Hepatocellular Carcinoma (HCC) is the primary malignancy of the liver, which is typically associated with underlying chronic liver diseases, such as cirrhosis, hepatitis B, or hepatitis C infections. Inflammation is a prevailing concern for liver disorders with documented impacts on the tumorigenic and metastatic propensities of individuals afflicted with HCC. Portal vein tumor thrombus (PVTT) is a widespread problem among patients with HCC, manifesting in approximately 50% of cases. A comprehensive understanding of the PVTT mechanism is imperative to comprehend and address the challenges associated with HCC progression. The intricate nature of the mechanism underlying PVTT formation and its influence on metastasis progression remains to be fully eluci-dated. Given that the portal venous system's microenvironment is conducive to tumor cells' survival and further metastasis, a critical exploration of the associations and parallels among metastasis, epithelial-mesenchymal transition (EMT), and PVTT becomes paramount. Signaling pathways play diverse roles in the progression of various diseases, with particular significance attributed to their role in HCC advancement, which highlights the necessity for precise determination of their effects in the context of HCC and PVTT. We highlight the significance of understanding the interplay between EMT, inflammation, and PVTT in the HCC context. Furthermore, we revisit the signaling pathways impacting this interconnected network, providing useful perspectives to support research initiatives. This review aims to guide research studies toward promising outcomes in exploring HCC complexities by defining the possible association between PVTT and EMT, thus identifying potential target areas for advanced therapeutics.

Objectives: The impact of graft type on the outcomes of liver transplantation (LT) for hepatocellular carcinoma (HCC) remains controversial. We aimed to evaluate the efficacy of living donor (LDLT) versus deceased donor LT (DDLT) by analyzing disease-free survival (DFS) and overall survival (OS).
Methods: We evaluated 356 HCC patients who underwent LT. There were two groups: LDLT and DDLT. We compared OS, DFS, demographic data, and clinical variables between the cohorts. The study also evaluated the impact of Milan criteria adherence on patient outcomes.
Results: The study population was 85.9% male, with a mean age of 52.69 (±0.61) years.While nearly half of the patients were within the Milan criteria, a significant majority of procedures, n=356 (94.7%), were LDLT. The OS and DFS were comparable between the groups, irrespective of Milan criteria compatibility. Patients with tumors within the Milan criteria demonstrated a significantly better OS and DFS compared to those with tumors beyond the criteria (p<0.001).
Conclusion: The Milan criteria remain the best prognostic indicator after liver transplantation for HCC. Liver graft type (LDLT vs. DDLT) did not affect liver transplantation (LT) outcomes for HCC, regardless of Milan criteria adherence.

Objectives: Hepatocellular carcinoma (HCC) is a primary liver tumor that exhibits significant resistance to conventional chemotherapeutic treatments. Phenethyl isothiocyanate (PEITC), a phytochemical derived from Cruciferae plants, has emerged as a promising therapeutic candidate. We aimed to assess the effects of PEITC on cell proliferation and migration in the SNU-449 HCC cells.
Methods: To evaluate the effect of PEITC (2.5-100 µM) on cell viability and migratory rate in SNU-449 cells, MTT, Sulforhodamine B (SRB), colony formation and wound healing assays were analyzed. All data are presented as the median and interquartile range (IQR).
Results: The results indicated that cell viability in response to PEITC began to decrease at 10 µM after 72 hours, with absorbance values of 0.431 (IQR: 0.458) for the 10 µM treatment and 0.67 (IQR: 0.049) for the control group, respectively (p<0.05). The SRB assay results for PEITC-treated and control groups were 0.581 (IQR: 0.789) and 0.381 (IQR: 0.365), respectively (p>0.05). The surviving fraction of cells treated with PEITC was 19.35% relative to untreated controls. Wound closure percentages in the PEITC and control groups were 10.35% (IQR: 10.3) and 59.75% (IQR: 15.4), respectively (p<0.05).
Conclusion: Our results suggest that PEITC may be beneficial in ameliorating hepatocellular carcinoma. Further comprehensive studies are planned to elucidate the molecular mechanisms underlying the antitumoral effect of PEITC.

