Search Results (6,212)

Metabolic dysfunction-associated fatty liver disease (MAFLD) is now the leading cause of hepatocellular carcinoma (HCC) globally. HCC surveillance is currently restricted to patients with cirrhosis, leaving those without cirrhosis, who present with more advanced disease and poorer outcomes without adequate risk stratification tools. This study compared lipid profiles across MAFLD and MAFLD-related HCC (MAFLD-HCC) patients, with and without cirrhosis, to characterise metabolic dysregulation underlying non-cirrhotic MAFLD-HCC (ncMAFLD-HCC). Plasma and liver lipidomic profiles were obtained from 221 patients (140 MAFLD, 66 cirrhotic MAFLD-HCC (cMAFLD-HCC), and 15 ncMAFLD-HCC) using untargeted liquid chromatography mass spectrometry. Univariate, multivariable and enrichment analyses were performed for statistically determining the lipid profile difference between the groups. Seventy percent of lipid classes were more abundant in MAFLD than in ncMAFLD-HCC and cMAFLD-HCC. Multivariate analysis revealed distinct lipid profiles across the three groups in both plasma and liver. Over 100 lipid species including diglyceride (DAG), sphingomyelin (SM), triglyceride (TG), dihydroceramide (DHCer), and linoleic acid derivatives were differentially expressed in ncMAFLD-HCC versus MAFLD, with enrichment in pathways such as glycerolipid metabolism, G-protein signalling, MAPK signalling, EGFR-TKI resistance pathway, implicated in HCC development. ncMAFLD-HCC exhibits a distinct lipid signature, offering preliminary mechanistic insight and a foundation for non-invasive biomarker development. Full article

Yttrium-90 (⁹⁰Y) is a pivotal pure beta-emitting radionuclide extensively employed in the targeted therapy of malignant tumors, such as hepatocellular carcinoma and lymphoma. The ⁹⁰Sr-⁹⁰Y generator system represents the most effective method for producing no-carrier-added (NCA) ⁹⁰Y to meet escalating clinical demands. However, safe clinical application necessitates the stringent separation of its parent isotope, ⁹⁰Sr, which poses significant radiotoxicological risks due to its long half-life and bone-seeking behavior. This review comprehensively summarizes recent advances in solid-phase adsorbent materials developed for the high-efficiency separation of Y³⁺ and Sr²⁺. We systematically analyze the design strategies, molecular recognition mechanisms, and performance evaluation metrics of various functional systems. Key materials discussed include extraction chromatography (EXC) resins based on organophosphorus extractants, diglycolamide (DGA) derivatives, and crown ethers, as well as inorganic ion exchangers such as antimony-based materials, manganese oxides, and zeolite-like molecular sieves. Special attention is given to composite modification strategies, including silica-based and polymer-matrix composites, and metal doping techniques aimed at enhancing radiation resistance, acid stability, and Sr-Y separation factors (SF). Finally, we provide an outlook on the future development of next-generation ⁹⁰Sr-⁹⁰Y generator materials, highlighting the imperative of transitioning from idealized simulated environments to robust, field-ready applications. Full article

Hepatocellular carcinoma (HCC) is a heterogeneous primary liver malignancy characterized by limited treatment options and low overall survival rates. Recent studies have explored the role of programmed death ligand 1 (PD-L1), tumor-associated macrophages (TAMs), and epithelial-mesenchymal transition (EMT) in modulating tumor progression and the response to immunotherapy. This study aimed to investigate the association among PD-L1 expression, TAMs, and EMT in HCC, highlighting the recently proposed immunophenotypic variant—gastric-type HCCs. A retrospective cohort of 50 surgically resected HCC patients was analyzed. Immunohistochemical staining was performed for PD-L1 (clones 28-8 and 22C3), CD68 (TAMs), and EMT markers (VSIG-1, TTF-1, and vimentin). PD-L1 expression was detected in 52% of the patients and was significantly associated with high TAM counts (p < 0.001). Compared with PD-L1-negative patients, those with gastric-type HCCs, which are characterized by VSIG-1 and TTF-1 co-expression and vimentin negativity, demonstrated improved survival outcomes (p = 0.03). Integration of immune and EMT profiling of tumor cells in routine diagnostics may guide prognosis and immunotherapeutic strategies in HCC. Further molecular validation is required to confirm the biological significance of the proposed gastric-type HCC immunophenotype. Full article

