomes. Nonetheless, improving outcomes and preventing adverse events is a major challenge when selecting an appropriate treatment for alcoholic hepatitis. Currently, steroids are the standard of care for SAH with Maddrey's discriminant function > 32 and model for end stage liver disease > 20; however, they have limited usage due to ineligibility in approximately two-third of such patients. Approximately 25% of patients do not respond to steroids and require alternative therapies. An array of evolving therapies, such as granulocyte colony-stimulating factors, plasma exchange, fecal microbiota transplantation, antibiotics, anti-cytokine therapies, and N-acetylcysteine, showing variable success, are emerging. Hence, it is also crucial to select appropriate therapy. The present review discusses the standard of care, the existing therapies, risk stratification for outcomes, and the selection of appropriate therapy to improve survival in SAH patients.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"109118"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Prognostic value of dynamic changes in C-reactive protein to albumin ratio in patients with acute-on-chronic liver failure.","authors":"Zong-Yi Zhu, Li-Juan Yan","doi":"10.4254/wjh.v17.i9.110652","DOIUrl":"10.4254/wjh.v17.i9.110652","url":null,"abstract":"<p><strong>Background: </strong>Acute-on-chronic liver failure (ACLF) is a life-threatening syndrome associated with high short-term mortality. Accurate risk stratification is crucial for the management of ACLF.</p><p><strong>Aim: </strong>To evaluate the prognostic value of the C-reactive protein to albumin ratio (CAR) and its dynamic changes in patients with ACLF defined by the Chinese Group on Study of Severe Hepatitis B (COSSH) criteria.</p><p><strong>Methods: </strong>A total of 126 consecutive patients diagnosed with COSSH-ACLF were prospectively enrolled. CAR was calculated at admission and on days 4, 7, and 14. The primary and secondary outcomes were 28-day and 90-day mortality, respectively. Multivariate Cox regression analysis was conducted to identify independent predictors of mortality. A novel prognostic model (COSSH-CAR), integrating baseline and dynamic variables, was developed and compared with established prognostic scoring systems.</p><p><strong>Results: </strong>The 28-day and 90-day mortality rates were 27.8% and 40.5%, respectively. Baseline CAR was significantly higher in 28-day non-survivors than in survivors (2.68 <i>vs</i> 1.42, <i>P</i> < 0.001). The dynamic change in CAR from baseline to day 7 (ΔCAR-7) showed stronger predictive power for 28-day mortality [area under the receiver operating characteristic curve (AUC) = 0.765] than baseline CAR (AUC = 0.698), ΔCAR-4 (AUC = 0.706) or ΔCAR-14 (AUC = 0.712). Multivariate analysis identified ΔCAR-7 (HR = 1.53), baseline Model for End-Stage Liver Disease-Sodium (MELD-Na) score (HR = 1.08), and hepatic encephalopathy grade (HR = 1.92) as independent predictors of 28-day mortality (all <i>P</i> < 0.05). The COSSH-CAR model, which incorporated these parameters, showed superior predictive performance (AUC = 0.832) for 28-day mortality compared with established prognostic scores, including Child-Pugh (AUC = 0.721), MELD-Na (AUC = 0.768) and COSSH-ACLF (AUC = 0.786) and effectively stratified patients into three risk categories with significantly different survival rates (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>Dynamic changes in CAR during the first week provide important prognostic information in patients with COSSH-ACLF, surpassing baseline values and conventional inflammatory markers. The novel COSSH-CAR model improves risk stratification and may support clinical decision-making in the management of ACLF, pending external validation in diverse populations.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"110652"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xue Feng, Nan-Nan Li, Gui-Jian Liu, Cheng An, Chao Liu
{"title":"Anti-hepatitis B virus effects of traditional Chinese medicine: Learning from clinical trials in the past twenty years.","authors":"Xue Feng, Nan-Nan Li, Gui-Jian Liu, Cheng An, Chao Liu","doi":"10.4254/wjh.v17.i9.107806","DOIUrl":"10.4254/wjh.v17.i9.107806","url":null,"abstract":"<p><p>Hepatitis B virus (HBV) is a serious global public health concern. Although nucleoside drugs and interferons can significantly inhibit HBV replication, issues such as drug resistance and low clinical cure rates remain. Traditional Chinese medicine (TCM) is widely used in the treatment of chronic hepatitis B (CHB) in China, with anti-inflammatory, anti-fibrotic, and liver-protective effects; however, reports on its antiviral effects are still inconsistent. We retrieved multicenter clinical studies and meta-analyses of TCM treatment for CHB over the past two decades. The results revealed that TCM has a certain anti-HBV effect, and when combined with antiviral drugs, it can significantly improve antiviral efficacy. It was demonstrated that TCM most effectively promotes serum HBV e antigen conversion to negative, followed by the ability to reduce HBV DNA levels, facilitating HBV surface antigen loss, and improving the treatment of CHB.