Clinical and Molecular Hepatology

"OMICS"

Review Article

Hepatocellular Carcinoma Surveillance: A Health Economic Evaluation: Qi-Feng Chen, Xiong-Ying Jiang, Song Chen, Jiongliang Wang, Ming Zhao; Received September 19, 2025 Accepted January 1, 2026 Published online January 9, 2026; DOI: https://doi.org/10.3350/cmh.2025.1060 [Accepted]

Abstract
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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 (AFP) 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 MRI, multi-biomarker models (e.g., GALAD), 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 (AI) 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.

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Review

Panomics in metabolic dysfunction-associated steatotic liver disease: unravelling the drivers of disease heterogeneity: Carlos José Pirola, Silvia Sookoian; Clin Mol Hepatol 2026;32(1):156-169.
Published online October 27, 2025; DOI: https://doi.org/10.3350/cmh.2025.0960

Abstract
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The knowledge accumulated over the past two decades has revealed that the natural history of metabolic dysfunction-associated steatotic liver disease (MASLD) and the drivers of the disease severity are not only complex but also exhibit variation among patients. This intricate clinical scenario entails major therapeutic and management implications. In this review, we provide a comprehensive examination of recent advancements in our understanding of MASLD heterogeneity, drawing insights from multiomics and panomics studies. The discussion herein explores the instrumental role of panomics in MASLD research, elucidating the potential for the identification of molecular subtypes that exhibit divergent survival outcomes or heterogeneous responses to various treatments. Furthermore, we provide insights into the challenges in addressing disease heterogeneity and potential solutions. Finally, the most advanced technological advancements and prospective research directions in the domain of MASLD research are delineated, with the objective of facilitating the implementation of personalized diagnosis and interventions.

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Original Article

Integrative multi-omics profiling identifies infiltrative hepatocellular carcinoma as an immunotherapy-resistant subtype with distinct molecular features: Won Suk Lee, Seonjeong Woo, Sung Hwan Lee, Gae Hoon Jo, Ilhwan Kim, Hyeyeong Kim, Chansik An, Sanghoon Jung, Gwangil Kim, Haeyoun Kang, Beodeul Kang, Jung Sun Kim, Ho Yeong Lim, Incheon Kang, Hannah Yang, So Jung Kong, Dahyeon Son, Dong Jun Shin, Woo Young Kwon, Da-Yeon Lee, Ju-Seog Lee, Junho Park, Youngsoo Kim, Sohyun Hwang, Chan Kim, Hong Jae Chon; Clin Mol Hepatol 2026;32(1):258-275.
Published online October 27, 2025; DOI: https://doi.org/10.3350/cmh.2025.0792

Background/Aims
Hepatocellular carcinoma (HCC) exhibits substantial morphological and biological heterogeneity. Clinical and molecular relevance of the infiltrative subtype remains poorly defined in the context of cancer immunotherapy. We aimed to evaluate the prognostic impact and molecular features of infiltrative HCC in patients treated with first-line atezolizumab plus bevacizumab (Ate/Bev).
Methods
We included 307 patients with advanced HCC treated with Ate/Bev and classified them into four gross morphological types based on imaging. Multi-omics profiling was conducted on tumor samples. Type IV infiltrative signature was derived and externally validated using five independent HCC cohorts, including IMbrave150.
Result
s: Infiltrative morphology, encompassing pure and mixed forms, was present in 42.7% of advanced HCC and associated with advanced disease features and compromised liver function. Patients with type IV infiltrative HCC showed lowest objective response rate (14.6%) and worst progression-free (median, 2.8 months) and overall survival (median, 7.1 months). Infiltrative morphology remained an independent predictor of poor outcomes after multivariable adjustment for confounders, including intrahepatic tumor extent. Genomic profiling revealed enriched TP53 and ATM loss-of-function mutations in type IV infiltrative HCC. Transcriptomic and proteomic analyses identified consistent activation of tumor proliferation, epithelial-mesenchymal transition, TGF-β signaling, and immunosuppressive pathways in type IV infiltrative HCC. Type IV infiltrative signature was significantly associated with poor survival across external datasets and retained independent prognostic value.
Conclusions
Infiltrative HCC is a clinically aggressive and molecularly distinct subtype of advanced HCC. Morphological classification and type IV infiltrative signatures may guide risk stratification and therapeutic decision-making in advanced HCC treated with immunotherapy.