The widespread adoption of prostate-specific membrane antigen (PSMA)-targeted PET/CT has profoundly reshaped molecular imaging in prostate cancer and has substantially reduced the routine use of radiolabeled choline tracers. However, the transition from choline to PSMA imaging should not be interpreted simply as the replacement of one radiopharmaceutical by another, but rather as part of a broader evolution from metabolism-based imaging toward receptor-targeted and biology-driven imaging strategies. This narrative review critically reassesses the residual and emerging role of choline PET/CT in the PSMA era, with particular attention to the biological rationale of choline uptake, selected prostate cancer scenarios, and extra-prostatic applications. In prostate cancer, PSMA PET/CT remains the dominant imaging modality because of its superior diagnostic performance, particularly in biochemical recurrence; nevertheless, choline PET/CT may provide complementary metabolic information in highly selected settings, including PSMA-low or heterogeneous disease, aggressive or dedifferentiated variants, neuroendocrine transformation, equivocal PSMA findings, and limited PSMA availability. These prostate cancer applications, however, are supported mainly by biological rationale, indirect evidence, and limited clinical data and should therefore be regarded as exploratory rather than established indications. By contrast, ¹⁸F-fluorocholine PET/CT has emerged as a clinically established imaging modality in primary hyperparathyroidism, particularly after negative or inconclusive conventional imaging, with prospective studies and meta-analyses demonstrating high detection rates and superior performance compared with conventional scintigraphic techniques. Additional applications in hepatocellular carcinoma and selected neuro-oncologic settings remain exploratory and require further validation. Overall, choline PET/CT should not be considered obsolete in the PSMA era, but selectively repositioned within biology-driven and multiparametric imaging strategies, with its strongest evidence currently supporting primary hyperparathyroidism and its other applications requiring cautious interpretation and further prospective validation. Full article

Fibrosis is a common extracellular matrix pathology characterized by increased scarring, representing a critical checkpoint toward cirrhosis and hepatocellular carcinoma. Its onset involves coordinated interplay among hepatocytes, Kupffer, and hepatic stellate cells (HSCs). Extracellular ATP and its derivates act as crucial damage-associated molecular patterns when released by injured liver cells, binding to specific purinergic receptors (P2X, P2Y, and P1) to establish an autocrine–paracrine signaling loop. The hepatic fibrotic response underlies the activation of ATP receptors that generate second messengers and cationic conductance. In parallel, extracellular nucleotidases hydrolyze ATP towards less phosphorylated intermediates and adenosine. This review focuses on the role of P2X and P2Y receptors in liver injury. The P2X7 receptor regulates the NLRP3 inflammasome in Kupffer cells and HSCs, while the P2X4 receptor is upregulated in myofibroblasts, modulating migration and matrix synthesis. Among P2Y receptors, P2Y2 drives inflammation and steatosis but promotes HIF-1α-mediated DNA repair. The P2Y6 receptor promotes alcohol-induced injury but restrains metabolic-dysfunction-associated steatohepatitis. P2Y2 and P2Y4 receptors maintain biliary homeostasis in cholangiocytes, whereas the P2Y1 receptor preserves HSC quiescence by blocking YAP translocation. Finally, UDP-glucose–P2Y14 induces HSC activation. Targeting these specific purinergic receptors or ecto-nucleotidases represents a promising pharmacological frontier against hepatic fibrosis. Full article

Hepatocellular carcinoma (HCC) remains one of the leading causes of cancer-related mortality worldwide and is characterized by extensive vascularization, aggressive progression, and limited therapeutic responsiveness. Angiogenesis plays a central role in HCC development by supporting tumor growth, metabolic adaptation, invasion, and metastatic dissemination. Although anti-angiogenic therapies targeting the vascular endothelial growth factor (VEGF) pathway have improved clinical management, their overall survival benefit remains modest because of compensatory signaling, adaptive resistance, and the highly complex nature of the tumor microenvironment (TME). Astrocyte elevated gene-1/metadherin (AEG-1/MTDH) has emerged as a multifunctional oncogene that functions by orchestrating interconnected angiogenic, inflammatory, metabolic, and immune-regulatory programs within the hepatic tumor microenvironment. AEG-1 regulates angiogenesis through modulation of VEGF-family signaling, NF-κB activation, hypoxia-responsive pathways, PI3K/AKT signaling, endothelial remodeling, and translational control of pro-angiogenic mediators. Emerging evidence further implicates AEG-1 in hypoxia adaptation, immune evasion, extracellular vesicle signaling, and metabolic reprogramming, supporting its role as a systems-level regulator of HCC angiogenesis. This review summarizes the current understanding of the molecular mechanisms through which AEG-1 regulates angiogenesis in HCC, discusses its interactions with the TME and anti-angiogenic resistance pathways, and highlights future translational opportunities for developing multi-targeted therapeutic strategies beyond conventional VEGF-centric approaches. Full article