Objectives: Early hepatic artery thrombosis (eHAT) is a primary cause of graft dysfunction, significantly contributing to mortality and morbidity in liver transplant (LT) recipients. This study aims to identify factors influencing the development of eHAT in LT patients at our institution.
Methods: This retrospective study included 428 adult patients who underwent living donor liver transplantation (LDLT) at our institution. The demographic, clinical, and operative characteristics of the remaining 428 patients were analyzed to evaluate risk factors for eHAT development.
Results: eHAT developed in 12 patients (2.8%). The recipient population had a male-to-female ratio of 294: 136, a median age of 52 years (range: 18-73), a mean graft-to-recipient weight ratio (GRWR) of 1.06±0.23, and a mean Model for End-Stage Liver Disease (MELD) score of 15.4±6.3. The incidence of eHAT was significantly higher in patients with hepaticojejunostomy (HJ) (5% vs. 2.4%; p<0.05) and in those who received cryopreserved artery grafts (CAG) (p<0.05). Among the 173 patients (40.2%) with a GRWR <0.98, 9 (5.2%) developed eHAT (p<0.05). Furthermore, both erythrocyte suspension (ES) and fresh frozen plasma (FFP) transfusion rates were significantly higher in patients who developed eHAT (p<0.05). Preoperative portal vein thrombosis (PVT) was also significantly associated with a higher rate of eHAT (p<0.05). Multivariate analysis identified CAG use for arterial reconstruction, HJ for biliary anastomosis, intraoperative FFP transfusion, GRWR <0.98, and t preoperative PVT as independent risk factors for eHAT.
Conclusion: Our findings indicate that hepaticojejunostomy, a graft-to-recipient weight ratio below 0.98, intraoperative FFP transfusion, pre-transplant PVT, and the use of CAG in hepatic arterial reconstruction are significant risk factors for early hepatic artery thrombosis following living donor liver transplantation.

Objectives: A Network Phenotyping Strategy (NPS) was recently created to stage hepatocellular carcinoma (HCC) from an Italian dataset into 25 discrete phenotypes sT, s=1→τ1, …, s=25→τ25 ordered (τ1<τ2,…,<τ25 ) according to the dynamics of the HCC progression from its onset.
Methods: To use NPS methodology on an ethnically different, Turkish HCC cohort that had, in addition, been stratified according to patients selected for liver transplantation or not.
Results: The Turkish patients had only a smaller subset of 16 out of the 25 HCC phenotypes of the Italian patients. HCC progression through phenotypes, which are exclusive to the Italian population, is a dominantly tumor biology-driven process, occurring within a constant extent of liver microenvironment damage. In contrast, in phenotypes shared by the minority of Italian patients and the majority of Turkish patients, the HCC progresses by a more complex disease burden generating mechanism, consisting of simultaneous tumor biology-driven damage, accompanied by advancing liver microenvironmental impairment.
NPS objective stratification of a “real world clinical practice” patient cohort into subpopulations with identical HCC clinical phases enabled the simulation of clinician-dependent selection for liver transplantation or not in this cohort, using specific baseline variables. A clearer understanding of HCC biology has allowed us to identify differing biological phenotypes. The predominant 12T phenotype was examined in detail and combined with surgical knowledge obtained retrospectively as to the difference between transplanted and non-transplanted patients to then derive models that may be useful for biology-dependent surgical decision support in future patients.
Conclusion: Only a subset of all HCC phenotypes appeared in the Turkish cohort and may be explained by the non-screened patients having HCC as a secondary problem, and is primarily driven by the liver microenvironment, in contrast to Italy, where HCC develops (predominantly) in healthier livers.

Objectives: Hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA) are the most common primary liver cancers that differ in origin and histopathological features. This study aimed to identify the differentially expressed genes and dysregulated pathways between HCC and iCCA using transcriptomic and bioinformatics analyses.
Methods: Gene expression data were obtained from the GEO database (accession number GSE241466), comprising RNA-seq profiles from 3 HCC and 5 iCCA tumor samples. Data were processed and analyzed using the limma package in R, applying a |log2 fold change| > 1 and adjusted p-value < 0.05 as significance thresholds. Visualization techniques including UMAP, volcano plots, were employed. Functional enrichment analysis of DEGs was conducted via the clusterProfiler package, integrating gene ontology terms and gene-concept network plots to explore relevant biological processes and molecular functions.
Results: Out of 17,637 genes, a total of 1,248 genes were found to be significantly differentially expressed between HCC and iCCA. UMAP analysis demonstrated clear clustering and separation between the two cancer types. Enrichment analyses revealed key biological differences, notably in metabolic reprogramming, extracellular matrix organization, and neuron projection develop-ment. Notably, genes such as NLGN1, EPHA6, and SEMA3E, involved in neural differentiation and signaling, were significantly enriched in iCCA, suggesting a potential role of neuron-like features in its progression. Conversely, HCC samples were characterized by upregulation of genes linked to amino acid metabolism and hepatocellular-specific functions.
Conclusion: This study elucidates the molecular divergence between HCC and iCCA, identifying distinct gene expression profiles and enriched biological pathways. The activation of neural signaling pathways in iCCA, coupled with differential engagement of metabolic and morphogenetic processes, suggests subtype-specific mechanisms that could inform future diagnostic and therapeutic strategies. These findings provide a foundation for the development of tailored clinical interventions in primary liver cancers.

HIV-infected individuals may develop co-infection and liver failure due to hepatitis viruses sharing similar transmission routes. While HIV infection was considered a contraindication for liver transplantation in the past, liver transplantation can be performed in these patients today as a result of the progress made in antiretroviral therapies. In this article, we described the liver transplantation procedure we performed on a patient infected with HIV and Hepatitis B virus and on antiretroviral therapy. Post-transplant follow-up and treatment of these patients should be performed carefully and meticulously by a multidisciplinary team.