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Prognostic Significance of Glypican-3 Expression in Hepatocellular Carcinoma Treated with Atezolizumab-Bevacizumab
Ji Hoon Kim, Ji Won Han, Hee Sun Cho, Jeong Won Jang, Kwon Yong Tak, Pil Soo Sung
Cancers.2025; 17(24): 3967. CrossRef

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Letters to the Editor

Plasma lipidomic and fungal signatures predict early mortality in acute liver failure: Yu Ji Kim, Jong-Won Kim; Clin Mol Hepatol 2026;32(1):e21-e23.
Published online August 20, 2025; DOI: https://doi.org/10.3350/cmh.2025.0813

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Letter to the editor on “Radiogenomics of intrahepatic cholangiocarcinoma predicts immunochemotherapy response and identifies therapeutic target”: Yuqian Liu, Ruiyun Guo, Jun Ma; Clin Mol Hepatol 2026;32(1):e13-e15.
Published online April 23, 2025; DOI: https://doi.org/10.3350/cmh.2025.0377

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Editorial

A novel link between tumor cell metabolism and patient prognosis: Editorial on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”: Eun Ji Jang, Pil Soo Sung; Clin Mol Hepatol 2026;32(1):420-422.
Published online April 16, 2025; DOI: https://doi.org/10.3350/cmh.2025.0395

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Correspondence to editorial on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”
Tomoko Aoki, Naoshi Nishida, Masatoshi Kudo
Clinical and Molecular Hepatology.2026; 32(1): e79. CrossRef
Reply to correspondence on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”
Eun Ji Jang, Pil Soo Sung
Clinical and Molecular Hepatology.2026; 32(1): e115. CrossRef
Fluorine-18 Fluorodeoxyglucose Positron Emission Tomography: A Potential Imaging Biomarker for Predicting Response to Combination Immunotherapy in Hepatocellular Carcinoma
Masatoshi Kudo
Liver Cancer.2025; 14(5): 511. CrossRef

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Research Letter

Lipidomic analysis of alcohol use disorder patients revealed the biomarkers for alcohol-related liver disease susceptibility: Dongyao Wang, Hongwei Zhang, Yuxiao Tang; Clin Mol Hepatol 2025;31(3):e259-e262.
Published online April 2, 2025; DOI: https://doi.org/10.3350/cmh.2025.0227

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Discovery of Bufalin as a Molecular Glue Degrader of NCAPG to Inhibit the Proliferation of Hepatoma Cells
Chenghua Wu, Xiaobin Zhuo, Jianxin Yang, Yuxiao Tang, Weili Wang, Mengpu Wu, Gen Miao, Chenqi Li, Hui Shen, Jianxin Qian, Dongyao Wang
Drug Development Research.2026;[Epub] CrossRef
Targeting Annexin A2 to reactivate tumor-associated antigens presentation and relieve immune tolerance in liver cancer
Yuxiao Tang, Jianxin Yang, Qicong Shen, Zelong Gao, Mengpu Wu, Chenghua Wu, Jicong Du, Min Li, Changquan Ling, Feng Lu, Yifeng Chai, Xin Dong, Jianxin Qian, Chenqi Li, Feng Xie, Zhenhong Guo, Hui Shen, Dongyao Wang
Journal for ImmunoTherapy of Cancer.2025; 13(6): e011716. CrossRef

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Original Article

Radiogenomics of intrahepatic cholangiocarcinoma predicts immunochemotherapy response and identifies therapeutic target: Gu-Wei Ji, Zheng-Gang Xu, Shuo-Chen Liu, Shu-Ya Cao, Chen-Yu Jiao, Ming Lu, Biao Zhang, Yue Yang, Qing Xu, Xiao-Feng Wu, Ke Wang, Yong-Xiang Xia, Xiang-Cheng Li, Xue-Hao Wang; Clin Mol Hepatol 2025;31(3):935-959.
Published online February 10, 2025; DOI: https://doi.org/10.3350/cmh.2024.0895

Background/Aims
Identifying patients with intrahepatic cholangiocarcinoma (ICC) likely to benefit from immunochemotherapy, the new front-line treatment, remains challenging. We aimed to unveil a novel radiotranscriptomic signature that can facilitate treatment response prediction by multi-omics integration and multiscale modelling.
Methods
We analyzed bulk, single-cell and spatial transcriptomic data comprising 457 ICC patients to identify an immune-related score (IRS), followed by decoding its spatial immune context. We mapped radiomics profiles onto spatial-specific IRS using machine learning to define a novel radiotranscriptomic signature, followed by multi-scale and multi-cohort validation covering 331 ICC patients. The signature was further explored for the potential therapeutic target from in vitro to in vivo.
Result
s: We revealed a novel 3-gene (PLAUR, CD40LG, and FGFR4) IRS whose down-regulation correlated with better survival and improved sensitivity to immunochemotherapy. We highlighted functional IRS-immune interactions within tumor epithelium, rather than stromal compartment, irrespective of geospatial locations. Machine learning pipeline identified the optimal 3-feature radiotranscriptomic signature that was well-validated by immunohistochemical assays in molecular cohort, exhibited favorable external prognostic validity with C-index over 0.64 in resection cohort, and predicted treatment response with an area under the curve of up to 0.84 in immunochemotherapy cohort. We also showed that anti-uPAR/PLAUR alone or in combination with anti-programmed cell death protein 1 therapy remarkably curbed tumor growth, using in vitro ICC cell lines and in vivo humanized ICC patient-derived xenograft mouse models.
Conclusions
This proof-of-concept study sheds light on the spatially-resolved radiotranscriptomic signature to improve patient selection for emerging immunochemotherapy and high-order immunotherapy combinations in ICC.

