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Purpose: The impact of visceral adiposity on overall survival (OS) in hepatocellular carcinoma (HCC) receiving immunotherapy was unclear. We aimed to determine how visceral adiposity affected OS and explore the interrelationships between visceral adiposity, body mass index (BMI), and other body compositions. Patients and Methods: Data from three centers were retrospectively analyzed. Skeletal muscle index (SMI), skeletal muscle density (SMD), visceral adipose tissue index (VATI), and subcutaneous adipose tissue index (SATI) were used to define each body composition. The BMI subgroups included the underweight, the normal weight, and the obesity. The Log rank test compared survival curves calculated by the Kaplan-Meier method. The relationships between body compositions and BMI with OS were examined using Cox proportional risk regression models. Results: A total of 305 patients who met the criteria were included. Patients with low VATI had significantly worse OS (P = 0.001). The protections of VATI (P = 0.011) on OS were independent of covariates. However, after additional adjustment of SMI, the effect of VATI on OS disappeared (P = 0.146), but the effect of SMD on OS did not (P = 0.021). BMI has a significant U-shaped relationship with OS, and the effect of BMI on OS equally disappeared after additional adjustment by SMI. Conclusion: This study first demonstrated that high VATI and mid-level BMI were protective for the survival of patients with HCC receiving immunotherapy. Skeletal muscle status (including SMI and SMD) may be the better predictor for outcomes of patients with HCC receiving immunotherapy. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to compare the clinical efficacy of laparoscopic liver resection (LLR) and radiofrequency ablation (RFA) in treating solitary hepatocellular carcinoma (HCC) of the hepatic caudate lobe. Methods: Patients with hepatic caudate lobe HCC who underwent LLR or RFA at three hospitals in China between February 2015 and February 2021 were included. In total, 112 patients met the inclusion criteria, of whom 52 underwent RFA and 60 underwent LLR. The outcomes of the two groups were compared and analyzed using propensity score matching (PSM) method. Results: There were no significant differences between the two groups in terms of sex, HBV/HCV positivity, AFP positivity (>100 ng/mL), tumor position, Child–Pugh score, or preoperative liver function tests (ALT, AST, TBIL, ALB, and PT) (p > 0.05). Compared to the LLR group, the RFA group had a shorter operation time, less intraoperative bleeding, and shorter postoperative hospital stay (p < 0.05). There was no statistically significant difference in overall postoperative complications between the two groups (p > 0.05). Despite the larger tumor size, the LLR group had better postoperative recurrence‐free survival (RFS) (p = 0.00027) and overall survival (OS) (p = 0.0023) than the RFA group. After one‐to‐one PSM, 31 LLR patients and 31 RFA patients were selected for further analyses. The advantages of LLR over RFA were observed in terms of RFS (p < 0.0001) and OS (p = 0.00029). Conclusion: LLR should probably be recommended as the preferred method for solitary caudate lobe HCC. [ABSTRACT FROM AUTHOR]

To compare the efficacy and complications of ultrasound-guided percutaneous radiofrequency ablation of hepatocellular carcinoma (HCC) in the hepatocaval confluence with those of HCC in the non-hepatocaval confluence and to explore the risk factors that lead to radiofrequency ablation failure and patient local tumor progression (LTP). From January 2017 to January 2022, 86 patients with HCC in the hepatocaval confluence who had radiofrequency ablation were included. A 1:1 propensity-matched group of patients with HCC in the non-hepatocaval confluence with comparable clinical baseline traits, such as tumor diameter and tumor number, served as the control group. The two groups' complications, primary efficacy rate (PER), technical success rate (TSR), and prognosis were estimated. After PSM, no significant difference of TSR (91.7% vs 95.8%, p = 0.491) and PER (95.8% vs 97.2%, p = 1.000) and 1-, 3-, and 5-year LTP rate (12.5% vs 9.9%, 28.2% vs 27.7%, 40.8% vs 43.8%, p = 0.959) and 1-, 3-, and 5-year DFS rate (87.5% vs 87.5%, 62.3% vs 54.2%, 18.1% vs 22.6%, p = 0.437) and 1-, 3-, and 5-year OS rate (94.3% vs 95.7%, 72.7% vs 69.6%, 20.9% vs 33.6%, p = 0.904) was detected between the two groups. The tumor-to-IVC distance was an independent risk factor for radiofrequency ablation failure in HCC patients in the hepatocaval confluence (OR = 0.611, p = 0.022). Besides, tumor diameter was an independent risk factor for predicting LTP in patients with HCC in the hepatocaval confluence (HR = 2.209, p = 0.046). HCC in the hepatocaval confluence can be effectively treated with radiofrequency ablation. To maximize treatment efficacy, the tumor-to-IVC distance and tumor diameter should be assessed before the operation begins. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Reclassification of therapeutic response of unresectable hepatocellular carcinoma to anti-angiogenic therapy and immunotherapy using alpha RECIST" published in the journal European Radiology. The correction addresses an error in the Graphical Abstract, specifically the deletion of the value "20" in typesetting. The corrected Graphical Abstract provides accurate information on the therapeutic response and prognostic stratification for hepatocellular carcinoma. The publisher, Springer Nature, maintains a neutral stance on jurisdictional claims and institutional affiliations. [Extracted from the article]

