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Review

Hepatocyte Plasticity in Liver Health and Disease: Zonation, Regeneration, Lineage Conversion, and Hepatic Malignancy
Xuan Wang, Yunfang Wang, Shuyong Wang
Received May 19, 2026  Accepted September 9, 2026  Published online September 11, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0630    [Accepted]
Hepatocytes are highly specialized epithelial cells that maintain liver metabolic homeostasis, yet they also display remarkable plasticity in response to physiological demands, injury, disease, and oncogenic stress. In this review, we propose hepatocyte plasticity as an integrative framework that links homeostatic metabolic zonation, injury‑ and disease‑induced zonal remodeling and regeneration, hepatobiliary lineage conversion, and zonally biased malignant transformation. We first delineate homeostatic liver zonation as the baseline spatial architecture that constrains, rather than itself constitutes, hepatocyte plasticity, whereas dynamic re-zonation and state conversion represent plastic responses to perturbation. We further propose a conceptual framework that categorizes these plastic responses into four distinct yet interconnected modalities: transient adaptive state transitions, partial lineage conversion, transdifferentiation, and malignant lineage switching. We delineate the multiscale regulatory mechanisms underpinning each category, and critically assess the translational gaps between murine models and human disease. We further explore the therapeutic duality of this plasticity, evaluating emerging approaches that seek either to exploit its regenerative potential for liver repair and disease regression, or to counteract its pathological roles in cancer progression. By integrating these insights, this review establishes a comprehensive framework for understanding hepatocyte plasticity as a central determinant of liver pathobiology and highlights its translational potential for precision therapeutics in liver disease and cancer.
  • 118 View
  • 11 Download

Original Article

Co-repression of Yap1 and Sox9 abrogates established cholangiocarcinoma by eliminating transcriptional compensation
Minwook Kim, Shikai Hu, Yoojeong Park, Joseph Kwon, Laura Molina, Li-Ju Wang, Jia-Jun Liu, Silvia Liu, Aatur Singhi, Yu-Chiao Chiu, Sungjin Ko
Clin Mol Hepatol 2026;32(3):1305-1320.
Published online April 3, 2026
DOI: https://doi.org/10.3350/cmh.2025.1170
Background/Aims
Intrahepatic cholangiocarcinoma (iCCA) represents an unmet clinical need due to its increasing incidence, aggressive biology, and limited treatment options. The extremely low-response rates to current systemic regimens and the emergence of adaptive resistance to targeted therapies underscore the urgent need for alternative therapeutic strategies. Given that the lineage-defining transcription factors SOX9 and YAP1 are central regulators of cholangiocyte and iCCA identity, we investigated their functional roles as potential therapeutic vulnerabilities across multiple preclinical models.
Methods
Patient tissue-microarray analysis, Sleeping Beauty hydrodynamic tail vein injection–based iCCA models, and Cre-mediated inducible gene deletion systems were used to investigate the roles of Sox9 and Yap1. Deep-learning– based prediction, RNA-seq, chromatin immunoprecipitation sequencing and immunohistochemistry analyses were performed to delineate transcriptional networks and downstream effectors associated with SOX9/ YAP1 signaling.
Results
Dual deletion of Sox9 and Yap1 effectively eradicated advanced iCCA while preserving intrahepatic bile ducts, regardless of oncogenic drivers. Mechanistically, SOX9 and YAP1 transcriptionally compensated for each other when one was absent, and ILF2 and MGAT5 were identified as key downstream effectors mediating this compensatory mechanism. Loss of Ilf2 and Mgat5 suppressed iCCA, whereas overexpression of Ilf2 following Sox9/Yap1 co-deletion restored tumor development, indicating that ILF2 can functionally substitute for YAP1 and SOX9 in sustaining iCCA.
Conclusions
Co-targeting SOX9 and YAP1 offers a promising and safe broad-spectrum preventive/therapeutic approach for iCCA, potentially overcoming resistance to YAP1 inhibition. The adaptive resistance mechanism identified may extend to other malignancies, providing insights for addressing the advanced resistance to YAP1-TEAD-directed therapies.
  • 2,884 View
  • 185 Download

Review

From steatosis to metastasis: microenvironmental reprogramming of the liver in metabolic dysfunction-associated steatotic liver disease
Gyu Jeong Cho, Sun Myoung Kim, Yoon Mee Yang, Ekihiro Seki
Clin Mol Hepatol 2026;32(3):1135-1157.
Published online March 25, 2026
DOI: https://doi.org/10.3350/cmh.2025.1389
Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently gained attention as a risk factor for primary liver cancer and extrahepatic cancers. Increasing evidence shows that MASLD creates a fibrotic, immunosuppressive tumor microenvironment that supports metastatic growth, making it a risk factor for liver metastasis from extrahepatic tumors, such as colorectal cancer. In steatotic liver, tumor-stromal interactions promote colorectal liver metastasis through several mechanisms, including extracellular vesicles enriched with oncogenic microRNAs, hyaluronan synthase 2-mediated hyaluronic acid production by activated hepatic stellate cells and cancer-associated fibroblasts, M2-polarized tumor-associated macrophage infiltration, and Yes-associated protein-dependent tumor signaling. In this review, we summarize key pathways involved in a pre- and pro-metastatic niche in the liver, such as extracellular vesicle-mediated intercellular communication, feed-forward loops between tumor cells and stromal fibroblasts, and hyaluronic acid-induced extracellular matrix remodeling and immune cell modulation, all of which impair antitumor immunity and promote immune escape. We also discuss how targeting hyaluronic acid synthesis, interleukin-1 signaling, or CXCR2 can restore antitumor immunity and improve responses to programmed cell death protein-1 blockade. These therapeutic approaches may offer promising benefits for patients with colorectal cancer liver metastasis.
  • 2,180 View
  • 167 Download

Original Article

Interleukin-1β as target to induce synthetic lethality in KRAS mutant biliary tract cancer
Shijie Li, Yukai Shan, Tianen Chen, Win Topatana, Sarun Juengpanich, Ziyi Lu, Yuchao Sun, Tianao Xie, Ruijing Ruijing, Lidan Hou, Jiang Chen, Guojun Chen, Jiemin Lv, Xianjue Ma, Pengjuan Guo, Dan Gabriel Duda, Xiujun Cai, Mingyu Chen
Clin Mol Hepatol 2026;32(2):904-918.
Published online February 20, 2026
DOI: https://doi.org/10.3350/cmh.2025.1278
Background/Aims
Biliary tract cancer (BTC) frequently harbors KRAS mutations, which are associated with resistance to traditional treatment and a poor prognosis. Synthetic lethality (SL) strategy may provide other targets of KRAS. Therefore, we aim to identify and validate potential therapeutic targets of KRAS for the treatment of BTC via SL.
Methods
The dependency (DepMap) projects were used to predict the synthetic lethal gene of KRAS. FDA-approved anticancer drug library was applied to screen potential drugs effective against KRAS-mutant BTC. Furthermore, the synthetic lethal effects or corresponding mechanisms of potential genes and drugs on BTC were investigated using KRAS-mutant and KRAS-wild type BTC cell lines, patient-derived xenografts (PDX), and KRAS oncogene-driven tumor models, as well as other KRAS-mutant cancer cell lines.
Results
Initially, we discovered that the loss of GATA2 reduced the viability of KRAS-mutant but not KRAS-wild-type BTC. Subsequently, the drug library screened out disulfiram, which primarily exerts a synthetic lethal effect by inhibiting interleukin-1β (IL-1β) in KRAS-mutant BTC. Mechanistically, GATA2 specifically enhanced the transcription of IL-1β to promote NF-κB signaling in KRAS-mutant BTC. IL-1β inhibition phenocopied GATA2 deficiency, leading to reduced KRAS-mutant BTC viability. These synthetically lethal effects were confirmed using PDX, a KRAS oncogene-driven tumor model, as well as in other KRAS-mutant cancer cell lines.
Conclusions
In summary, these results indicate that inhibiting GATA2/IL1β could be a therapeutic strategy in KRAS-mutant BTC and potentially other cancers.
  • 2,203 View
  • 156 Download

Correspondences

Correspondence to editorial 1 on “Aspirin and hepatocellular carcinoma risk in metabolic dysfunction-associated steatotic liver disease: nationwide cohort study with genetic risk analysis”
Moon Haeng Hur, Hyunjae Shin, Yoon Jun Kim
Clin Mol Hepatol 2026;32(3):e378-e380.
Published online January 27, 2026
DOI: https://doi.org/10.3350/cmh.2026.0038

Citations

Citations to this article as recorded by  Crossref logo
  • Reply to correspondence on “Aspirin and hepatocellular carcinoma risk in metabolic dysfunction-associated steatotic liver disease: nationwide cohort study with genetic risk analysis”
    Yang-Hyun Baek
    Clinical and Molecular Hepatology.2026; 32(3): e439.     CrossRef
  • 1,536 View
  • 33 Download
  • 1 Web of Science
  • Crossref
Correspondence to editorial 2 on “Aspirin and hepatocellular carcinoma risk in metabolic dysfunction-associated steatotic liver disease: nationwide cohort study with genetic risk analysis”
Hyunjae Shin, Moon Haeng Hur, Yoon Jun Kim
Clin Mol Hepatol 2026;32(3):e381-e383.
Published online January 27, 2026
DOI: https://doi.org/10.3350/cmh.2026.0037
  • 1,409 View
  • 30 Download