Citations

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Bioinformatics analysis of PLAUR and its oncogenic role of promoting colorectal cancer progression through the AKT/p53 signaling
You Chen, Rui Ma, Chuyue Wang, Zhiying Yang, Ying Shi, Yingying Zhao, Xiaofen Pan, Bo Wang, Weili Wu, Ping Yuan
Experimental Cell Research.2026; 455(2): 114850. CrossRef
Letter to the editor on “Radiogenomics of intrahepatic cholangiocarcinoma predicts immunochemotherapy response and identifies therapeutic target”
Yuqian Liu, Ruiyun Guo, Jun Ma
Clinical and Molecular Hepatology.2026; 32(1): e13. CrossRef
Characterization of hypoxia-related molecular clusters and prognostic riskScore for glioma
Xiang Fang, Xinhao Wu, Chengran Xu
Frontiers in Oncology.2025;[Epub] CrossRef
Artificial intelligence in the diagnosis and prognosis of intrahepatic cholangiocarcinoma: Applications and challenges
Liang Qiao, Yu-Gang Luo, Qing-Ying Wang, Tian Yuan, Meng Xu, Guang-Bing Xiong, Feng Zhu
World Journal of Gastrointestinal Oncology.2025;[Epub] CrossRef

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Correspondence

Hepatic neoplasm

Correspondence to editorial on “Aberrant fragmentomic features of circulating cell-free mitochondrial DNA enable early detection and prognosis prediction of hepatocellular carcinoma”: Yang Liu, Fan Peng, Siyuan Wang, Jinliang Xing; Clin Mol Hepatol 2025;31(2):e166-e168.
Published online January 6, 2025; DOI: https://doi.org/10.3350/cmh.2024.1185

Citations

Citations to this article as recorded by

Reply to correspondence on “Aberrant fragmentomic features of circulating cell-free mitochondrial DNA enable early detection and prognosis prediction of hepatocellular carcinoma”
Hyuk Soo Eun
Clinical and Molecular Hepatology.2025; 31(2): e215. CrossRef

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Original Articles

Plasma lipidomics and fungal peptide-based community analysis identifies distinct signatures for early mortality in acute liver failure: Neha Sharma, Sushmita Pandey, Gaurav Tripathi, Manisha Yadav, Nupur Sharma, Babu Mathew, Abhishak Gupta, Vasundhra Bindal, Sadam H. Bhat, Yash Magar, Rimsha Saif, Sanju Yadav, Amritpal Kaur, Rakhi Maiwall, Shvetank Sharma, Shiv Kumar Sarin, Jaswinder Singh Maras; Clin Mol Hepatol 2025;31(4):1233-1251.
Published online December 13, 2024; DOI: https://doi.org/10.3350/cmh.2024.0554

Background/Aims
Acute liver failure (ALF) has high mortality predominantly due to compromised immune system and increased vulnerability to bacterial and fungal infections.
Methods
Plasma lipidome and fungal peptide-based community (mycobiome) analysis were performed in discovery cohort (ALF=40, healthy=5) and validated in a validation cohort of 230 patients with ALF using high-resolution-mass-spectrometry, artificial neural network (ANN) and machine learning (ML).
Result
s: Untargeted lipidomics identified 2,013 lipids across 8 lipid group. 5 lipid-species—phosphatidylcholine (PC)[15:0/17:0], PC[20:1/14:1], PC[26:4/10:0], PC[32:0] and TG[4:0/10:0/23:6]—significantly differentiated ALF-NS (FC>10, P<0.05, FDR<0.01). Mycobiome alpha/beta diversity was significantly higher and showed 4 phyla and >20 species significantly dysregulated in ALF-NS linked with lipid metabolism, fatty acid elongation in ER, and others (P<0.05). Lipid and mycobiome diversity values in ALF-NS were strongly correlated (r²>0.7, P<0.05). Multi-modular correlation network showed striking associations between lipid, fungal peptide modules, and clinical parameters specific to ALF-NS (P<0.05). Cryptococcus amylolentus CBS6039 and Penicillium oxalicum 1142 directly correlated with phosphatidylcholine, triglycerides, and severity in ALF-NS (r²>0.85, P<0.05). POD-fungus and POD-lipids showed direct association with infection, necrosis, and hepatic encephalopathy (Beta>1.2, P<0.05). POD-lipid (AUC=0.969 and HR=1.99 [1.02–2.04]) superseded POD-fungus and severity indices for early-mortality prediction. Finally, significant increase in PC (15:0/17:0) level showed highest normalized importance, and ANNs and ML predicted early mortality with >95% accuracy, sensitivity, and specificity. Interestingly, fungal surveillance protein Clec7a was significantly downregulated (>2-fold), leading to a notable increase in fungal infection-mediated choline/phosphatidylcholine and associated enzymes (FC>1.5; Kennedy cycle). This contributed to phosphatidic acid-mediated hyper-inflammation in ALF-NS.
Conclusions
In ALF, the plasma lipidome and mycobiome are dysregulated. Increased circulating phosphatidylcholine could stratify ALF predisposed to early mortality or require emergency liver transplantation.