Cancer cells sustain high levels of glycolysis and glutaminolysis via reprogramming of intracellular metabolism, which represents a driver of hepatocellular carcinoma (HCC) progression. Understanding the mechanisms of cell metabolic reprogramming may present a new basis for liver cancer treatment. Herein, we collected HCC tissues and noncancerous liver tissues and found hepatitis B virus X‐interacting protein (HBXIP) was found to be upregulated in HCC tissues and associated with poor prognosis. The N6‐methyladenosine (m6A) level of hypoxia‐inducible factor‐1α (HIF‐1α) in HCC cells was evaluated after the intervention of METTL3. The possible m6A site of HIF‐1α was queried and the binding relationship between METTL3 and HIF‐1α was verified. The interference of HBXIP suppressed HCC malignant behaviors and inhibited the Warburg effect in HCC cells. METTL3 was upregulated in HCC tissues and positively regulated by HBXIP. Overexpression of METTL3 restored cell metabolic reprogramming in HCC cells with partial loss of HBXIP. HBXIP mediated METTL3 to promote the metabolic reprogramming and malignant biological behaviors of HCC cells. The levels of total m6A in HCC cells and m6A in HIF‐1α were increased. METTL3 had a binding relationship with HIF‐1α and mediated the m6A modification of HIF‐1α. In conclusion, HBXIP drives metabolic reprogramming in HCC cells via METTL3‐mediated m6A modification of HIF‐1α. [ABSTRACT FROM AUTHOR]

Infection of hepatitis C virus (HCV) is associated with primary hepatocellular carcinoma (HCC). However, its underlying molecular mechanisms remain enigmatic. Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2), a new negative regulator of immunity, plays significant roles in modulating inflammation and tumorigenesis. We hypothesized that TIPE2 might be involved in the development of HCV-induced HCC. To test this hypothesis, the expression of TIPE2 was determined by Western blot in the tumor and pericarcinomatous tissues collected from ten HCV-positive HCC patients; the interaction between TIPE2 and HCV-encoded non-structural proteins was analyzed by immunoprecipitation and immunofluorescence assays, and tumorigenesis and its mechanisms were studied in cell models and nude mice. Our results demonstrated that the expression of TIPE2 was significantly reduced in HCC tissues compared to that in the paracarcinoma tissues. HCV-encoded non-structural protein NS5A could specifically interact with TIPE2 and induce its degradation. Downregulation of TIPE2 by shRNA in cell lines increased genomic DNA damage and promoted cell colony formation in vitro and tumorigenesis in nude mice. In contrast, overexpression of TIPE2 had an opposite effect. Downregulation of TIPE2 by NS5A is associated with genomic DNA instability and HCV-induced HCC development. Thus, TIPE2 may be a new therapeutic target for the treatment of HCV-associated HCC. [ABSTRACT FROM AUTHOR]

Background: The aim of this research was to investigate the mechanism of miR-96 affecting hepatocellular carcinoma (HCC). Methods: mRNA and protein expression was detected by qRT-PCR and Western blot, respectively. HepG2 cells were transfected and grouped as follows: miR-NC group, miR-mimics group, NC + Vector group, mimics + Vector group, mimics + FOXO1 group. Luciferase reporter assay was performed. MTT and Transwell assay was conducted. In vivo studies by nude mice were performed. Immunohistochemistry and immunofluorescence was executed. Results: Up-regulated miR-96 and down-regulated FOXO1 was found in tumor tissues and HepG2 cells (P < 0.01). FOXO1 was directly suppressed by miR-96. Compared with NC + Vector group, mimics + Vector group has higher OD495 value (P < 0.05), higher migration and invasion cells (P < 0.01), larger transplanted tumor volume (P < 0.01), lower FOXO1 positive cell numbers (P < 0.01), higher p-AKT and p-GSK-3β expression (P < 0.01), lower p-β-catenin expression (P < 0.01), more β-catenin expression in the nucleus (P < 0.01). Compared with mimics + Vector group, mimics + FOXO1 group has lower OD495 value (P < 0.05), lower migration and invasion cells (P < 0.01), smaller transplanted tumor volume (P < 0.01), higher FOXO1 positive cells (P < 0.01), lower p-AKT and p-GSK-3β expression (P < 0.01), higher p-β-catenin expression (P < 0.01), less β-catenin expression in the nucleus (P < 0.01). Conclusion: miR-96 exerts carcinogenic effect by activating AKT/GSK-3β/β-catenin signaling pathway through targeting inhibition of FOXO1 in HCC. [ABSTRACT FROM AUTHOR]