Original Article

COLEC12high tumor-associated macrophages orchestrate lenvatinib resistance and cancer stemness in hepatocellular carcinoma via paracrine NRG1-HER2/HER3 signaling
Jianxing Zhang, Liang Qiao, Zongfeng Wu, Dinglan Zuo, Shanshan Huang, Shaoru Liu, Zhenkun Huang, Yi Zeng, Yu Li, Yichuan Yuan, Chenwei Wang, Wei He, Jiliang Qiu, Yunfei Yuan, Yi Niu, Binkui Li
Clin Mol Hepatol 2026;32(2):772-786.
Published online January 20, 2026
DOI: https://doi.org/10.3350/cmh.2025.1059
Background/Aims
Lenvatinib resistance remains a critical barrier in advanced hepatocellular carcinoma (HCC) therapy. However, the underlying mechanisms and strategies for reversing resistance remain incompletely understood.
Methods
Integrated transcriptomics of lenvatinib-resistant patient tumors and an acquired-resistance murine model identified a novel macrophage subpopulation. Functional validation employed CRISPR-SAM screening, conditioned medium (CM) assays, subcutaneous/orthotopic xenografts, patient-derived organoids (PDOs), and patient-derived xenografts (PDXs). Mechanistic studies included ChIP-qPCR, co-immunoprecipitation, and pharmacologic targeting. Clinical relevance was assessed in a retrospective cohort.
Results
Resistant HCC exhibited significant enrichment of a COLEC12high TAM subset , which correlated with poor survival and treatment response. These TAMs secreted neuregulin-1 (NRG1) , activating HER2/HER3-AKT signaling in tumor cells to drive cancer stemness and lenvatinib resistance. Mechanistically, in TAMs COLEC12 sequestered STAT1 in the cytoplasm, preventing its phosphorylation, and thereby derepressing STAT3-mediated NRG1 transcription. Depletion of NRG1 reversed the stemness phenotypes and resensitized tumors to lenvatinib both in vitro and in vivo. Clinically, high NRG1 expression predicted an inferior lenvatinib response and shorter survival. Crucially, the bispecific anti-HER2/HER3 antibody zenocutuzumab restored lenvatinib efficacy in PDOs, PDXs, and murine models.
Conclusions
Our work establishes the COLEC12high TAM/NRG1 axis as a master regulator of therapeutic resistance and identifies NRG1 as a predictive biomarker, providing a clinically actionable strategy to overcome lenvatinib resistance in HCC.

Citations

Citations to this article as recorded by  Crossref logo
  • COLEC12high tumor-associated macrophages: A novel paracrine axis driving lenvatinib resistance in hepatocellular carcinoma: Editorial on “COLEC12high tumor-associated macrophages orchestrate lenvatinib resistance and cancer stemness in hepatocellular carc
    Ji Won Han
    Clinical and Molecular Hepatology.2026; 32(3): 1463.     CrossRef
  • 3,103 View
  • 292 Download
  • 1 Web of Science
  • Crossref

Review

Hepatocellular carcinoma surveillance: a health economic evaluation
Qi-Feng Chen, Xiong-Ying Jiang, Song Chen, Jiongliang Wang, Ming Zhao
Clin Mol Hepatol 2026;32(2):536-564.
Published online January 9, 2026
DOI: https://doi.org/10.3350/cmh.2025.1060
Hepatocellular carcinoma (HCC) imposes a major health and economic burden worldwide, with disproportionate effects in low- and middle-income countries (LMICs). Surveillance in high-risk populations, typically using semiannual ultrasound and alpha-fetoprotein testing, has been shown to be cost-effective by enabling earlier detection and improving survival. Yet, its overall value is reduced by poor adherence and the limited sensitivity of ultrasound, particularly in patients with metabolic-associated steatotic liver disease. Emerging approaches—including abbreviated magnetic resonance imaging, multi-biomarker models (e.g., gender, age, AFP, AFP-L3, and DCP), and liquid biopsy assays such as methylated DNA markers—demonstrate greater diagnostic accuracy and potential economic advantages compared with conventional methods. Integration of artificial intelligence into imaging may further enhance efficiency and reduce downstream costs. Moving toward precision surveillance, guided by individualized risk stratification that incorporates etiology, fibrosis stage, and molecular profiles, can optimize allocation of resources and maximize cost-effectiveness at the population level. Interventions to improve adherence, including mailed outreach and behavioral economic incentives, have shown both clinical benefit and cost savings, underscoring the role of implementation science. Because socioeconomic disparities influence both access and outcomes, economic models must explicitly address equity to achieve sustainable impact. Future research should prioritize prospective trials that evaluate not only clinical performance but also the real-world cost-effectiveness of novel technologies and stratified surveillance strategies. For LMICs, adapting proven models into affordable, context-appropriate programs is essential. By combining prevention, precision risk assessment, innovative technologies, and equitable implementation, HCC surveillance can deliver both clinical and economic value, reducing the global burden of disease.

Citations

Citations to this article as recorded by  Crossref logo
  • Toward Precise Risk Stratification after the Functional Cure of Chronic Hepatitis B
    Moon Haeng Hur
    The Korean Journal of Gastroenterology.2026; 86(2): 71.     CrossRef
  • Burden and Regional Disparities of MASH‐Related Liver Cancer in the Asia‐Pacific Region From 1990 to 2023
    Xiao‐Dong Zhou, Qin‐Fen Chen, Daniel Q. Huang, Hung N. Luu, Giovanni Targher, Christopher D. Byrne, Huai Zhang, Mazen Noureddin, Renyi Su, Jacob George, Zobair M. Younossi, Frank Tacke, Ming‐Hua Zheng
    Liver International.2026;[Epub]     CrossRef
  • The impact of alcohol consumption on the risk of hepatocellular carcinoma across different age groups: A nationwide cohort study
    Mi Na Kim, Kyungdo Han, Dong Yun Kim, Jae Seung Lee, Hye Won Lee, Beom Kyung Kim, Seung Up Kim, Jun Yong Park, Sang Hoon Ahn, Do Young Kim
    JHEP Reports.2026; : 101975.     CrossRef
  • 3,047 View
  • 151 Download
  • 2 Web of Science
  • Crossref

Original Articles

Acetyl-coenzyme A synthetase 2-mediated acetyl-coenzyme A accumulation promotes mitophagy and tumor growth via increased H3K27ac in hepatitis B virus-related hepatocellular carcinoma
Shan Li, Jie Hu, Yihan Yan, Xinrui Liu, Xiao Dong, Huijun Liang, Xin Tang, Junji Tao, Rong Zhang, Yuan Hu, Ailong Huang, Kai Wang, Ni Tang
Clin Mol Hepatol 2026;32(2):661-682.
Published online December 19, 2025
DOI: https://doi.org/10.3350/cmh.2025.0754
Background/Aims
Acetyl coenzyme A (acetyl-CoA) is one of the most essential metabolites in cell metabolism but its function and concentration in hepatocellular carcinoma (HCC) remain elusive and controversial.
Methods
A comprehensive analysis of acetyl-CoA levels and acetyl-CoA synthetase 2 (ACSS2) expression across a range of samples, including patient specimens from both hepatitis B virus (HBV) positive and HBV negative HCC individuals, HBV-transgenic mouse HCC models, and multiple cell lines. Furthermore, to evaluate the functional significance of ACSS2 in HBV-related HCC, we implemented both genetic and pharmacological inhibition strategies targeting ACSS2. Molecular mechanism and mitophagy assessment were revealed by cleavage under target and tagmentation sequencing, RNA sequencing, bioinformatic analyses, transmission electron microscopy and JC-1 staining.
Results
Our study revealed a distinct metabolic signature of HBV-related HCC, marked by elevated acetyl-CoA, which was driven by ACSS2. ACSS2 was upregulated by the carbohydrate response element-binding protein in HBV-related HCC. Furthermore, ACSS2 improved tumor cell proliferation, an effect that was dependent on its enzymatic activity. Mechanistically, ACSS2-induced acetyl-CoA accumulation activated voltage-dependent anion channels 1 transcription through increased H3K27ac occupancy, which subsequently promoted mitophagy and HBV-related HCC tumorigenesis. Notably, targeting ACSS2 by depletion or inhibition with a catalytic inhibitor significantly suppressed tumor growth.
Conclusions
These findings not only illustrate the interplay between metabolic reprogramming, epigenetic modification, and tumorigenesis in the context of HBV infection, but also highlight ACSS2 as a novel metabolic vulnerability in HBV-related HCC. Therefore, targeting ACSS2 could be a novel strategy against HBV-related HCC.