Citations

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Acute-on-chronic liver failure: pathophysiological mechanisms and clinical management
S. K. Sarin, Ashok Choudhury, Anupam Kumar, Nadim Mahmud, G. H. Lee, Qin Ning, Soek-Siam Tan, Kessarin Thanapirom, Vinod Arora, Nobuaki Nakayama, Jun Li, Constantine J. Karvellas
Nature Reviews Gastroenterology & Hepatology.2026;[Epub] CrossRef
Plasma lipidomic and fungal signatures predict early mortality in acute liver failure
Yu Ji Kim, Jong-Won Kim
Clinical and Molecular Hepatology.2026; 32(1): e21. CrossRef

10,334 View
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Hepatic neoplasm

Integrated molecular characterization of sarcomatoid hepatocellular carcinoma: Rong-Qi Sun, Yu-Hang Ye, Ye Xu, Bo Wang, Si-Yuan Pan, Ning Li, Long Chen, Jing-Yue Pan, Zhi-Qiang Hu, Jia Fan, Zheng-Jun Zhou, Jian Zhou, Cheng-Li Song, Shao-Lai Zhou; Clin Mol Hepatol 2025;31(2):426-444.
Published online December 10, 2024; DOI: https://doi.org/10.3350/cmh.2024.0686

Backgrounds/Aims
Sarcomatoid hepatocellular carcinoma (HCC) is a rare histological subtype of HCC characterized by extremely poor prognosis; however, its molecular characterization has not been elucidated.
Methods
In this study, we conducted an integrated multiomics study of whole-exome sequencing, RNA-seq, spatial transcriptome, and immunohistochemical analyses of 28 paired sarcomatoid tumor components and conventional HCC components from 10 patients with sarcomatoid HCC, in order to identify frequently altered genes, infer the tumor subclonal architectures, track the genomic evolution, and delineate the transcriptional characteristics of sarcomatoid HCCs.
Result
s: Our results showed that the sarcomatoid HCCs had poor prognosis. The sarcomatoid tumor components and the conventional HCC components were derived from common ancestors, mostly accessing similar mutational processes. Clonal phylogenies demonstrated branched tumor evolution during sarcomatoid HCC development and progression. TP53 mutation commonly occurred at tumor initiation, whereas ARID2 mutation often occurred later. Transcriptome analyses revealed the epithelial–mesenchymal transition (EMT) and hypoxic phenotype in sarcomatoid tumor components, which were confirmed by immunohistochemical staining. Moreover, we identified ARID2 mutations in 70% (7/10) of patients with sarcomatoid HCC but only 1–5% of patients with non-sarcomatoid HCC. Biofunctional investigations revealed that inactivating mutation of ARID2 contributes to HCC growth and metastasis and induces EMT in a hypoxic microenvironment.
Conclusions
We offer a comprehensive description of the molecular basis for sarcomatoid HCC, and identify genomic alteration (ARID2 mutation) together with the tumor microenvironment (hypoxic microenvironment), that may contribute to the formation of the sarcomatoid tumor component through EMT, leading to sarcomatoid HCC development and progression.

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Sequential anlotinib and camrelizumab combination therapy achieves exceptional survival in multi-driver mutated, TMB-low/PD-L1-low/MSS pulmonary sarcomatoid carcinoma: case report and literature review
Jun Zhu, Ai Zhu, Gang Li, Lidong Liu, Ziran Gao, Jiayun Liu, Yunfei Ye, Xunzhi Zhu, Yi Li, Hong Chen, Meijin Huang
Frontiers in Immunology.2026;[Epub] CrossRef
Curative response to combined targeted-immunotherapy for post-hepatectomy lymph node metastasis in sarcomatoid hepatocellular carcinoma: case report and literature review
Pan Liu, Song Zhang, Xiao-Ming Xin, Min Jing, Lie-Dong Wen, Xin Xiang, Shun-Hai Liu
Frontiers in Oncology.2025;[Epub] CrossRef
Comparison of stereotactic body radiotherapy following transcatheter arterial chemoembolization vs transcatheter arterial chemoembolization alone in hepatocellular carcinoma
Lin Chen, Liang Wang, Hui Wang
World Journal of Gastrointestinal Surgery.2025;[Epub] CrossRef