Hepatocellular carcinoma is one of the most aggressive malignancies worldwide, with limited therapeutic options. Boswellia serrata Roxb., an Indian medicinal tree, produces a resin rich in essential oil and boswellic acids, particularly acetyl-11-keto-β-boswellic acid (AKBA), with demonstrated antiproliferative and pro-apoptotic activities. This study investigated the cytotoxic effects of B. serrata essential oil and AKBA on hepatocarcinoma Huh-7 cells in both monolayer and three-dimensional spheroid cultures and characterized the underlying molecular targets. Essential oil was extracted and analyzed by gas chromatography-mass spectrometry (GC-MS). Cytotoxicity was assessed using the cell counting kit-8 (CCK-8). Three-dimensional spheroid cultures were also established to evaluate anti-tumoral potential. Expression of cyclin D1, cyclin-dependent of kinase 4 (CDK4) (cyclin-dependent kinase inhibitor 1A (p21), E-cadherin, (alpha fetoprotein) AFP, epithelial cell adhesion molecule (EpCAM), Myeloid cell leukemia-1 (Mcl-1), and caspase-3 was analyzed by western blot. In addition, an in silico analysis was performed on the main constituents of B. serrata essential oil targeting 5-lipoxygenase (5LO). The results showed cytotoxic effects, with AKBA exhibiting greater potency than the essential oil. Cytotoxicity was associated with caspase-3-mediated apoptosis, with minimal effects on cell cycle and epithelial–mesenchymal transition markers. The in silico analysis predicted that some compounds may act as competitive inhibitors of the 5LO at the catalytic site and partially activate pro-apoptotic pathways. These data support the potential of B. serrata-derived compounds as novel anti-hepatocarcinoma agents, with AKBA and longifolene as leads for further preclinical and clinical research. Full article

Background/Objectives: The prevalence and management options of bland (non-neoplastic) portal vein thrombosis (PVT) in patients with hepatocellular carcinoma (HCC) are poorly characterized and data remain limited. Methods: We performed a retrospective analysis of a prospectively collected single-center cohort of 638 patients with HCC. Bland PVT was identified at baseline or during follow-up. Treatment exposure was modeled as time-varying to account for differences in timing of anticoagulation initiation. Results: Bland PVT was identified in 39 patients (25 at baseline and 14 during follow-up). Patients with PVT showed features of more advanced portal hypertension (lower platelet count and higher prevalence of ascites) and had a higher tumor burden (more often outside the Milan criteria; higher AFP). A total of 30 patients received anticoagulation. Anticoagulation was associated with partial or complete recanalization in 30% of cases at three months and with decrease in bilirubin, but was not associated with improved 1 year survival. Bleeding events occurred in four anticoagulated patients (13.3%). Conclusions: Bland PVT in HCC is associated with more severe liver disease. Our data indicate that anticoagulation in patients with HCC and concomitant bland PVT was generally well-tolerated and was associated with thrombus regression in one-third of cases. However, we did not observe an improved survival in patients on anticoagulation. Full article