Citations

Citations to this article as recorded by  Crossref logo
  • From metabolites to chromatin: ACSS2-driven acetyl-CoA fuels H3K27ac chromatin remodeling in HBV-associated HCC: Editorial on “Acetyl-coenzyme A synthetase 2-mediated acetyl-coenzyme A accumulation promotes mitophagy and tumor growth via increased H3K27ac
    Hyeong-Jin Cho, Sung-Gyoo Park
    Clinical and Molecular Hepatology.2026; 32(3): 1444.     CrossRef
  • Metabolic Reprogramming at the Tumor–Immune Interface in Hepatocellular Carcinoma
    Weiming Zhao, Ping Li
    Cells.2026; 15(15): 1357.     CrossRef
  • Crosstalk between mitophagy and metabolism in cancer: Mechanisms and therapeutic opportunities
    Jingyi Cheng, Ting Xiao, Zhangui Tang, Yuhan Chen
    Free Radical Biology and Medicine.2026; 255: 573.     CrossRef
  • 5,922 View
  • 558 Download
  • 3 Web of Science
  • Crossref
Aspirin and hepatocellular carcinoma risk in metabolic dysfunction-associated steatotic liver disease: nationwide cohort study with genetic risk analysis
Juhee Ahn, Moon Haeng Hur, Hyunjae Shin, Min Kyung Park, Sungho Won, Jeayeon Park, Yunmi Ko, Youngsu Park, Yun Bin Lee, Eun Ju Cho, Jeong-Hoon Lee, Su Jong Yu, Jung-Hwan Yoon, Yoon Jun Kim
Clin Mol Hepatol 2026;32(1):339-352.
Published online November 25, 2025
DOI: https://doi.org/10.3350/cmh.2025.0528
Background/Aims
The association between aspirin use and hepatocellular carcinoma (HCC) risk in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) remains unclear. This study evaluated the effect of aspirin on HCC development in MASLD patients using Korean National Health Insurance Service (NHIS) and UK Biobank (UKB) databases.
Methods
A retrospective cohort analysis was conducted using the NHIS database with a 3-year landmark design. Baseline characteristics were balanced using inverse probability of treatment weighting (IPTW) and 1:3 propensity score matching (PSM). Additionally, Mendelian randomization analysis was performed in the UKB cohort using a genomic risk score (GRS) for salicylic acid, based on genetic variants related to aspirin metabolism, as a proxy for aspirin use.
Results
In the NHIS cohort, 6,584,155 eligible patients were included, of whom 1,723,435 had MASLD. After PSM, aspirin use was associated with a significantly lower risk of HCC compared to no aspirin use, in both the overall population (adjusted subdistribution hazard ratio [ASHR]=0.86; 95% confidence interval [CI] 0.78–0.95; P=0.002) and MASLD group (ASHR=0.86; 95% CI 0.75–0.99; P=0.036). Similar results were reproduced in the IPTW population and several sensitivity and subgroup analyses. In the UKB cohort, individuals in the top 95% of GRS had a significantly lower risk of HCC compared to those in the bottom 5%, in both the overall population (ASHR=0.61; 95% CI 0.39–0.95; P=0.028) and MASLD group (ASHR=0.47; 95% CI 0.29–0.76; P=0.002).
Conclusions
Findings from both population-based and genetic analyses suggest a possible protective association between aspirin use and HCC in patients with MASLD, which warrants further validation.

Citations

Citations to this article as recorded by  Crossref logo
  • The role of platelets in the hepatocellular carcinoma immune microenvironment and their clinical prospects: a comprehensive review
    Zirong Yang, Li Qi, Dan Liu, Wenjing Wang, Junfeng Lu
    Medical Oncology.2026;[Epub]     CrossRef
  • 4,902 View
  • 317 Download
  • 7 Web of Science
  • Crossref

Reviews

Stratifying cholangiocarcinoma: tumor microenvironment, molecular drivers, and novel immunotherapeutic approaches
Cindy Xinqi Liu, Carmen Chak-Lui Wong
Clin Mol Hepatol 2026;32(1):127-155.
Published online October 14, 2025
DOI: https://doi.org/10.3350/cmh.2025.0889
Cholangiocarcinoma (CCA) is an epithelial cell cancer of the biliary tract. CCA can be further classified into intrahepatic cholangiocarcinoma (iCCA), perihilar cholangiocarcinoma (pCCA), and distal cholangiocarcinoma (dCCA) depending on the anatomical location. Until recently, the treatment for advanced CCA has remained highly reliant on chemotherapy, with gemcitabine plus cisplatin used in first-line treatment. Recent developments have led to the addition of immune checkpoint blockade (ICB) to the chemotherapy regimen, highlighting the promising potential of immunotherapies for CCA treatment. Despite these developments, most patients still do not benefit from current treatments, and response rates to ICB monotherapy remain modest. This underscores the need to develop more effective immunotherapeutic strategies. A major obstacle to this is the highly heterogenous nature of the disease. CCA tumors exhibit high inter-tumor heterogeneity in terms of anatomical locations, driver mutations, etiologies, and tumor microenvironment (TME) composition, making each patient immunologically distinct and difficult to benefit from a one-size-fits-all approach. There is a need to stratify patients according to individual disease status to identify immunotherapies and combination therapies that are most beneficial to them. Here we describe the different ways inter-tumor heterogeneity may arise in CCA, including stromal cell abundance, anatomical location, driver mutations, etiologies, TME profile, and tertiary lymphoid structure (TLS) presence. We also discuss what these factors mean to the immune microenvironment and their potential to be used as biomarkers. Careful stratification of patients is crucial in designing personalized medicine to improve survival outcomes and treatment efficacy for CCA patients.

Citations

Citations to this article as recorded by  Crossref logo
  • Integrative single-cell and machine-learning analysis identifies ac4C-related S100A13 as a causal risk gene in cholangiocarcinoma
    Yi Zheng, Yan Lin, Zilin Wang, Fazong Wu
    BMC Cancer.2026;[Epub]     CrossRef
  • Development of a prediction model integrating cardiac ultrasound parameters for cardiac complications after distal cholangiocarcinoma surgery: a retrospective cohort study
    Fangfei Wang, Shan Jin, Shaocheng Lyu, Xin Zhao, Xiuzhang Lyu, Qiang He
    BMC Medical Imaging.2026;[Epub]     CrossRef
  • Combined Model of Inflammatory-Nutritional Indicators and Tumor Markers for Predicting Prognosis in Patients with Distal Cholangiocarcinoma: A Retrospective Cohort Study
    Fangfei Wang, Jinhao Li, Xin Zhao, Shaocheng Lyu, Qiang He
    Diseases.2026; 14(3): 97.     CrossRef
  • A pyroptosis-related molecular signature stratifies prognosis and highlights GSDMB-mediated malignancy in intrahepatic cholangiocarcinoma
    Binhan Zhao, Yongji Zhu, Ziyang Jin, Xiang Li, Kainan Lin, Yifan Wang, Yunkun Lu, Wen Hua
    Biology Direct.2026;[Epub]     CrossRef
  • Multidimensional Regulatory Networks of Immune Resistance in Intrahepatic Cholangiocarcinoma: Synergistic Mechanisms of Tumor Microenvironment, Immune Cells, and Microbiota, and Novel Therapeutic Strategies
    Lingyu Kong, Hongxin Piao
    Gastrointestinal Disorders.2026; 8(3): 32.     CrossRef
  • CircUBAP2 promotes intrahepatic cholangiocarcinoma progression via PRMT1–p65 methylation and the miR-642b-5p/IL-1β axis
    Chang Li, Shuochen Liu, Changan Chen, Kai Cao, Ruixiang Chen, Xiao Xu, Jiang Chang, Yaodong Zhang, Changxian Li, Xiangcheng Li
    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease.2026; 1872(7): 168337.     CrossRef
  • mTOR signaling in cholangiocarcinoma: mechanistic insights and therapeutic opportunities
    Zhenxuan Chen, Tao Peng
    Frontiers in Pharmacology.2026;[Epub]     CrossRef
  • Machine Learning–Guided Personalized Immunochemotherapy Strategies in Intrahepatic Cholangiocarcinoma
    Jun-Hao Mei, Kai Zhang, Ying Zhang, Zhen Li, Nai-Jian Ge, Xue Han, Sui-Xing Zhong, Xiu-Ping Zhang, Ping-Ping Wu, Wei-Fu Lv, Jun Wu, Jian-Xiong Wu, Chao Wang, Hui Yan, Tian Huang, Jie Liu, Kai-Zhi Jia, Yue Liu, Jin-He Guo, Rong Liu, Gao-Jun Teng, Jian Lu
    JHEP Reports.2026; : 102004.     CrossRef
  • 5,504 View
  • 189 Download
  • 6 Web of Science
  • Crossref
Harnessing the microbiome: unveiling the influence of the gut microbiota on hepatobiliary cancer therapeutic strategies
Melody Yusong Li, Xue Qian Wu, Terence Kin Wah Lee
Clin Mol Hepatol 2026;32(1):91-126.
Published online August 25, 2025
DOI: https://doi.org/10.3350/cmh.2025.0476
The gut microbiota significantly influences hepatobiliary cancer therapeutics. Growing evidence indicates that shifts in the gut microbial ecosystem are hallmarks of hepatocellular carcinoma and cholangiocarcinoma, strongly correlating with tumor development, therapeutic resistance, and patient survival. The composition of gut microbiota has emerged as a biomarker associated with treatment outcomes across various modalities, including chemotherapy, radiotherapy, targeted therapy, and immunotherapy. Beneficial bacterial communities enhance antitumor immunity, while pathogenic taxa are linked to reduced therapeutic efficacy. Multi-omics analyses have identified microbial metabolite signatures, such as short-chain fatty acids and bile acids, as potential targets for boosting antitumor responses. This review highlights the transformative potential of leveraging the gut microbiota to enhance precision oncology in hepatobiliary cancer. Future directions should prioritize personalized microbiota modulation approaches, combinatorial therapies targeting gut-liver axis crosstalk, and large-scale validation of microbial biomarkers across diverse populations.

