Minimally invasive needle-based interventions are commonly used in cancer diagnosis and treatment, including procedures, such as biopsy, brachytherapy, and microwave ablation. Although MR-guided needle placement offers several distinct advantages, such as high-resolution target visualization and accurate device tracking, one of the primary limitations that affect its widespread adoption is the ergonomic constraints of the closed-bore MRI environment, requiring the patients to be frequently moved in and out to perform the needle-based procedures. This paper introduces a low-profile, body-mounted, MR-guided robot designed to address this limitation by streamlining the operation workflow and enabling accurate needle placement within the MRI scanner.

The robot employs piezoelectric linear actuators and stacked Cartesian XY stages to precisely control the position and orientation of a needle guide. A kinematic model and control framework was developed to facilitate accurate targeting. Additionally, clinical workflow for the liver interventions was developed to demonstrate the robot's capability to replicate existing procedures. The proposed system was validated in benchtop environment and 3T MRI scanner to quantify the system performance.

Experimental validations conducted in free space demonstrated a position accuracy of 2.38 ± 0.94 mm and orientation error of 1.40 ± 2.89°. Additional tests to confirm MR-conditionality and MR-guided phantom placements were carried out to assess the system's performance and safety in MRI suite, yielding a position error of 2.01 ± 0.77 mm and an orientation error of 1.57 ± 1.31°.

The presented robot shows exceptional compatibility with a wide range of patients and bore sizes while maintaining clinically significant accuracy. Future work will focus on the validations in dynamic liver environments.

Portal vein embolization (PVE) allows for liver regeneration to enhance reduced residual liver volume before resection in hepatocellular carcinoma (HCC) patients with systemic liver disease. A retrospective review of medical records was conducted, including patients who underwent PVE and subsequent major hepatectomy to treat resectable non-metastatic HCC at the University Medical Center in Ho Chi Minh City between 01/2016 and 6/2023. Patient demographics, timing of procedures, surgical interventions, intra- and postoperative complications, pattern of recurrence, and survival were analyzed. A total of 58 patients with HCC were included, and the median length of stay after surgery was 8 days (range 5-24). Post-hepatectomy liver failure (PHLF) occurred with an overall incidence of 31% (18/58 cases). Severe PHLF occurred in 6 cases: grade B in 5 cases (8.6%) and grade C in 1 case (1.7%), resulting in patient death. Postoperative bleeding and bile leak each occurred in 1 case (1.7%). Univariable and multivariable analyses identified portal vein pressure (PVP) after PVE as the only significant preoperative parameter associated with outcomes, correlating with PHLF occurrence (OR 1.27, p = 0.009) at a cut-off of 15 mmHg (p = 0.018). The overall survival at 3, 6, and 12 months was 96%, 94%, and 94%, respectively, with disease-free survival rates of 94%, 90%, and 87%, respectively. Major hepatectomy can be performed safely and effectively in HCC patients who have PVE-induced liver hypertrophy (sFLR ≥ 40%) and preserved liver function (Child-Pugh A) maintaining low morbidity. Multivariate analysis revealed that a post-PVE PVP cutoff of 15 mmHg significantly correlated with perioperative parameters, including operating time, blood loss, and PHLF occurrence.

Primary liver cancer, predominantly hepatocellular carcinoma (HCC), is a major global health concern. Liver transplantation is a critical therapeutic option for HCC, offering potential tumor eradication and cure of underlying liver disease. Enhanced Recovery After Surgery (ERAS) protocols aim to improve patient outcomes by optimizing perioperative care. This study evaluates the efficacy of ERAS in elderly liver transplant recipients.

A retrospective study was conducted on elderly liver transplant patients treated from January 2016 to March 2023. Patients were divided into two groups: conventional care (n = 58) and ERAS-based care (n = 57). Propensity score matching controlled for confounding variables. Perioperative care interventions included preoperative education, intraoperative management, and postoperative strategies emphasizing early mobilization, pain management, and nutrition. Outcomes included postoperative recovery times, complication rates, and anxiety levels.