The new therapeutic options now available for patients with hepatocellular carcinoma (HCC) have made their assessment more complex, especially due to the different stages of liver cirrhosis typically associated with this tumor. The management of the disease therefore requires an interdisciplinary approach aimed at identifying the most appropriate treatment based on the risk–benefit profile and residual liver function, as well as in relation to the patient’s age and potential for a full or partial recovery, risk of complications, and cancer recurrence. Another factor to be carefully considered in patients with hepatocellular carcinoma is the frequent comorbidities and the associated socio-health variables (substance abuse, addictions, unfavorable economic or family circumstances), which can impact patient management or the possibilities for long-term monitoring, thus influencing the choice of the most appropriate therapeutic pathway. The healthcare services offered in the Province of Salerno (Campania Region, Southern Italy) to ensure all possible diagnostic and therapeutic options for these patients can be difficult to access due to the territorial extension of the Local Health Authority, characterized by clinics and hospitals located in distant locations, as well as the potential fragmentation of expertise between the University Hospital and ambulatorial facilities or small hospitals. An interdisciplinary consensus conference on the management of patients with HCC has been set with the aim of involving clinicians and surgeons working in healthcare facilities located in Salerno and its Province for the optimal care and effective management of these patients, taking into account all the clinical characteristics of the disease and individual health needs or expectations, from the perspective of personalized medicine. Full article

Background: Statins have pleiotropic anti-inflammatory, antifibrotic, and potential antineoplastic effects. Although several studies have linked statin exposure to lower hepatocellular carcinoma (HCC) incidence, their effect on survival after HCC diagnosis remains uncertain. We evaluated whether statin therapy before HCC diagnosis was associated with overall survival in a real-world cohort. Methods: We performed a retrospective single-center cohort study of consecutive patients with HCC managed at a tertiary referral center between January 2000 and January 2025. Demographic, clinical, laboratory, tumor-related, and treatment variables were collected at diagnosis and during follow-up. Patients were classified according to statin use before HCC diagnosis. Overall survival (OS) was assessed using Kaplan–Meier analysis and Cox proportional hazards regression. Results: Overall, 190 patients were included; 172 (90.5%) were male, 136 (71.6%) had cirrhosis, and 42 (22.1%) received statins. Statin users more frequently had diabetes mellitus, elevated body mass index and arterial hypertension, but baseline liver function, alpha-fetoprotein levels, tumor burden, and treatment allocation were broadly comparable between groups. Among 159 patients with available survival data, statin users had longer OS than non-users (mean 82.5 vs. 41.7 months; median 57 vs. 31 months; log-rank p < 0.001). In univariate Cox analysis, statin therapy was associated with reduced mortality risk (HR 0.45, 95% CI 0.28–0.70, p < 0.001). This association remained significant across multivariable models adjusting for baseline liver function, tumor stage, vascular invasion, and diagnostic era. Conclusions: Pre-diagnostic statin therapy was independently associated with improved OS in patients with HCC. These hypothesis-generating findings warrant prospective multicenter validation and careful assessment of confounding by indication. Full article

Background: Effects of neoadjuvant immunotherapy (NIT) before liver resection are not well-described in hepatocellular carcinoma (HCC). Survival and R0 resection rates in HCC patients undergoing curative-intent resection with or without NIT were evaluated. Methods: A retrospective study of stage I-III HCC patients undergoing hepatectomy from the 2017–2022 National Cancer Database was performed. Patients receiving NIT were exactly matched 1:3 to non-NIT patients by clinical stage. Primary outcomes were margin positivity, 30- and 90-day mortality, and overall survival. Results: After matching 510 patients, 97 received NIT and 291 did not (non-NIT). Resections included segmental (178, 45.9%), lobar (149, 38.4%), and extended hepatectomy (61, 15.7%). The NIT group included ablation (6, 6.2%), radiation (25, 25.8%), and Y90 (18, 18.6%). The non-NIT group included 124 (42.6%) chemotherapy, 23 (7.9%) chemotherapy plus ablation, 31 (10.7%) chemotherapy plus radiation, four (1.4%) radiation, and 109 (37.5%) upfront surgery. NIT patients were treated more at high-volume (41.2% vs. 0%) and academic/research centers (85.4% vs. 50.5%). NIT R0 resection rates were higher (97.9% vs. 93.2%, p = 0.009). Median survival was higher in the NIT group (59.1 vs. 50.4 months, p = 0.002); 30- and 90-day mortality were similar. NIT was not independently associated with improved survival in multivariable Cox regression (HR 0.73, 95% CI [0.35, 1.55]), although the effect estimate indicates a protective effect may be present. Conclusions: NIT was associated with higher R0 resection rates and overall survival without increasing short-term mortality in selected patients at high-volume academic centers, but was not independently associated with survival when adjusting for confounders. As we continue to see increasing use of immunotherapy in the neoadjuvant setting, these findings should be considered hypothesis-generating and warrant prospective validation before widespread adoption for HCC. Full article