Citations

Citations to this article as recorded by  Crossref logo
  • Liver Transplantation Following Immune Checkpoint Inhibitor Therapy: What Do We Need to Know from Clinical and Immunological Perspective?
    Hee Sun Cho, Soon Kyu Lee
    International Journal of Molecular Sciences.2026; 27(6): 2680.     CrossRef
  • Dental prophylactic interventions are associated with lower decompensation-related hospitalizations over 2 years in cirrhosis
    Jasmohan S. Bajaj, Scott Silvey, Anas Aljabi, Janina Golob Deeb, Nilang Patel
    JHEP Reports.2026; 8(5): 101821.     CrossRef
  • Multidimensional Regulatory Networks of Immune Resistance in Intrahepatic Cholangiocarcinoma: Synergistic Mechanisms of Tumor Microenvironment, Immune Cells, and Microbiota, and Novel Therapeutic Strategies
    Lingyu Kong, Hongxin Piao
    Gastrointestinal Disorders.2026; 8(3): 32.     CrossRef
  • 4,829 View
  • 157 Download
  • 2 Web of Science
  • Crossref

Correspondence

Correspondence to letter to the editor 1 on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study”
Xianhua Mao, Mindie H. Nguyen
Clin Mol Hepatol 2026;32(2):e231-e232.
Published online July 8, 2025
DOI: https://doi.org/10.3350/cmh.2025.0704
  • 2,472 View
  • 29 Download

Letter to the Editor

Letter to the editor on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”
Dibin Liu
Clin Mol Hepatol 2026;32(2):e153-e154.
Published online May 27, 2025
DOI: https://doi.org/10.3350/cmh.2025.0537

Citations

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  • Reply to correspondence 2 on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”
    Dibin Liu
    Clinical and Molecular Hepatology.2026; 32(2): e264.     CrossRef
  • Correspondence to letter to the editor on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”
    Pojsakorn Danpanichkul, Luis Antonio Diaz, Juan Pablo Arab, Amit G. Singal, Ju Dong Yang
    Clinical and Molecular Hepatology.2026; 32(2): e246.     CrossRef
  • 3,574 View
  • 52 Download
  • 2 Web of Science
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Editorial

Rising burden of alcohol-associated liver disease and cancers: Insights into sex disparities and policy implications: Editorial on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”
Sung-Eun Kim
Clin Mol Hepatol 2026;32(1):439-442.
Published online May 15, 2025
DOI: https://doi.org/10.3350/cmh.2025.0516

Citations

Citations to this article as recorded by  Crossref logo
  • Advancing policy and practice in alcohol-associated liver disease and alcohol-attributable cancer: Correspondence to the editorial on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the Unite
    Pojsakorn Danpanichkul, Donghee Kim, Karn Wijarnpreecha, Amit G. Singal, Ju Dong Yang
    Clinical and Molecular Hepatology.2026; 32(1): e96.     CrossRef
  • Reply to correspondence 1 on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”
    Sung-Eun Kim
    Clinical and Molecular Hepatology.2026; 32(1): e125.     CrossRef
  • Hidden Burden of Alcohol Use Disorder in MASLD and MetALD: Clinical and Nomenclatural Implications
    Yuri Cho
    Gut and Liver.2025; 19(5): 637.     CrossRef
  • 3,281 View
  • 37 Download
  • Crossref

Original Article

Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study
Xianhua Mao, Xinrong Zhang, Rongtao Lai, Ka-Shing Cheung, Man-Fung Yuen, Ramsey Cheung, Wai-Kay Seto, Mindie H. Nguyen
Clin Mol Hepatol 2025;31(3):1084-1099.
Published online April 23, 2025
DOI: https://doi.org/10.3350/cmh.2024.1096
Background/Aims
Information about the association of glucagon-like peptide-1 receptor (GLP-1RA) with liver and non-liver complications is insufficient in patients with type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD). We conducted a target trial emulation study to evaluate whether GLP-1RA decreases the risk of liver and non-liver outcomes.
Methods
Patients with T2D and MASLD initiating GLP-1RA or dipeptidyl peptidase-4 inhibitor (DPP-4i) were included from 2013 to 2022 in Merative™ Marketscan® Research Databases. Primary outcomes included incidences of (1) hepatocellular carcinoma (HCC) and cirrhosis, and (2) cardiovascular disease (CVD), chronic kidney disease (CKD), and non-liver cancer. Inverse probability of treatment weighting was applied to balance baseline characteristics and Cox regression models were conducted to estimate hazard ratio (HR) and 95% confidence interval (CI).
Results
In the intention-to-treat design, GLP-1RA, compared with DPP-4i, had a significantly lower incidence (per 1,000 person-years) of HCC (0.8 vs. 1.7; HR 0.53, 95% CI 0.39–0.71), of cirrhosis (29.3 vs. 32.9; HR 0.91, 95% CI 0.86–0.96), of CVD (57.2 vs. 73.9; HR 0.90, 95% CI 0.86–0.95), of CKD (4.5 vs. 6.8; HR 0.73, 95% CI 0.64–0.84), and of non-liver cancer (16.9 vs. 22.9; HR 0.82, 95% CI 0.77–0.89). In the per-protocol design, significant inverse associations for these study outcomes still were observed, with HR 0.60–0.77.
Conclusions
In this emulated target trial of nationwide patients with T2D and MASLD, GLP-1RA use, when compared with DPP-4i, was associated with a significantly lower risk of liver and non-liver complications.

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Revisiting unmet needs in clinical research on direct-acting antiviral therapy for HCC patients: Correspondence to letter to the editor on “Direct-acting antiviral therapy for patients with HCV-related hepatocellular carcinoma: A nationwide cohort study”
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Correspondence to letter to the editor on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
Hyung Seok Kim, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun
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  • 6,307 View
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Emerging evidence supports direct-acting antiviral therapy for HCC patients beyond the early stage: Correspondence to editorial on “Direct-acting antiviral therapy for patients with HCV-related hepatocellular carcinoma: A nationwide cohort study”
Teng-Yu Lee, Pei-Chien Tsai, Shou-Wu Lee, Ming-Lung Yu
Clin Mol Hepatol 2026;32(1):e68-e71.
Published online March 4, 2025
DOI: https://doi.org/10.3350/cmh.2025.0235

Citations

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    Clinical and Molecular Hepatology.2026; 32(1): e99.     CrossRef
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Clin Mol Hepatol 2026;32(1):371-373.
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Original Articles

GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma
Hyung Seok Kim, Jung Hwan Yoon, Ji Yi Choi, Moon Gyeong Yoon, Geum Ok Baek, Minji Kang, Se Ha Jang, Won Park, Yunjin Go, Jestlin Tianthing Ng, Suk Woo Nam, Jee-Yeong Jeong, Ji Eun Han, Hyo Jung Cho, Su Bin Lim, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun
Clin Mol Hepatol 2025;31(3):914-934.
Published online February 6, 2025
DOI: https://doi.org/10.3350/cmh.2024.1038
Background/Aims
Hepatocellular carcinoma (HCC) is characterized by high recurrence and mortality, necessitating the identification of reliable biomarkers. In this study, we aimed to identify the predictive gene signatures for HCC recurrence and evaluate the efficiency of GULP PTB domain-containing engulfment adaptor 1 (GULP1) as a predictive and diagnostic marker and therapeutic target for HCC.
Methods
We analyzed genomic datasets from The Cancer Genome Atlas and Gene Expression Omnibus databases via least absolute shrinkage and selection operator Cox regression and 10-fold cross-validation, leading to the development of a 15-gene risk score model, which was validated using three independent datasets. Serum GULP1 and α-fetoprotein levels were assessed to determine the diagnostic accuracy of the model. Using clinical cohorts and patient sera, GULP1 roles were examined, and functional assays in vitro and in vivo were used to evaluate its effects on cell growth, epithelial–mesenchymal transition (EMT), ADP-ribosylation factor 6 (ARF6) activation, and β-catenin signaling.
Results
Our newly developed risk-score model accurately predicted recurrent HCC in all datasets. Among the 15 genes in the risk score model, GULP1 was overexpressed in patients with HCC and independently predicted HCC recurrence. Its expression modulation influenced cell growth and EMT, with observed effects on ARF6 activation and β-catenin signaling pathways.
Conclusions
GULP1 is a crucial biomarker for HCC, serving as a non-invasive diagnostic and predictive tool. It also plays key roles in HCC progression. Our findings highlight the potential use of GULP1 in treatment strategies targeting EMT and HCC recurrence to improve the personalized care and patient outcomes.