11,551 View
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5 Web of Science
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Hepatic neoplasm

Aberrant fragmentomic features of circulating cell-free mitochondrial DNA enable early detection and prognosis prediction of hepatocellular carcinoma: Yang Liu, Fan Peng, Siyuan Wang, Huanmin Jiao, Kaixiang Zhou, Wenjie Guo, Shanshan Guo, Miao Dang, Huanqin Zhang, Weizheng Zhou, Xu Guo, Jinliang Xing; Clin Mol Hepatol 2025;31(1):196-212.
Published online October 15, 2024; DOI: https://doi.org/10.3350/cmh.2024.0527

Background/Aims
Early detection and effective prognosis prediction in patients with hepatocellular carcinoma (HCC) provide an avenue for survival improvement, yet more effective approaches are greatly needed. We sought to develop the detection and prognosis models with ultra-sensitivity and low cost based on fragmentomic features of circulating cell free mtDNA (ccf-mtDNA).
Methods
Capture-based mtDNA sequencing was carried out in plasma cell-free DNA samples from 1168 participants, including 571 patients with HCC, 301 patients with chronic hepatitis B or liver cirrhosis (CHB/LC) and 296 healthy controls (HC).
Result
s: The systematic analysis revealed significantly aberrant fragmentomic features of ccf-mtDNA in HCC group when compared with CHB/LC and HC groups. Moreover, we constructed a random forest algorithm-based HCC detection model by utilizing ccf-mtDNA fragmentomic features. Both internal and two external validation cohorts demonstrated the excellent capacity of our model in distinguishing early HCC patients from HC and highrisk population with CHB/LC, with AUC exceeding 0.983 and 0.981, sensitivity over 89.6% and 89.61%, and specificity over 98.20% and 95.00%, respectively, greatly surpassing the performance of alpha-fetoprotein (AFP) and mtDNA copy number. We also developed an HCC prognosis prediction model by LASSO-Cox regression to select 20 fragmentomic features, which exhibited exceptional ability in predicting 1-year, 2-year and 3-year survival (AUC=0.8333, 0.8145 and 0.7958 for validation cohort, respectively).
Conclusions
We have developed and validated a high-performing and low-cost approach in a large clinical cohort based on aberrant ccf-mtDNA fragmentomic features with promising clinical translational application for the early detection and prognosis prediction of HCC patients.

Citations

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Integrative metabolomic and transcriptomic profiling reveals distinct metabolic signatures of hepatocellular carcinoma arising from cirrhosis
Junxi Ni, Qiuming Song, Daoli Liu, Yongwei Zhang, Yun Sun
Computational Biology and Chemistry.2026; 121: 108863. CrossRef
Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential
Yijia Chen, Hanzhe Shi, Mingming Xiao, Haoqi Pan, Xiaoning Yu, Yicheng Zhu, Jing Yang, Wei Wang, Jin Xu, Xianjun Yu, Si Shi
Biomarker Research.2026;[Epub] CrossRef
Clinical utilization of testing for cell-free DNA in hepatocellular cancer
Jasmine J. Wang, Yi-Te Lee, Amy K. Kim, Augusto Villanueva, Amit G. Singal, Ju Dong Yang
Hepatology.2026;[Epub] CrossRef
Hepatic mitochondrial signaling as a systemic hub: inter-organ communication networks in aging and aging-related diseases
Yishuo Ji, Ying Wang, Xiaowei Yu, Yi Jin, Kai Zhao, Yue Hu, Zhenglin He
Frontiers in Cell and Developmental Biology.2026;[Epub] CrossRef
Transcriptome combined with single-cell sequencing explored prognostic markers associated with T cell exhaustion characteristics in head and neck squamous carcinoma
Jie Liu, Penghui Li, Yuanyuan Zhang, Lian Zheng
Scientific Reports.2025;[Epub] CrossRef
Hepatocyte mitochondrial DNA activated store-operated Ca2+ entry via Stim1/Orai1-induced podocyte injury in trichloroethylene sensitized mice: A new insight in liver and kidney crosstalk
Luo-lun Dong, Xue-qian Jia, Hai-bo Xie, Li-fu Zhu, Peng-cheng Zhou, Rui-xuan Cheng, Chun-lin Cao, Qi-xing Zhu, Jia-xiang Zhang
Toxicology and Applied Pharmacology.2025; 503: 117465. CrossRef
Mitochondrial metabolism and cancer therapeutic innovation
Hongxiang Du, Tianhan Xu, Sihui Yu, Sufang Wu, Jiawen Zhang
Signal Transduction and Targeted Therapy.2025;[Epub] CrossRef
Mitochondrial echoes in the bloodstream: decoding ccf-mtDNA for the early detection and prognosis of hepatocellular carcinoma
Yu-De Chu, Wei-Ting Chen, Wey-Ran Lin, Ming-Wei Lai, Chau-Ting Yeh
Cell & Bioscience.2025;[Epub] CrossRef
Circulating Cell‐Free Mitochondrial DNA as a Prognostic Biomarker in Patients With HBV‐Related Acute‐on‐Chronic Liver Failure
Qiankun Hu, Jiajia Han, Chong Chen, Shuai Tao, Chenlu Huang, Jiacheng Lin, Xun Qi, Zhiping Qian, Mengxin Lu, Xinyan Li, Yi Zhang, Xuhua Jiang, Jianming Zheng, Huazhen Zhao, Feifei Yang, Jiming Zhang, Liang Chen, Xiaoni Kong, Xueyun Zhang, Yuxian Huang
Journal of Medical Virology.2025;[Epub] CrossRef
Mitochondrial damage-associated molecular patterns (mito-DAMPs): Determinants of hepatopathy progression and therapeutic implications
Ranyi Luo, Yun Yang, Yinhao Zhang, Xiaoyong Xue, Mengyu Guo, Xiaojiaoyang Li
Pharmacological Research.2025; 221: 107980. CrossRef
Targeting liver cancer stem cells: the prognostic significance of MRPL17 in immunotherapy response
Jingjing Shao, Tianye Zhao, Jibin Liu, Peipei Kang
Frontiers in Immunology.2024;[Epub] CrossRef