Hepatocellular carcinoma (HCC) remains a malignancy with poor prognosis and limited therapeutic targets. Emerging evidence suggests a critical role for iron metabolism and ferroptosis in tumor progression. However, the involvement of hematopoietic lineage cell-specific protein 1 (HAX1) in HCC, particularly its regulatory role in ferroptosis, remains largely unknown. Here, we report that HAX1 is significantly upregulated in HCC tissues and correlates with advanced pathological stages and poor patient survival, suggesting its potential as an oncogene. Functionally, HAX1 overexpression promotes the proliferation and migration of HCC cells, while its knockdown inhibits these malignant phenotypes. Mechanistically, we demonstrate that HAX1 acts as a negative regulator of ferroptosis. Silencing HAX1 sensitizes HCC cells to the ferroptosis inducer IKE, leading to abnormal accumulation of intracellular ferrous iron (Fe²⁺) and increased lipid reactive oxygen species (ROS). Conversely, HAX1 overexpression suppresses iron overload and lipid peroxidation. Furthermore, we reveal that HAX1 maintains redox homeostasis by regulating the GSH/GPX4 antioxidant pathway. Knockdown of HAX1 depletes reduced glutathione (GSH), reduces glutathione peroxidase activity, and downregulates key ferroptosis defense proteins, including GPX4, FSP1, and SLC7A11. Our findings identify HAX1 as a critical promoter of HCC progression that functions by inhibiting ferroptosis through the modulation of iron homeostasis and the GSH/GPX4 pathway. Targeting the HAX1-mediated anti-ferroptotic mechanism may represent a promising therapeutic strategy for HCC treatment. Full article

Background: Hepatitis delta (HDV) is the most severe form of chronic viral hepatitis, with rapid progression to cirrhosis and hepatocellular carcinoma, and remains neglected in the Amazon Basin. The state of Acre, in the Western Brazilian Amazon, is endemic for HDV, with a high prevalence of genotype 3 (HDV-3). This study aimed to analyze epidemiological data, quantify HDV RNA, identify genotypes, and describe the phylogeny and phylogeography of HDV in Acre. Methods: This cross-sectional study included patients positive for HBsAg and anti-HDV under follow-up at the Specialized Assistance Service (SAE) in Rio Branco, Acre, between March and November 2023. Blood samples were collected for HDV RNA quantification using one-step RT-qPCR. Samples with detectable viremia (Ct ≤ 30) underwent Nested-PCR, Sanger sequencing, phylogenetic analysis (Maximum Likelihood), temporal signal evaluation, and Bayesian phylogeographic reconstruction. Results: Among 108 patients (median age 43; 55.6% female), HDV RNA was detected in 48.1%, with viral loads ranging from 140 to 24,000,000 copies/mL. Of these, 55.8% had >100,000 copies/mL. Genotyping (n = 41) identified exclusively HDV-3. Phylogenetic analysis revealed genetic heterogeneity among HDV-3 isolates, with the formation of two major phylogenetic clades. Bayesian analysis estimated tMRCA around 1818 and suggested dispersion from Amazonas to Acre and neighboring regions. Conclusion: HDV-3 predominates in Acre with high genetic diversity, indicating sustained viral circulation in the Western Amazon and reinforcing the need for improved surveillance and diagnosis. Full article

Background/Objectives: Hepatocellular carcinoma (HCC) arises through heterogeneous pathways involving chronic hepatitis B virus infection, hepatitis C virus infection, alcohol-related liver disease, metabolic dysfunction-associated steatotic liver disease, fibrosis, cirrhosis, and environmental exposures. Genome-wide association studies (GWASs) have identified host germline loci associated with HCC susceptibility, but interpretation is complicated by aetiology, ancestry, liver disease stage, and the definition of controls. This narrative review examines current GWAS evidence for HCC, with emphasis on aetiology-specific susceptibility, functional interpretation, cross-disorder genetic effects, and clinical translation. Methods: Studies were identified through iterative searches of PubMed/PMC, publisher pages, academic search tools, and citation tracking, supplemented by targeted searches for major HCC-associated loci. Sources were chosen based on relevance to GWAS discovery, replication, meta-analysis, functional interpretation, polygenic risk modelling, or HCC risk stratification, rather than by a formal systematic review protocol. Results: Viral HCC studies most often implicate immune regulation and antigen presentation, including MICA, HLA-DQ, HLA-DQB1, HLA class I, HCP5, STAT4, DEPDC5, and FAM114A1. Alcohol-related, metabolic, and non-viral HCC studies more often implicate hepatic lipid metabolism, telomere biology, iron metabolism, steatosis, and cirrhosis-related pathways, including PNPLA3, TM6SF2, TERT, HSD17B13, APOE, HFE, and MTARC1. Recent studies increasingly combine GWASs with fine-mapping, functional annotation, transcriptomic analyses, and risk modelling. Conclusions: HCC genetic susceptibility is highly aetiology-specific and overlaps with other liver and metabolic disorders, but discoveries from genetic studies have not yet been translated into routine clinical practice. Future work should prioritise multi-ancestry cohorts, disease-stage-aware controls, functional validation, and prospectively tested genetic risk models. Full article