Citations

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  • Correspondence to letter to the editor on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
    Hyung Seok Kim, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun
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  • GULP1, a multifaceted diagnostic biomarker and potential therapeutic target in hepatocellular carcinoma: Editorial on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
    Yuhao Xie, Lu-Qi Cao, John Wurpel, Zhe-Sheng Chen
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    Juan Yang, Xinyi Li, Sheng Zheng
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    Yuhao Xie, Lu-Qi Cao, John Wurpel, Zhe-Sheng Chen
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    Soon Sun Kim, Hyung Seok Kim, Jae Youn Cheong, Jung Woo Eun
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    Pengde Lu, Ning Wang
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Direct-acting antiviral therapy for patients with hepatitis C virus-related hepatocellular carcinoma: A nationwide cohort study
Shou-Wu Lee, Sheng-Shun Yang, Pei-Chien Tsai, Chung-Feng Huang, Chi-Yi Chen, Chao-Hung Hung, Chien-Hung Chen, Chi-Ming Tai, Pin-Nan Cheng, Hsing-Tao Kuo, Kuo-Chih Tseng, Lein-Ray Mo, Ching-Chu Lo, Yi-Hsiang Huang, Han-Chieh Lin, Pei-Lun Lee, Ming-Jong Bair, Te-Sheng Chang, Chun-Yen Lin, Szu-Jen Wang, Tsai-Yuan Hsieh, Tzeng-Hue Yang, Cheng-Yuan Peng, Chi-Chieh Yang, Lee-Won Chong, Chien-Wei Huang, Chih-Wen Lin, Cheng-Hsin Chu, Ming-Chang Tsai, Jia-Horng Kao, Chun-Jen Liu, Wan-Long Chuang, Teng-Yu Lee, Ming-Lung Yu, on behalf of TACR investigators
Clin Mol Hepatol 2025;31(3):899-913.
Published online February 5, 2025
DOI: https://doi.org/10.3350/cmh.2024.1015
Background/Aims
The survival benefit of direct-acting antiviral (DAA) therapy for hepatitis C virus (HCV) infection in patients with hepatocellular carcinoma (HCC), particularly in Barcelona Clinic Liver Cancer (BCLC) stages B/C, remains largely uncertain. We aimed to explore the impact of DAA therapy on overall survival (OS) in HCC patients using a nationwide cohort study.
Methods
We utilized the nationwide Taiwan Association for the Study of the Liver (TASL) HCV Registry (TACR) database to include all adults receiving a DAA therapy for HCV, excluding those with other viral infections, liver transplantation, non-HCC malignancies, and terminal-staged HCC. We respectively analyzed the adjusted odds ratio (aOR) for sustained virological response (SVR) and adjusted hazard ratio (aHR) for OS.
Results
Between December 2013 and December 2020, 2,205 (9.3%) patients with HCC and 21,569 (90.7%) patients without HCC were include. The SVR rates were 96.6% in the HCC group and 98.8% in the non-HCC group (P<0.001), with HCC being an independent risk factor affecting SVR (aOR 0.41; 95% CI 0.31–0.54; P<0.001). In the whole patient cohort, SVR was independently associated with improved OS (aHR 0.46; 95% CI 0.35–0.60; P<0.001). Among patients with baseline HCC, SVR remained an independent factor related to OS (aHR 0.41; 95% CI 0.28–0.59; P<0.001). The impact of SVR on OS persisted significantly across BCLC stages 0/A and stages B/C.
Conclusions
High SVR rates among HCC patients underscore the importance of DAA therapy in enhancing OS, reaffirming its efficacy across various HCC stages.

Citations

Citations to this article as recorded by  Crossref logo
  • Revisiting unmet needs in clinical research on direct-acting antiviral therapy for HCC patients: Correspondence to letter to the editor on “Direct-acting antiviral therapy for patients with HCV-related hepatocellular carcinoma: A nationwide cohort study”
    Teng-Yu Lee, Pei-Chien Tsai, Shou-Wu Lee, Ming- Lung Yu
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    Teng-Yu Lee, Pei-Chien Tsai, Shou-Wu Lee, Ming-Lung Yu
    Clinical and Molecular Hepatology.2026; 32(1): e68.     CrossRef
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    Teng-Yu Lee, Sheng-Shun Yang, Pei-Chien Tsai, Chung-Feng Huang, Chi-Yi Chen, Chao-Hung Hung, Chien-Hung Chen, Chi-Ming Tai, Pin-Nan Cheng, Hsing-Tao Kuo, Kuo-Chih Tseng, Lein-Ray Mo, Ching-Chu Lo, Yi-Hsiang Huang, Han-Chieh Lin, Pei-Lun Lee, Ming-Jong Bai
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Review

Unveiling the intratumor microbiome in liver cancer: Current insights and prospective applications
Xindi Ke, Shangze Jiang, Qiaoxin Wei, Minghao Sun, Hang Sun, Mingchang Pang, Mei Liu, Lejia Sun, Huayu Yang, Yilei Mao
Clin Mol Hepatol 2025;31(3):685-705.
Published online January 22, 2025
DOI: https://doi.org/10.3350/cmh.2024.1039
The role of the gut microbiome in the development and progression of liver cancer has long been recognized. However, the presence of microbes in tumors that were previously considered sterile has only recently been discovered. The intratumor microbiome in liver cancer likely originates from various sources, including the gut, hematogenous spread from other mucosal locations, adjacent non-cancerous tissues, and co-metastasis with the tumor cells. As a newly discovered component of the tumor microenvironment, it regulates host immune responses, promotes chronic inflammation, modulates metabolic pathways, and exerts other influences in liver cancer. These unique features offer potential new biomarkers for liver cancer prognosis and treatment response. Exploring the complex interactions between intratumor microbiome and the host to modulate or target the intratumor microbiome may provide new avenues for liver cancer treatment. This article provides a comprehensive review of our current understanding regarding the potential origins of the intratumor microbiome in liver cancer, its unique characteristics, and the underlying mechanisms by which it affects liver cancer. Furthermore, we discuss the promising clinical implications and potential challenges that remain before this knowledge can be fully integrated into clinical practice.

Citations

Citations to this article as recorded by  Crossref logo
  • Intratumoral Microbe Correlated with Expression of DNA Methylation Genes in Hepatocellular Carcinoma
    Ashish Kumar, Ajeet Raj, Karan Chaman Lal, Puja
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    Zhiyue Wang, Tianqi Zhang, Yang Liu
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    Yaru Miao, Dongdong Cui, Yanghui Bi, Ruiping Zhang
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    Kaiyuan Yu, Xinyu Sun, Wanxia Ma, Jianming Yang, Xuan Sun, Lisong Zhang, Yumeng Liu, Tianshu Ren, Qi Wang, Jingyu Wang, Xiao Li, Xianping Peng, Liu Yang, Junqiang Lv, Zhi Yao, Zhi‐Song Zhang, Quan Wang
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    Shilin Wang, Ziyi Liu, Chunyun Jiang, Yanting Wei, Guohong Liu, Yunbao Pan
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    Haiyang Liu, Zun Fan, Zhen Liu, Lei Qin, Xin Zhao
    Advanced Science.2026;[Epub]     CrossRef
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    You-Peng Ding, Cui-Cui Liu, Ke-Da Yu
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  • Crossref

Original Article

High Steatosis-Associated Fibrosis Estimator scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction-associated steatotic liver disease
Tung-Hung Su, Sheng-Shun Yang, Mei-Hsuan Lee, Wei-Yu Kao, Shang-Chin Huang, Fen-Fang Chen, Francis SK Poon, Lung-Wen Tsai, Yi-Ting Chen, Che Lin, Weichung Wang, W Ray Kim, Jia-Horng Kao
Clin Mol Hepatol 2025;31(3):796-809.
Published online January 6, 2025
DOI: https://doi.org/10.3350/cmh.2024.0822
Background/Aims
There are no hepatocellular carcinoma (HCC) surveillance recommendations for non-viral chronic liver diseases (CLD), such as metabolic dysfunction-associated steatotic liver disease (MASLD). We explored the Steatosis-Associated Fibrosis Estimator (SAFE) score to predict HCC in MASLD and other CLD etiologies.
Methods
Patients with various CLDs were included from medical centers in Taiwan. The SAFE score, consisting of age, body mass index, diabetes, and laboratory data, was calculated at baseline, and patients were traced for new development of HCC. The predictability of the SAFE score for HCC was analyzed using the sub-distribution hazard model with adjustments for competing risks.
Results
Among 12,963 CLD patients with a median follow-up of 4 years, 258 developed HCC. The SAFE score classifies 1-, 3-, and 5-year HCC risk regardless of CLD etiologies. High (≥100) and intermediate (0–100) SAFE scores increased 11 and 2 folds HCC risks compared to low (<0) SAFE scores. Combining two lower risk tiers (SAFE<100), a high SAFE score (≥100) was associated with a 7.5-fold risk of HCC (adjusted sub-distributional hazard ratio [aSHR] 7.54; 95% confidence interval (CI) 5.38–10.60). A high SAFE score increased the risks of HCC in subgroups of viral hepatitis, non-viral hepatitis (aSHR 11.10; 95% CI 3.97–31.30) and MASLD (aSHR 4.23; 95% CI 1.43–12.50). A hospital cohort (n=8,103) and a community MASLD cohort (n=120,166) validated the high SAFE score (≥100) for HCC risk prediction.
Conclusions
The SAFE score stratifies high risks for HCC in CLD patients regardless of etiologies and helps to select at-risk candidates for HCC surveillance.

Citations

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  • HCC predictors in routine practice for patients with chronic liver diseases: Correspondence to editorial on “High SAFE scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction associated steatotic liver disease”
    Tung-Hung Su, Jia-Horng Kao
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    Michael Kwan-Lung Ko, Loey Lung-Yi Mak
    Clinical and Molecular Hepatology.2026; 32(1): 371.     CrossRef
  • Risk stratification for hepatocellular carcinoma in metabolic dysfunction-associated steatotic liver disease: Editorial on “High Steatosis-Associated Fibrosis Estimator scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic
    Ho Soo Chun, Minjong Lee
    Clinical and Molecular Hepatology.2026; 32(1): 368.     CrossRef
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    Heechul Nam, Sung Won Lee
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  • Crossref

Reviews

Hepatic neoplasm

Gut microbiota-mediated gut-liver axis: a breakthrough point for understanding and treating liver cancer
Chenyang Li, Chujun Cai, Chendong Wang, Xiaoping Chen, Bixiang Zhang, Zhao Huang
Clin Mol Hepatol 2025;31(2):350-381.
Published online December 11, 2024
DOI: https://doi.org/10.3350/cmh.2024.0857
The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

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Hepatic neoplasm

Liquid biopsy in hepatocellular carcinoma: Challenges, advances, and clinical implications
Jaeho Park, Yi-Te Lee, Vatche G. Agopian, Jessica S Liu, Ekaterina K. Koltsova, Sungyong You, Yazhen Zhu, Hsian-Rong Tseng, Ju Dong Yang
Clin Mol Hepatol 2025;31(Suppl):S255-S284.
Published online November 28, 2024
DOI: https://doi.org/10.3350/cmh.2024.0541
Hepatocellular carcinoma (HCC) is an aggressive primary liver malignancy often diagnosed at an advanced stage, resulting in a poor prognosis. Accurate risk stratification and early detection of HCC are critical unmet needs for improving outcomes. Several blood-based biomarkers and imaging tests are available for early detection, prediction, and monitoring of HCC. However, serum protein biomarkers such as alpha-fetoprotein have shown relatively low sensitivity, leading to inaccurate performance. Imaging studies also face limitations related to suboptimal accuracy, high cost, and limited implementation. Recently, liquid biopsy techniques have gained attention for addressing these unmet needs. Liquid biopsy is non-invasive and provides more objective readouts, requiring less reliance on healthcare professional’s skills compared to imaging. Circulating tumor cells, cell-free DNA, and extracellular vesicles are targeted in liquid biopsies as novel biomarkers for HCC. Despite their potential, there are debates regarding the role of these novel biomarkers in the HCC care continuum. This review article aims to discuss the technical challenges, recent technical advancements, advantages and disadvantages of these liquid biopsies, as well as their current clinical application and future directions of liquid biopsy in HCC.