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Correspondence

Hepatic neoplasm

Correspondence to editorial on “Multiomics profiling of buffy coat and plasma unveils etiology-specific signatures in hepatocellular carcinoma”: Su Bin Lim, Hyo Jung Cho; Clin Mol Hepatol 2024;30(4):1009-1011.
Published online May 20, 2024; DOI: https://doi.org/10.3350/cmh.2024.0368

Citations

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Matrisomics: Beyond the extracellular matrix for unveiling tumor microenvironment
Jiwon Hong, Hyo Joon Jin, Mi Ran Choi, Darren Wan-Teck Lim, Jong-Eun Park, You-Sun Kim, Su Bin Lim
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer.2024; 1879(6): 189178. CrossRef

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Original Article

Hepatic neoplasm

Multiomics profiling of buffy coat and plasma unveils etiology-specific signatures in hepatocellular carcinoma: Jiwon Hong, Jung Woo Eun, Geum Ok Baek, Jae Youn Cheong, Seryoung Park, Soon Sun Kim, Hyo Jung Cho, Su Bin Lim; Clin Mol Hepatol 2024;30(3):360-374.
Published online March 15, 2024; DOI: https://doi.org/10.3350/cmh.2024.0042

Background/Aims
Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality worldwide. Despite identification of several biomarkers for HCC diagnosis, challenges such as low sensitivity and intratumoral heterogeneity have impeded early detection, highlighting the need for etiology-specific blood biomarkers.
Methods
We generated whole-transcriptome sequencing (WTS) and targeted proteome data from buffy coat and plasma samples from HCC patients. By integrating etiological information on viral infection, we investigated the etiology-specific gene expression landscape at the blood level. Validation of differentially expressed genes (DEGs) was performed using publicly available RNA-seq datasets and qRT‒PCR with AUC analyses.
Result
s: Differential expression analyses with multiomics data revealed distinct gene expression profiles between HBV-associated HCC and nonviral HCC, indicating the presence of etiology-specific blood biomarkers. The identified DEGs were validated across multiple independent datasets, underscoring their utility as biomarkers. Additionally, single-cell RNA-seq analysis of HCC confirmed differences in DEG expression across distinct immune cell types.
Conclusions
Our buffy coat WTS data and plasma proteome data may serve as reliable sources for identifying etiology-specific blood biomarkers of HCC and might contribute to discovery of therapeutic targets for HCC across different etiologies.