Background and Objectives: Sevoflurane, a widely used inhalational anesthetic, is frequently administered during hepatocellular carcinoma (HCC) surgery, including hepatic resection and orthotopic liver transplantation. Because such procedures often require prolonged anesthetic exposure, the potential influence of sevoflurane on HCC cell behavior is of clinical interest. We aimed to evaluate the effects of sevoflurane on the proliferation and migration of HepG2 cells in vitro and on tumor growth in a xenograft mouse model in vivo, and to explore whether hypoxia-inducible factor-1α (HIF-1α) might be involved in this process. Materials and Methods: For the in vitro experiments, HepG2 cells were exposed to room air (0%), 2%, or 4% sevoflurane. A scratch wound healing assay was used to assess cell migration, and the number of viable cells was quantified by hemocytometer counting on day 4 to estimate proliferation. For the in vivo experiments, BALB/c nude mice bearing HepG2 xenografts were exposed to room air, 2% sevoflurane, or 4% sevoflurane for 3 h, three times weekly for 5 weeks. Tumor size and tumor weight were measured at the end of the exposure period. HIF-1α protein levels in tumor tissue were measured by enzyme-linked immunosorbent assay (ELISA) in tumor lysates and normalized to total tumor protein as an exploratory mechanistic analysis. Given the small sample available for this endpoint, the analysis had limited sensitivity to detect modest differences. Results: When wound closure was quantified and pooled across the analyzable experiments, no statistically significant difference was detected among the room air, 2% sevoflurane, and 4% sevoflurane groups (day-2 closure 19.9 ± 32.1%, 22.1 ± 25.8%, and 22.3 ± 28.8%, respectively; repeated-measures ANOVA p = 0.82), with variability dominated by between-experiment rather than treatment differences. In the proliferation assay, the number of viable HepG2 cells on day 4 was significantly lower in the 2% sevoflurane group (62.6 ± 3.3 × 10⁵) than in the room air group (68.5 ± 4.2 × 10⁵; p < 0.05); the 4% sevoflurane group (66.0 ± 3.2 × 10⁵) showed an intermediate value that did not reach statistical significance. In the xenograft model, mean tumor size in the room air, 2% sevoflurane, and 4% sevoflurane groups was 7.1 ± 1.9, 2.7 ± 2.0, and 2.1 ± 0.9 cm³, respectively (p = 0.041 for room air vs. 2% sevoflurane; p = 0.034 for room air vs. 4% sevoflurane). Tumor weight was likewise lower in the sevoflurane groups (room air, 7.88 ± 2.2 g; 2% sevoflurane, 2.95 ± 2.1 g; 4% sevoflurane, 2.3 ± 1.6 g; p = 0.044 for room air vs. 2% sevoflurane; p = 0.067 for room air vs. 4% sevoflurane). No statistically significant differences in tumor HIF-1α protein levels were observed among the three groups. Conclusions: In this exploratory study, sevoflurane exposure was associated with reduced HepG2 xenograft tumor growth in vivo, whereas its in vitro effects were more limited: a reduction in viable cell number was observed only at 2% sevoflurane, and an effect on cell migration could not be confirmed when analyzed across experiments. Tumor HIF-1α levels did not differ significantly between groups, suggesting that other molecular pathways may be involved. Further mechanistic and clinical studies are warranted before any conclusions can be drawn about the relevance of these findings to the perioperative management of patients with HCC. Full article