ERAS group patients showed significantly improved recovery metrics: reduced times to first oral intake (29.26 vs. 38.42 h, p = 0.011), first ambulation (3.93 vs. 5.46 days, p = 0.008), and first flatus (3.07 vs. 4.33 days, p = 0.003). ICU and total hospital stays were shorter (2.89 vs. 4.52 days, p = 0.007; 22.18 vs. 27.14 days, p = 0.014). The ERAS group had lower complication rates (31.6% vs. 56.9%, p = 0.009) and reduced anxiety levels.

ERAS protocols significantly enhance postoperative recovery and reduce complications in elderly liver transplant recipients. These findings support the integration of ERAS principles into liver transplantation care to improve patient outcomes.

Hepatocellular carcinoma is one of the most common and malignant tumors worldwide. Although aloe-emodin (AE), a pure natural drug, can effectively kill hepatocellular carcinoma cells, its internal molecular mechanism has not been fully elucidated. In this study, the anti-hepatocellular carcinoma targets of AE were predicted using network pharmacology and bioinformatics.

The differentially expressed genes between hepatocellular carcinoma and normal tissues were first identified and then further intersected with the potential pharmacological target genes of AE for subsequent analysis. Moreover, the potential targets of AE were enriched and analyzed to identify potential downstream pathways. The binding ability and interaction between the above drug targets and AE were analyzed by molecular docking. The prognostic model of hepatocellular carcinoma was subsequently constructed via univariate Cox regression analysis, LASSO regression analysis and multivariate Cox regression analysis. Finally, the potential targets that can stably bind to AE were further screened through molecular dynamics simulation. Finally, we validated the potential utility of AE in treating hepatocellular carcinoma through in vitro experiments.

After 90 target genes related to AE were crossed with hepatocellular carcinoma differential genes, 13 cross genes were obtained. The above 13 genes might act on hepatocellular carcinoma through the following pathways: p53 signaling pathway, cell cycle, cellular sense, mismatch repair, apoptosis-multiple specifications, base example repair and DNA replication. Molecular docking revealed that the combination of the BAX, FASN, CDK1, PCNA, CLIC1, VWF, RAN, FOXM1, TGM3, CANT1, and NSMCE2 proteins with AE was relatively stable. A 4-gene prognostic model was further constructed. The area under the curve (AUC) values of the 1-year, 3-year and 5-year survival rates from the ROC curve were 0.809, 0.673 and 0.641, respectively. Molecular dynamics analysis revealed that CDK1 and PCNA were the most stable binding targets among the above proteins. CCK8 and wound healing assays revealed that AE inhibited the proliferation and migration of hepatocellular carcinoma cells at increasing concentrations. Western blot experiments revealed that AE achieved therapeutic effects on hepatocellular carcinoma by promoting apoptosis of hepatocellular carcinoma cells.

Based on network pharmacology, bioinformatics, molecular dynamics simulation, and in vitro experimental verification, we found that AE achieved a therapeutic effect on hepatocellular carcinoma by promoting apoptosis of hepatocellular carcinoma cells.

Flavonoids are a group of polyphenolic compounds distributed in vegetables, fruits and other plants, which have considerable antioxidant, anti‑tumor and anti‑inflammatory activities. Several types of gastrointestinal (GI) cancer are the most common malignant tumors in the world. A large number of studies have shown that flavonoids have inhibitory effects on cancer, and they are recognized as a class of potential anti‑tumor drugs. Therefore, the present review investigated the molecular mechanisms of flavonoids in the treatment of different types of GI cancer and summarized the drug delivery systems commonly used to improve their bioavailability. First, the classification of flavonoids and the therapeutic effects of various flavonoids on human diseases were briefly introduced. Then, to clarify the mechanism of action of flavonoids on different types of GI cancer in the human body, the metabolic process of flavonoids in the human body and the associated signaling pathways causing five common types of GI cancer were discussed, as well as the corresponding therapeutic targets of flavonoids. Finally, in clinical settings, flavonoids have poor water solubility, low permeability and inferior stability, which lead to low absorption efficiency in vivo. Therefore, the three most widely used drug delivery systems were summarized. Suggestions for improving the bioavailability of flavonoids and the focus of the next stage of research were also put forward.

We sought to develop a machine learning (ML) preoperative model to predict bile leak following hepatectomy for primary and secondary liver cancer.