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Relevance of proteomics and metabolomics approaches to overview the tumorigenesis and better management of cancer
Pooja Singh, Yashika W. Dhir, Shagun Gupta, Ankur Kaushal, Deepak Kala, Rupak Nagraiik, Naveen K. Kaushik, Md Salik Noorani, Abdul R. Asif, Bharat Singh, Shahbaz Aman, Sunny Dhir
3 Biotech.2025;[Epub] CrossRef
Development of a big data platform for collecting and utilizing clinical information from the Korea Biobank Network
Yun Seon Im, Seol Whan Oh, Ki Hoon Kim, Wona Choi, In Young Choi
BMC Medical Informatics and Decision Making.2025;[Epub] CrossRef
Harnessing plasma transcriptomics for non-invasive cancer biomarker identification: a comprehensive review
Nur Mazidah Haji Noor Mohamed, Nurulisa Zulkifle, Siti Razila Abdul Razak
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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
Clinical and Molecular Hepatology.2024; 30(4): 689. CrossRef
Technology and Future of Multi-Cancer Early Detection
Danny A. Milner, Jochen K. Lennerz
Life.2024; 14(7): 833. 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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Correspondence

Steatotic liver disease

Correspondence on Editorial regarding “Identification of signature gene set as highly accurate determination of MASLD progression”: Sungju Jung, Sumin Yoon, Jong Hoon Park, Yeon-Su Lee, Kyung Hyun Yoo; Clin Mol Hepatol 2024;30(2):287-290.
Published online February 23, 2024; DOI: https://doi.org/10.3350/cmh.2024.0136

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The effects of next generation probiotics on metabolic dysfunction-associated steatotic liver disease: a parallel, double-blind, randomized, placebo-controlled trial
Sung-Min Won, Hyunchae Joung, In Gyu Park, Sang Hak Han, Young Lim Ham, Ji Sook Han, Yoojin Kwon, Dong Joon Kim, Ki Tae Suk
Journal of Translational Medicine.2025;[Epub] CrossRef
The role of SPP1 in MASLD pathogenesis: Therapeutic insights into ursolic acid’s mechanisms of action: Correspondence to editorial on “Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against metabolic dysfunction-associated steatotic
Yiyuan Zheng, Zhekun Xiong, Lina Zhao, Chaoyuan Huang, Qiuhong Yong, Dan Fang, Fengbin Liu, Yong Li
Clinical and Molecular Hepatology.2024; 30(4): 1019. CrossRef

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Editorial

Steatotic liver disease

The gene expression signature of metabolic dysfunction- associated steatotic liver disease from a multiomics perspective: Carlos Jose Pirola, Silvia Sookoian; Clin Mol Hepatol 2024;30(2):174-176.
Published online February 5, 2024; DOI: https://doi.org/10.3350/cmh.2024.0082

Citations

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Early portal hypertension in metabolic dysfunction-associated steatotic liver disease: a concise review
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Original Article

Steatotic liver disease

Identification of signature gene set as highly accurate determination of metabolic dysfunction-associated steatotic liver disease progression: Sumin Oh, Yang-Hyun Baek, Sungju Jung, Sumin Yoon, Byeonggeun Kang, Su-hyang Han, Gaeul Park, Je Yeong Ko, Sang-Young Han, Jin-Sook Jeong, Jin-Han Cho, Young-Hoon Roh, Sung-Wook Lee, Gi-Bok Choi, Yong Sun Lee, Won Kim, Rho Hyun Seong, Jong Hoon Park, Yeon-Su Lee, Kyung Hyun Yoo; Clin Mol Hepatol 2024;30(2):247-262.
Published online January 26, 2024; DOI: https://doi.org/10.3350/cmh.2023.0449

Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by fat accumulation in the liver. MASLD encompasses both steatosis and MASH. Since MASH can lead to cirrhosis and liver cancer, steatosis and MASH must be distinguished during patient treatment. Here, we investigate the genomes, epigenomes, and transcriptomes of MASLD patients to identify signature gene set for more accurate tracking of MASLD progression.
Methods
Biopsy-tissue and blood samples from patients with 134 MASLD, comprising 60 steatosis and 74 MASH patients were performed omics analysis. SVM learning algorithm were used to calculate most predictive features. Linear regression was applied to find signature gene set that distinguish the stage of MASLD and to validate their application into independent cohort of MASLD.
Result
s: After performing WGS, WES, WGBS, and total RNA-seq on 134 biopsy samples from confirmed MASLD patients, we provided 1,955 MASLD-associated features, out of 3,176 somatic variant callings, 58 DMRs, and 1,393 DEGs that track MASLD progression. Then, we used a SVM learning algorithm to analyze the data and select the most predictive features. Using linear regression, we identified a signature gene set capable of differentiating the various stages of MASLD and verified it in different independent cohorts of MASLD and a liver cancer cohort.
Conclusions
We identified a signature gene set (i.e., CAPG, HYAL3, WIPI1, TREM2, SPP1, and RNASE6) with strong potential as a panel of diagnostic genes of MASLD-associated disease.