Citations

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    Clinical and Molecular Hepatology.2026; 32(3): e427.     CrossRef
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    Ruikang Ming, Xuemeng Gao, Xiaoying Hu, Zhihan Yang, Chunzi Liang, Guo-Jun Zhang, Baoping Luo, Shi-Bo Cheng, Yu-Tao Li
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Correspondences

Hepatic neoplasm

Correspondence to letter to the editor on “Transarterial radioembolization versus tyrosine kinase inhibitor in hepatocellular carcinoma with portal vein thrombosis”
Moon Haeng Hur, Yoon Jun Kim
Clin Mol Hepatol 2025;31(1):e93-e95.
Published online November 6, 2024
DOI: https://doi.org/10.3350/cmh.2024.0943
  • 6,008 View
  • 54 Download

Hepatic neoplasm

Correspondence to editorial 2 on “Genomic biomarkers to predict response to atezolizumab plus bevacizumab immunotherapy in hepatocellular carcinoma: insights from the IMbrave150 trial”
Sun Young Yim, Sung Hwan Lee, Ji Hoon Kim, Sunyoung S Lee, Ahmed O Kaseb, Ju-Seog Lee
Clin Mol Hepatol 2025;31(1):e84-e86.
Published online October 7, 2024
DOI: https://doi.org/10.3350/cmh.2024.0830
  • 6,077 View
  • 51 Download

Hepatic neoplasm

Correspondence to editorial 1 on “Genomic biomarkers to predict response to atezolizumab plus bevacizumab immunotherapy in hepatocellular carcinoma: insights from the IMbrave150 Trial”
Sung Hwan Lee, Sun Young Yim, Ji Hoon Kim, Sunyoung S. Lee, Ahmed O. Kaseb, Ju-Seog Lee
Clin Mol Hepatol 2025;31(1):e81-e83.
Published online October 7, 2024
DOI: https://doi.org/10.3350/cmh.2024.0829

Citations

Citations to this article as recorded by  Crossref logo
  • Reply to correspondence on “Genomic biomarkers to predict response to atezolizumab plus bevacizumab immunotherapy in hepatocellular carcinoma: Insights from the IMbrave150 trial”
    Hiroaki Kanzaki, Yujin Hoshida
    Clinical and Molecular Hepatology.2025; 31(1): e121.     CrossRef
  • 6,512 View
  • 48 Download
  • Crossref

Hepatic neoplasm

Correspondence to letter to the editor on “Genomic biomarkers to predict response to atezolizumab plus bevacizumab immunotherapy in hepatocellular carcinoma: Insights from the IMbrave150 trial”
Sung Hwan Lee, Sun Young Yim, Ji Hoon Kim, Sunyoung S Lee, Ahmed O Kaseb, Peng Wei, Ju-Seog Lee
Clin Mol Hepatol 2025;31(1):e110-e112.
Published online October 2, 2024
DOI: https://doi.org/10.3350/cmh.2024.0828
  • 6,129 View
  • 59 Download

Viral hepatitis

Correspondence to letter to the editor on “Non-linear association between liver fibrosis scores and viral load in patients with chronic hepatitis B”
Gi-Ae Kim, Seung Won Choi, Young-Suk Lim
Clin Mol Hepatol 2025;31(1):e108-e109.
Published online August 5, 2024
DOI: https://doi.org/10.3350/cmh.2024.0619
  • 6,450 View
  • 41 Download

Editorial

From past to pandemic: Health disparities in US hepatobiliary cancer mortality before and during COVID-19: Editorial on “Burden of mortality from hepatocellular carcinoma and biliary tract cancers by race and ethnicity and sex in US, 2018–2023”
Ilona Argirion
Clin Mol Hepatol 2025;31(1):286-289.
Published online August 5, 2024
DOI: https://doi.org/10.3350/cmh.2024.0597
  • 8,062 View
  • 46 Download

Original Article

Viral hepatitis

Non-linear association between liver fibrosis scores and viral load in patients with chronic hepatitis B
Gi-Ae Kim, Seung Won Choi, Seungbong Han, Young-Suk Lim
Clin Mol Hepatol 2024;30(4):793-806.
Published online July 19, 2024
DOI: https://doi.org/10.3350/cmh.2024.0252
Background/Aims
Serum hepatitis B virus (HBV) DNA levels and non-invasive liver fibrosis scores are significantly associated with hepatocellular carcinoma (HCC) risk in chronic hepatitis B (CHB) patients. Nonetheless, the relationship between HBV DNA levels and liver fibrosis scores is unclear.
Methods
A historical cohort comprising 6,949 non-cirrhotic Korean CHB patients without significant alanine aminotransferase elevation was investigated. The association of HBV DNA levels with the aspartate aminotransferase to platelet ratio index (APRI) and fibrosis (FIB)-4 score at baseline was analyzed using general linear models.
Results
In HBeAg-negative patients (n=4,868), HBV DNA levels correlated linearly with both APRI and FIB-4 scores. In contrast, in HBeAg-positive patients (n=2,081), HBV DNA levels correlated inversely with both APRI and FIB-4 scores. Across the entire cohort, a significant non-linear parabolic relationship was identified between HBV DNA levels and fibrosis scores, independent of age and other covariates. Notably, moderate viral loads (6–7 log10 IU/mL) corresponded to the highest APRI and FIB-4 scores (p<0.001). Over a median 10-year follow-up, 435 patients (6.3%) developed HCC. Higher APRI scores ≥0.5 and FIB-4 scores ≥1.45 were significantly associated with elevated HCC risk (p<0.001 for both). HBV DNA level remained a significant predictive factor for HCC development, even after adjusting for APRI or FIB-4 scores.
Conclusions
HBV viral load is significantly correlated with APRI and FIB-4 scores, and is also associated with HCC risk independent of those scores in CHB patients. These findings suggest that HBV DNA level is associated with hepatocarcinogenesis through both direct and indirect pathways.

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Reply to Correspondence

Viral hepatitis

Reply to correspondence on “Metformin and statins reduce hepatocellular carcinoma risk in chronic hepatitis C patients with failed antiviral therapy”
Seren M. Gedallovich, Paul Y. Kwo
Clin Mol Hepatol 2024;30(4):1050-1052.
Published online July 12, 2024
DOI: https://doi.org/10.3350/cmh.2024.0546
  • 6,165 View
  • 40 Download

Letter to the Editor

Hepatic neoplasm

Dipeptidyl peptidase-4 inhibitors are associated with improved survival of patients with diabetes mellitus and hepatocellular carcinoma receiving immunotherapy: Letter to the editor on “Statin and aspirin for chemoprevention of hepatocellular carcinoma: Time to use or wait further?”
Dorothy Cheuk-Yan Yiu, Huapeng Lin, Vincent Wai-Sun Wong, Grace Lai-Hung Wong, Ken Liu, Terry Cheuk-Fung Yip
Clin Mol Hepatol 2024;30(4):970-973.
Published online July 4, 2024
DOI: https://doi.org/10.3350/cmh.2024.0280

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Editorial

Hepatic neoplasm

Engineering HBV-specific T cells for the treatment of HBV-related HCC and HBV infection: Past, Present, and Future. Editorial on “Genetically-modified, redirected T cells target hepatitis B surface antigen-positive hepatocytes and hepatocellular carcinoma lesions in a clinical setting”
Antonio Bertoletti, Anthony T Tan
Clin Mol Hepatol 2024;30(4):728-734.
Published online June 27, 2024
DOI: https://doi.org/10.3350/cmh.2024.0469

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Original Article

Hepatic neoplasm

Burden of mortality from hepatocellular carcinoma and biliary tract cancers by race and ethnicity and sex in US, 2018–2023
Donghee Kim, Richie Manikat, Karn Wijarnpreecha, George Cholankeril, Aijaz Ahmed
Clin Mol Hepatol 2024;30(4):756-770.
Published online June 24, 2024
DOI: https://doi.org/10.3350/cmh.2024.0318
Backgrounds/Aims
The trends in mortality of hepatocellular carcinoma (HCC) and biliary tract cancers stratified by sex and race/ethnicity in the US continue to evolve. We estimated the sex- and race/ethnicity-based trends in HCC and biliary tract cancers-related mortality in US adults with a focus on disease burden.
Methods
We performed a population-based analysis using the US national mortality records from 2018 to 2023. We identified HCC and biliary tract cancer using appropriate ICD-10 codes. Temporal trends in mortality were calculated by joinpoint analysis with annual percentage change (APC).
Results
Annual age-standardized mortality from HCC decreased steadily with an APC of –1.4% (95% confidence interval [CI]: –2.0% to –0.7%). While there was a linear increase in intrahepatic cholangiocarcinoma-related mortality (APC: 3.1%, 95% CI: 1.2–4.9%) and ampulla of Vater cancer-related mortality (APC: 4.1%, 95% CI: 0.5–7.9%), gallbladder cancer-related mortality decreased (APC: –1.9%, 95% CI: –3.8% to –0.0%). Decreasing trends in mortality from HCC were noted in males, not females. HCC-related mortality decreased more steeply in racial and ethnic minority individuals compared with non-Hispanic White individuals. Racial and ethnic differences in trends in mortality for biliary tract cancers depended on the malignancy’s anatomical site.
Conclusions
While the annual mortality for HCC and gallbladder cancer demonstrated declining trends, ICC- and AVC-related mortality continued to increase from 2018 to 2023. Although racial and ethnic minority individuals in the US experienced disproportionately higher HCC and biliary tract cancer, recent declines in HCC may be primarily due to declines among racial and ethnic minority individuals and males.