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"107806"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Noninvasive prediction of clinically significant portal hypertension in metabolic dysfunction-associated steatotic liver disease compared to other chronic liver diseases.","authors":"Muaaz Masood, Ragesh Babu Thandassery","doi":"10.4254/wjh.v17.i9.109691","DOIUrl":"10.4254/wjh.v17.i9.109691","url":null,"abstract":"<p><p>Liver biopsy is rarely performed for the diagnosis of compensated advanced chronic liver disease (cACLD) in the current clinical hepatology practice. In the early stage, cACLD presents without portal hypertension, and in the later stage, it presents with portal hypertension. Hepatic venous pressure gradient measurement is the gold standard for diagnosing portal hypertension, but it is rarely used due to its invasive nature. The recent Baveno VII consensus recommends a noninvasive strategy for the diagnosis of cACLD and clinically significant portal hypertension (CSPH). However, there is some uncertainty regarding the diagnostic accuracy of Baveno VII criteria for predicting CSPH among patients with metabolic dysfunction-associated steatotic liver disease (MASLD). This is pertinent as MASLD has become the most important cause of cACLD in the United States. This mini-review outlines the diagnostic performance of Baveno VII criteria and other noninvasive criteria for predicting CSPH in patients with cACLD from MASLD compared to non-MASLD causes.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"109691"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Interleukin-36 subfamily cytokines in liver diseases.","authors":"Zhe-Kun Xiong, Si-Min Gu, Yi-Yuan Zheng","doi":"10.4254/wjh.v17.i9.109429","DOIUrl":"10.4254/wjh.v17.i9.109429","url":null,"abstract":"<p><p>In this letter, we discuss the recently published study by Pan <i>et al</i>, which investigated the relationships between interleukin-36 (IL-36) subfamily cytokines and the gut microbiota in patients diagnosed with liver cirrhosis. This observational study revealed that the serum levels of IL-36α, IL-36γ, and IL-38 were significantly elevated in liver cirrhosis patients, accompanied by a distinct gut microbiota profile. These findings provide novel insights into the role of inflammatory cytokines in the imbalance of the gut-liver axis. Meanwhile, in our studies, it was found that IL-36γ is considerably increased in a mouse model of metabolic dysfunction-associated liver disease, which may be linked to the activation of T helper type 17 cells and macrophages. Thus, this letter provides a brief introduction to the role of IL-36 in liver diseases and anticipates further studies aimed at elucidating the full potential of IL-36 in the development of liver diseases.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"109429"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trung Hieu Doan, Khue Minh Nguyen, Xung Van Nguyen, Anh Thi Ngoc Pham, Nhan Duc Le
{"title":"Evaluating thresholds of Mac-2 binding protein glycosylation isomer in association with clinical outcomes in patients with cirrhosis.","authors":"Trung Hieu Doan, Khue Minh Nguyen, Xung Van Nguyen, Anh Thi Ngoc Pham, Nhan Duc Le","doi":"10.4254/wjh.v17.i9.109179","DOIUrl":"10.4254/wjh.v17.i9.109179","url":null,"abstract":"<p><strong>Background: </strong>Cirrhosis is a progressive condition characterized by fibrosis that can lead to severe complications and increased mortality. The mac-2 binding protein glycosylation isomer (M2BPGi) is a prominent biomarker for predicting hepatocellular carcinoma (HCC) and cirrhosis-induced esophageal varices (EV).</p><p><strong>Aim: </strong>To investigate thresholds of M2BPGi associated with HCC, EV, and decompensation in patients with cirrhosis.</p><p><strong>Methods: </strong>This was a prospective study. A total of 153 patients with cirrhosis who met the inclusion criteria were enrolled. The patients were diagnosed with HCC and EV according to the Baveno VII and European Association for the Study of the Liver guidelines. Baseline serum M2BPGi levels were assessed along with other routine tests. The data analysis aimed to determine the cutoff values of M2BPGi for predicting EV and HCC.</p><p><strong>Results: </strong>In the study 85.6% of patients were Child-Pugh B and C. M2BPGi mean cutoff index was 7.1 ± 3.7, showing no significant etiological differences. However, M2BPGi levels varied significantly among Child-Pugh classes, EV classifications, and between patients with and without HCC (<i>P</i> < 0.01). M2BPGi cutoff values for predicting HCC, EV, and decompensated cirrhosis were 6.50, 6.64, and 5.25, respectively. Multivariate analysis confirmed M2BPGi as an independent risk factor for EV [adjusted odds ratio (aOR): 1.3, 95%CI: 1.08-1.64] and liver decompensation (aOR: 2.11, 95%CI: 1.37-3.83). Area under the curve of M2BPGi for HCC differentiation was 0.71. An algorithm combining alpha-fetoprotein (AFP) and M2BPGi detected 26 of 28 HCC cases with 98.04% accuracy <i>vs</i> 10 cases by AFP alone.