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Editorial

Steatotic liver disease

Non-obese or lean nonalcoholic fatty liver disease matters, but is it preventable or inevitable in light of its risk factors?: Heejoon Jang, Won Kim; Clin Mol Hepatol 2023;29(2):381-383.
Published online March 9, 2023; DOI: https://doi.org/10.3350/cmh.2023.0088

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Snapshot

Microbiome and metabolomics in alcoholic liver disease: Raja Ganesan, Ki Tae Suk; Clin Mol Hepatol 2022;28(3):580-582.
Published online July 1, 2022; DOI: https://doi.org/10.3350/cmh.2022.0171

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Reviews

Hepatic neoplasm

Radiomics and radiogenomics of primary liver cancers: Woo Kyoung Jeong, Neema Jamshidi, Ely Richard Felker, Steven Satish Raman, David Shinkuo Lu; Clin Mol Hepatol 2019;25(1):21-29.
Published online November 16, 2018; DOI: https://doi.org/10.3350/cmh.2018.1007

Abstract
PDF

Concurrent advancements in imaging and genomic biomarkers have created opportunities to identify non-invasive imaging surrogates of molecular phenotypes. In order to develop such imaging surrogates radiomics and radiogenomics/imaging genomics will be necessary; there has been consistent progress in these fields for primary liver cancers. In this article we evaluate the current status of the field specifically with regards to hepatocellular carcinoma and intrahepatic cholangiocarcinoma, highlighting some of the up and coming results that were presented at the annual Radiological Society of North America Conference in 2017. There are an increasing number of studies in this area with a bias towards quantitative feature measurement, which is expected to benefit reproducibility of the findings and portends well for the future development of biomarkers for diagnosis, prognosis, and treatment response assessment. We review some of the advancements and look forward to some of the exciting future applications that are anticipated as the field develops.

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Hepatic neoplasm

The mutational landscape of hepatocellular carcinoma: Ju-Seog Lee; Clin Mol Hepatol 2015;21(3):220-229.
Published online September 30, 2015; DOI: https://doi.org/10.3350/cmh.2015.21.3.220

Abstract
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The development of hepatocellular carcinoma (HCC) is a complex process, and HCC arises from the accumulation of multiple genetic alterations leading to changes in the genomic landscape. Current advances in genomic technologies have revolutionized the search for genetic alterations in cancer genomes. Recent studies in which all coding exons in HCC were sequenced have shed new light on the genomic landscape of this malignant disease. Catalogues of these somatic mutations and systematic analysis of catalogued mutations will lead us to uncover candidate HCC driver genes, although further functional validation is needed to determine whether these genes play a causal role in the development of HCC. This review provides an overview of previously known oncogenes and new oncogene candidates in HCC that were uncovered from recent exome or whole-genome sequencing studies. This knowledge provides direction for future personalized treatment approaches for patients with HCC.

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Original Article

Protein Expression Profiles in a Rat Cirrhotic Model Induced by Thioacetamide: Jeung Hee An, Ph.D.1,3, Jinsil Seong, M.D.1,3, Haejin Oh, M.S.1,3, Wonwoo Kim, M.S.1,3, Kwang-Hyub Han, M.D.2,3 and Yong Han Paik, M.D.2; Korean J Hepatol 2006;12(1):93-102.

Abstract
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Background/Aims
The reactive oxygen species from thioacetamide (TAA) induces rat liver cirrhosis that resembles the human disease, and it can serve as a suitable animal model for studying human liver cirrhosis. The aim of this study was to identify the molecular protein signatures via a proteomics approach with using a rat model with TAA-induced liver cirrhosis. Methods: Male Wistar rats were treated with 0.3 g/L TAA in their drinking water. The animals were then sacrificed at 9 and 30 weeks after TAA administration. The development of liver cirrhosis was observed with histological study. The livers were processed for proteins extraction and the proteins were analyzed by 2-dimensional electrophoresis. The proteins were identified by matrix-assisted laser desorption ionizing time-of-flight mass spectrometry and this was validated by immunohistochemical staining. Results: On the proteomics analysis of the liver tissues, a total of 88 proteins showed significant change in their expression between the controls and the cirrhotic rats. When the proteins were categorized by their function, they included ECM/cellular skeleton, cell proliferation/death signal, metabolism, DNA damage/stress and immune response related proteins. The level of expression gradually increased up to 30 weeks for interleukin-6 (IL-6) precursor, transforming growth factor-beta (TGF-β) induced protein, TIMP-1 and MMP-9. Cytochrome P450 2B, which is required for the metabolic activation of TAA, also showed the same increasing pattern. In contrast, the expression level of the proteins did not show a significant change at 9 weeks, but this increased to 3-fold at 30 weeks for carbonic anhydrase VII, ras related protein Rab 6, Annexin A2, neurofibromatosis type 2 and aldehyde dehydrogenase. Conclusions: This study showed that there is a repertoire of proteins during the development of liver cirrhosis via TAA. In this model, IL-6, TGF-β, MMP-9 and TIMP-1 were reconfirmed as the molecular signatures during the development of TAA-induced liver cirrhosis. (Korean J Hepatol 2006;12:93-102)