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Editorial

Hepatic neoplasm

Unveiling etiology-specific blood biomarkers in hepatocellular carcinoma: A gateway to personalized medicine: Editorial on “Multiomics profiling of buffy coat and plasma unveils etiology-specific signatures in hepatocellular carcinoma”
Joseph C. Ahn, Ju Dong Yang
Clin Mol Hepatol 2024;30(4):689-691.
Published online May 14, 2024
DOI: https://doi.org/10.3350/cmh.2024.0348

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to letter to the editor on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
    Hyung Seok Kim, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun
    Clinical and Molecular Hepatology.2026; 32(1): e103.     CrossRef
  • Metabolites involvement in the growth and spread of liver cancer
    Anurag Kumar Gautam, Vipin Kumar, Archana Bharti Sonkar, Amita Singh, Deepankar Yadav, Nitin Rajan, Pranesh Kumar, Sanjay Singh, Sudipta Saha, Vijayakumar Mahalingam Rajamanickam
    Liver Research.2025; 9(4): 286.     CrossRef
  • Correspondence to editorial on “Multiomics profiling of buffy coat and plasma unveils etiology-specific signatures in hepatocellular carcinoma”
    Su Bin Lim, Hyo Jung Cho
    Clinical and Molecular Hepatology.2024; 30(4): 1009.     CrossRef
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Original Article

Viral hepatitis

Extrahepatic malignancies and antiviral drugs for chronic hepatitis B: A nationwide cohort study
Moon Haeng Hur, Dong Hyeon Lee, Jeong-Hoon Lee, Mi-Sook Kim, Jeayeon Park, Hyunjae Shin, Sung Won Chung, Hee Jin Cho, Min Kyung Park, Heejoon Jang, Yun Bin Lee, Su Jong Yu, Sang Hyub Lee, Yong Jin Jung, Yoon Jun Kim, Jung-Hwan Yoon
Clin Mol Hepatol 2024;30(3):500-514.
Published online May 10, 2024
DOI: https://doi.org/10.3350/cmh.2024.0055
Background/Aims
Chronic hepatitis B (CHB) is related to an increased risk of extrahepatic malignancy (EHM), and antiviral treatment is associated with an incidence of EHM comparable to controls. We compared the risks of EHM and intrahepatic malignancy (IHM) between entecavir (ETV) and tenofovir disoproxil fumarate (TDF) treatment.
Methods
Using data from the National Health Insurance Service of Korea, this nationwide cohort study included treatment-naïve CHB patients who initiated ETV (n=24,287) or TDF (n=29,199) therapy between 2012 and 2014. The primary outcome was the development of any primary EHM. Secondary outcomes included overall IHM development. E-value was calculated to assess the robustness of results to unmeasured confounders.
Results
The median follow-up duration was 5.9 years, and all baseline characteristics were well balanced after propensity score matching. EHM incidence rate differed significantly between within versus beyond 3 years in both groups (P<0.01, Davies test). During the first 3 years, EHM risk was comparable in the propensity score-matched cohort (5.88 versus 5.84/1,000 person-years; subdistribution hazard ratio [SHR]=1.01, 95% confidence interval [CI]=0.88–1.17, P=0.84). After year 3, however, TDF was associated with a significantly lower EHM incidence compared to ETV (4.92 versus 6.91/1,000 person-years; SHR=0.70, 95% CI=0.60–0.81, P<0.01; E-value for SHR=2.21). Regarding IHM, the superiority of TDF over ETV was maintained both within (17.58 versus 20.19/1,000 person-years; SHR=0.88, 95% CI=0.81–0.95, P<0.01) and after year 3 (11.45 versus 16.20/1,000 person-years; SHR=0.68, 95% CI=0.62–0.75, P<0.01; E-value for SHR=2.30).
Conclusions
TDF was associated with approximately 30% lower risks of both EHM and IHM than ETV in CHB patients after 3 years of antiviral therapy.

Citations

Citations to this article as recorded by  Crossref logo
  • Efficacy and Safety of Switching from Entecavir to Tenofovir Alafenamide in Chronic Hepatitis B: A Multicenter Randomized Trial in Korea
    Hyunjae Shin, Moon Haeng Hur, Yang Hyun Baek, Chun Kyon Lee, Yong Kyun Cho, June Sung Lee, Jae Yoon Jeong, Yong Jin Jung, Ja Kyung Kim, Moon Young Kim, Yeon Seok Seo, Woo Jin Chung, Moon Soo Koh, Jeong-Han Kim, Yun Bin Lee, Eun Ju Cho, Jeong-Hoon Lee, Su
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Editorial

Hepatic neoplasm

Unlocking the future: Machine learning sheds light on prognostication for early-stage hepatocellular carcinoma: Editorial on “Conventional and machine learning-based risk scores for patients with early-stage hepatocellular carcinoma”
Junlong Dai, Jimmy Che-To Lai, Grace Lai-Hung Wong, Terry Cheuk-Fung Yip
Clin Mol Hepatol 2024;30(4):698-701.
Published online May 7, 2024
DOI: https://doi.org/10.3350/cmh.2024.0327

Citations

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    Chun-Ting Ho, Elise Chia-Hui Tan, Chien-Wei Su
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Original Article

Hepatic neoplasm

Prognostic value of ultra-low-pass whole-genome sequencing of circulating tumor DNA in hepatocellular carcinoma under systemic treatment
Miguel Sogbe, Idoia Bilbao, Francesco P. Marchese, Jon Zazpe, Annarosaria De Vito, Marta Pozuelo, Delia D’Avola, Mercedes Iñarrairaegui, Carmen Berasain, Maria Arechederra, Josepmaria Argemi, Bruno Sangro
Clin Mol Hepatol 2024;30(2):177-190.
Published online December 29, 2023
DOI: https://doi.org/10.3350/cmh.2023.0426
Background/Aims
New prognostic markers are needed to identify patients with hepatocellular carcinoma (HCC) who carry a worse prognosis. Ultra-low-pass whole-genome sequencing (ULP-WGS) (≤0.5× coverage) of cell-free DNA (cfDNA) has emerged as a low-cost promising tool to assess both circulating tumor DNA (ctDNA) fraction and large structural genomic alterations. Here, we studied the performance of ULP-WGS of plasma cfDNA to infer prognosis in patients with HCC.
Methods
Plasma samples were obtained from patients with HCC prior to surgery, locoregional or systemic therapy, and were analyzed by ULP-WGS of cfDNA to an average genome-wide fold coverage of 0.3x. ctDNA and copy number alterations (CNA) were estimated using the software package ichorCNA.
Results
Samples were obtained from 73 HCC patients at different BCLC stages (BCLC 0/A: n=37, 50.7%; BCLC B/C: n=36, 49.3%). ctDNA was detected in 18 out of 31 patients who received systemic treatment. Patients with detectable ctDNA showed significantly worse overall survival (median, 13.96 months vs not reached). ctDNA remained an independent predictor of prognosis after adjustment by clinical-pathologic features and type of systemic treatment (hazard ratio 7.69; 95%, CI 2.09–28.27). Among ctDNA-positive patients under systemic treatments, the loss of large genomic regions in 5q and 16q arms was associated with worse prognosis after multivariate analysis.
Conclusions
ULP-WGS of cfDNA provides clinically relevant information about the tumor biology. The presence of ctDNA and the loss of 5q and 16q arms in ctDNA-positive patients are independent predictors of worse prognosis in patients with advanced HCC receiving systemic therapy.

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Review

Hepatic neoplasm

Recent advances in the management of hepatocellular carcinoma
Kamya Sankar, Jun Gong, Arsen Osipov, Steven A. Miles, Kambiz Kosari, Nicholas N. Nissen, Andrew E. Hendifar, Ekaterina K. Koltsova, Ju Dong Yang
Clin Mol Hepatol 2024;30(1):1-15.
Published online July 21, 2023
DOI: https://doi.org/10.3350/cmh.2023.0125
Liver cancer remains a challenge of global health, being the 4th leading cause of cancer death worldwide. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, and is usually precipitated by chronic viral infections (hepatitis B and C), non-alcoholic steatohepatitis, heavy alcohol use, and other factors which may lead to chronic inflammation and cirrhosis of the liver. There have been significant advances in the systemic treatment options for HCC over the past decades, with several approvals of both immune checkpoint inhibitors and tyrosine kinase inhibitors in patients with preserved liver function. These advances have led to improvement in survival outcomes, with expected survival of greater than 18 months, in those with sensitive tumors, adequate liver function, and those functionally fit to receive sequential therapies. Several ongoing and promising trials are now evaluating combinational strategies with novel systemic agents and combinations of systemic therapy with locoregional therapy. In view of these trials, further advances in the treatment of HCC are foreseen in the near future.