</p><p><strong>Conclusion: </strong>Serum M2BPGi predicted cirrhosis complications, including decompensation and varices, especially in HCC. Combined with AFP, it enhanced HCC detection. Future liver biopsy studies are needed for tissue confirmation.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"109179"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sayan Malakar, Umair Shamsul Hoda, Suprabhat Giri, Arghya Samanta, Akash Roy, Rajat Gupta, S Rakesh Kumar, Mayank Agarwal, Anubhav Pawar, Sumit Rungta, Uday C Ghoshal
{"title":"Difficult to treat and refractory autoimmune hepatitis: Recent advances in pharmacological management.","authors":"Sayan Malakar, Umair Shamsul Hoda, Suprabhat Giri, Arghya Samanta, Akash Roy, Rajat Gupta, S Rakesh Kumar, Mayank Agarwal, Anubhav Pawar, Sumit Rungta, Uday C Ghoshal","doi":"10.4254/wjh.v17.i9.110264","DOIUrl":"10.4254/wjh.v17.i9.110264","url":null,"abstract":"<p><p>Autoimmune hepatitis (AIH) is a rare cause of chronic liver disease. The exact pathophysiology of AIH is unknown. Breakdown of self-tolerance against hepatic antigens and molecular mimicry are often implicated in the pathogenesis of AIH. Immunosuppressive therapy is the mainstay of treatment; however, 10%-25% of patients with AIH may not respond to primary therapy. Those patients are often salvaged with second- and third-line immunosuppressive therapy. Workup for other concomitant diseases should be done for patients who fail to respond to primary immunosuppressive therapy. Concurrent metabolic dysfunction-associated steatotic liver disease, alcohol-related liver disease, overlap syndrome (AIH with primary biliary cholangitis or sclerosing cholangitis), chronic hepatitis B virus, hepatitis C virus, and human immunodeficiency virus infection should be ruled out in such cases. Targeting the concomitant etiology may lead to resolution of the clinical symptoms and induce biochemical and histological remission. Isolated AIH without other etiologies for liver injury should be managed with a higher dose of steroids, azathioprine, or other immunosuppressive agents. Second- and third-line immunosuppressive agents include mycophenolate mofetil, cyclosporine, tacrolimus, infliximab, and rituximab. Patients with AIH may present with acute severe AIH (AS-AIH) and AIH-related acute on chronic liver failure, and they often require liver transplantation. The terms refractory or difficult-to-treat AIH have been used interchangeably and have no distinct definition. Difficult-to-treat AIH includes patients with intolerable side effects, fulminant disease (AIH with acute on chronic liver failure and AS-AIH), AIH in pregnancy, and HIV infection. Patients who fail to respond to standard first-line immunosuppressive therapy should be classified as refractory AIH. This review addresses the issues in the management of difficult-to-treat AIH with recent advances in pharmacological management.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"110264"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Postoperative adjuvant management in hepatocellular carcinoma: A review of therapeutic efficacy and prognostic outcomes.","authors":"Fei Liu, Jing Zhang, Kai Li","doi":"10.4254/wjh.v17.i9.107631","DOIUrl":"10.4254/wjh.v17.i9.107631","url":null,"abstract":"<p><p>Primary liver cancer is the sixth most prevalent malignancy worldwide and the third leading cause of cancer-related death. According to the latest data from the National Cancer Center of China, its mortality rate has risen, making it the country's second-deadliest tumor. Hepatocellular carcinoma (HCC), the predominant histological subtype, remains a substantial therapeutic challenge. Hepatectomy is the treatment of choice for HCC; however, because of its insidious onset and aggressive progression, the global 5-year survival rate is only 14.1%, and up to 70% of patients experience recurrence within five years after surgery. Consequently, reducing postoperative recurrence and prolonging survival have become critical research priorities. Currently, no consensus or guidelines exist regarding the clinical efficacy or potential synergistic effects of diagnostic and therapeutic strategies to prevent postoperative recurrence. In recent years, interest has grown in systemic therapies and combined local modalities - particularly targeted agents and immune checkpoint inhibitors, as adjuvant treatments. This review synthesizes recent advances in targeted and immunotherapeutic adjuvant therapies for postoperative HCC to inform clinical practice and improve patient outcomes.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"107631"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}