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Correspondence

Artificial intelligence, epidemiology, methodology, or others

Correspondence on Letter 1 regarding “Assessing the performance of ChatGPT in answering questions regarding cirrhosis and hepatocellular carcinoma”
Yee Hui Yeo, Jamil S. Samaan, Wee Han Ng
Clin Mol Hepatol 2023;29(3):821-822.
Published online May 31, 2023
DOI: https://doi.org/10.3350/cmh.2023.0183

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Snapshot

Hepatic neoplasm

Systemic therapy in advanced hepatocellular carcinoma
Joseph C. Ahn, Nguyen H. Tran, Ju Dong Yang
Clin Mol Hepatol 2023;29(2):516-519.
Published online February 20, 2023
DOI: https://doi.org/10.3350/cmh.2023.0051

Citations

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Original Article

Hepatic neoplasm

Factors associated with unrecognized cirrhosis in patients with hepatocellular carcinoma
Yi-Te Lee, Mohammad A. Karim, Hye Chung Kum, Sulki Park, Nicole E. Rich, Mazen Noureddin, Amit G. Singal, Ju Dong Yang
Clin Mol Hepatol 2023;29(2):453-464.
Published online February 1, 2023
DOI: https://doi.org/10.3350/cmh.2022.0450
Background/Aims
Cirrhosis is the most important risk factor of hepatocellular carcinoma (HCC), and patients with cirrhosis are recommended to receive semiannual surveillance for early HCC detection. However, early cirrhosis is often asymptomatic and can go undiagnosed for years, leading to underuse of HCC surveillance in clinical practice. We characterized the frequency and associated factors of unrecognized cirrhosis in a national sample of patients with HCC from the United States.
Methods
HCC patients aged 68 years and older, diagnosed during 2011 to 2015 were included from the SEERMedicare Linked Database. If cirrhosis was diagnosed within 6 months immediately preceding HCC diagnosis or after HCC diagnosis, cases were categorized as unrecognized cirrhosis. Factors associated with unrecognized cirrhosis were identified using logistic regression analyses. Factors associated with overall survival were evaluated using Cox regression analyses.
Results
Among 5,098 HCC patients, 74.8% patients had cirrhosis. Among those with cirrhosis, 57.4% had unrecognized cirrhosis, with the highest proportion (76.3%) among those with NAFLD-related HCC. Male sex (aOR: 2.12, 95% CI: 1.83–2.46), non-Hispanic Black race (aOR: 1.93, 95% CI: 1.45–2.57), and NAFLD etiology (aOR: 4.46, 95% CI: 3.68–5.41) were associated with having unrecognized cirrhosis. Among NAFLD-related HCC patients, male sex (aOR: 2.32, 95% CI: 1.71–3.14) was associated with unrecognized cirrhosis. Unrecognized cirrhosis was independently associated with worse overall survival (aHR: 1.17, 95% CI: 1.08–1.27) compared to recognized cirrhosis.
Conclusions
Unrecognized cirrhosis is common in NAFLD-related HCC, particularly among male and Black patients, highlighting these groups as important intervention targets to improve HCC surveillance uptake and outcomes.

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Review

Hepatic neoplasm

Clinical practice guidelines and real-life practice in hepatocellular carcinoma: A Taiwan perspective
Tung-Hung Su, Chih-Horng Wu, Tsung-Hao Liu, Cheng-Maw Ho, Chun-Jen Liu
Clin Mol Hepatol 2023;29(2):230-241.
Published online January 30, 2023
DOI: https://doi.org/10.3350/cmh.2022.0421
Hepatocellular carcinoma (HCC) is the fourth most common cancer and the second leading cause of cancer-related death in Taiwan. The Taiwan Liver Cancer Association and the Gastroenterological Society of Taiwan developed and updated the guidelines for HCC management in 2020. In clinical practice, we follow these guidelines and the reimbursement policy of the government. In Taiwan, abdominal ultrasonography, alpha-fetoprotein, and protein induced by vitamin K absence or antagonist-II (PIVKA-II) tests are performed for HCC surveillance every 6 months or every 3 months for high-risk patients. Dynamic computed tomography, magnetic resonance imaging, and contrast-enhanced ultrasound have been recommended for HCC surveillance in extremely high-risk patients or those with poor ultrasonographic visualization results. HCC is usually diagnosed through dynamic imaging, and pathological diagnosis is recommended. Staging of HCC is based on a modified version of the Barcelona Clinic Liver Cancer (BCLC) system, and the HCC management guidelines in Taiwan actively promote curative treatments including surgery and locoregional therapy for BCLC stage B or C patients. Transarterial chemoembolization (TACE), drug-eluting bead TACE, transarterial radioembolization, and hepatic artery infusion chemotherapy may be administered for patients with BCLC stage B or C HCC. Sorafenib and lenvatinib are reimbursed as systemic therapies, and regorafenib and ramucirumab may be reimbursed in cases of sorafenib failure. First-line atezolizumab with bevacizumab is not yet reimbursed but may be administered in clinical practice. Systemic therapy and external beam radiation therapy may be used in specific patients. Early switching to systemic therapy in TACE-refractory patients is a recent paradigm shift in HCC management.

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Original Article

Hepatic neoplasm

Global burden of primary liver cancer and its association with underlying aetiologies, sociodemographic status, and sex differences from 1990–2019: A DALY-based analysis of the Global Burden of Disease 2019 study
Sungchul Choi, Beom Kyung Kim, Dong Keon Yon, Seung Won Lee, Han Gyeol Lee, Ho Hyeok Chang, Seoyeon Park, Ai Koyanagi, Louis Jacob, Elena Dragioti, Joaquim Radua, Jae Il Shin, Seung Up Kim, Lee Smith
Clin Mol Hepatol 2023;29(2):433-452.
Published online January 4, 2023
DOI: https://doi.org/10.3350/cmh.2022.0316
Background/Aims
Global distribution of dominant liver cancer aetiologies has significantly changed over the past decades. This study analyzed the updated temporal trends of liver cancer aetiologies and sociodemographic status in 204 countries and territories from 1990 to 2019.
Methods
The Global Burden of Disease 2019 report was used for statistical analysis. In addition, we performed stratification analysis to five quintiles using sociodemographic index and 21 geographic regions.
Results
The crude numbers of liver cancer disease-adjusted life years (DALYs) and deaths significantly increased during the study period (DALYs; 11,278,630 in 1990 and 12,528,422 in 2019, deaths; 365,215 in 1990 and 484,577 in 2019). However, the Age-standardized DALY and mortality rates decreased. Hepatitis B virus (HBV) remains the leading cause of liver cancer DALYs and mortality, followed by hepatitis C virus (HCV), alcohol consumption, and non-alcoholic steatohepatitis/non-alcoholic fatty liver disease (NASH/NAFLD). Although Age-standardized DALY and mortality rates of liver cancer due to HBV and HCV have decreased, the rates due to alcohol consumption and NASH/NAFLD have increased. In 2019, the population of the East Asia region had the highest Age-standardized DALY and mortality rates, followed by high-income Asia-Pacific and Central Asia populations. Although East Asia and high-income Asia-Pacific regions showed a decrease during the study period, Age-standardized DALY rates increased in Central Asia. High-income North American and Australasian populations also showed a significant increase in Age-standardized DALY.
Conclusions
Liver cancer remains an ongoing global threat. The burden of liver cancer associated with alcohol consumption and NASH/NAFLD is markedly increasing and projected to continuously increase.

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Review

Steatotic liver disease

Non-invasive biomarkers for liver inflammation in non-alcoholic fatty liver disease: present and future
Terry Cheuk-Fung Yip, Fei Lyu, Huapeng Lin, Guanlin Li, Pong-Chi Yuen, Vincent Wai-Sun Wong, Grace Lai-Hung Wong
Clin Mol Hepatol 2023;29(Suppl):S171-S183.
Published online December 12, 2022
DOI: https://doi.org/10.3350/cmh.2022.0426
Inflammation is the key driver of liver fibrosis progression in non-alcoholic fatty liver disease (NAFLD). Unfortunately, it is often challenging to assess inflammation in NAFLD due to its dynamic nature and poor correlation with liver biochemical markers. Liver histology keeps its role as the standard tool, yet it is well-known for substantial sampling, intraobserver, and interobserver variability. Serum proinflammatory cytokines and apoptotic markers, namely cytokeratin-18, are well-studied with reasonable accuracy, whereas serum metabolomics and lipidomics have been adopted in some commercially available diagnostic models. Ultrasound and computed tomography imaging techniques are attractive due to their wide availability; yet their accuracies may not be comparable with magnetic resonance imaging-based tools. Machine learning and deep learning models, be they supervised or unsupervised learning, are promising tools to identify various subtypes of NAFLD, including those with dominating liver inflammation, contributing to sustainable care pathways for NAFLD.

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Correspondence

Hepatic neoplasm

Correspondence on Editorial regarding “Impact of nationwide hepatocellular carcinoma surveillance on the prognosis in patients with chronic liver disease”
Won Sohn, Yong-Han Paik
Clin Mol Hepatol 2023;29(1):182-184.
Published online November 22, 2022
DOI: https://doi.org/10.3350/cmh.2022.0411

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to editorial on “Multiomics profiling of buffy coat and plasma unveils etiology-specific signatures in hepatocellular carcinoma”
    Su Bin Lim, Hyo Jung Cho
    Clinical and Molecular Hepatology.2024; 30(4): 1009.     CrossRef
  • 7,552 View
  • 57 Download
  • 1 Web of Science
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