An eXtreme Gradient Boosting (XGBoost) model was developed to predict post-hepatectomy bile leak using data from the ACS-NSQIP database. The model was externally validated using data from hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) multi-institutional databases.

Overall, 20,570 and 2253 patients were identified from the ACS-NSQIP and multi-institutional databases, respectively. The incidence rates of bile leak were 7.0 %, 6.3 % and 10.2 % in the ACS-NSQIP, HCC and ICC databases, respectively. The XGBoost model achieved areas under receiver operating characteristic curves (AUROC) of 0.748, 0.719 and 0.711 in the training, testing and external validation cohorts, respectively. The SHAP algorithm demonstrated that the factors most strongly predictive of postoperative bile leak were serum alkaline phosphatase, surgical approach and cancer diagnosis. An online tool was developed for ease-of-use and clinical applicability (https://altaf-pawlik-bileleak-calculator.streamlit.app/).

A novel ML model demonstrated strong discrimination power to preoperatively identify patients at high risk of developing bile leak post-hepatectomy. The online calculator may be used as a clinical tool to inform preoperative surgical planning, intraoperative decision-making, and postoperative recovery protocols for patients undergoing hepatectomy.

ERCC3, a crucial component of the nucleotide excision repair pathway, is implicated in the development and progression of various cancers and is a potential indicator of poor prognosis. However, the expression and function of ERCC3 in hepatocellular carcinoma (HCC) remain unclear. This study aimed to investigate the expression of ERCC3 in HCC tissues and its clinical significance, focusing on elucidating its potential mechanisms and therapeutic value in immunotherapy.

The differential expression and genetic variation characteristics of ERCC3 across various cancers were evaluated using the TCGA database. The expression and prognostic value of ERCC3 in HCC were analyzed by integrating TCGA, GEO, and ICGC datasets. Independent prognostic value of ERCC3 expression levels in HCC was assessed using Cox regression analysis, Kaplan-Meier survival analysis, receiver operating characteristic curves, and nomograms. Pathway association scores were determined using ssGSEA to reveal the biological functions of ERCC3 in HCC and its potential clinical efficacy in immunotherapy. Stable transient cell lines were established by infecting HepG2 cells with lentivirus overexpressing ERCC3. The effects of ERCC3 on HCC cell biological phenotypes were evaluated using RTCA, wound healing, and Transwell assays. Cell cycle distribution and apoptosis were detected by flow cytometry. Transcriptome sequencing was performed to explore the impact of ERCC3 overexpression on the expression of signaling pathway-related genes in HCC.

The study revealed that ERCC3 is aberrantly expressed in various tumors, with significantly higher mRNA and protein levels in HCC tissues compared to normal tissues. High ERCC3 expression was significantly correlated with poor survival outcomes in HCC patients. Multivariate Cox regression analysis revealed that ERCC3 expression level is an independent prognostic factor for overall survival (P = 0.014). Gene sets associated with the high ERCC3 group were significantly involved in multiple immune pathways and tumor progression-related pathways, and ERCC3 expression was significantly correlated with immune checkpoints in HCC. Overexpression of ERCC3 promoted the proliferation and migration of HCC cells and influenced cell cycle progression. Transcriptome sequencing analysis indicated that ERCC3 overexpression regulated the proliferation of HCC cells, participated in multiple pro-inflammatory pathways, induced the formation of an inflammatory tumor microenvironment, and promoted HCC progression.

This study is the first to reveal the association between high ERCC3 expression and poor prognosis in HCC and to elucidate its immunomodulatory role in HCC. Unlike previous studies, we found that ERCC3 promotes HCC progression by regulating the inflammatory microenvironment and immune checkpoints. These findings establish a novel theoretical foundation for the development of targeted immunotherapies for HCC and provide new insights into the molecular mechanisms underlying ERCC3's role in HCC.

Surgical site infections (SSIs) are a significant complication following liver surgery (LS) for primary liver cancer (PLC), contributing to increased morbidity, prolonged hospital stays, and higher healthcare costs. This study aimed to evaluate the association of perioperative nursing care (PNC) with the incidence of SSIs and short-term outcomes, comparing patients receiving structured PNC to those receiving standard care.

A retrospective study was conducted at [specific location] between January 2016 and February 2019. A total of 360 PLC patients undergoing LS were included and divided into an observation group (PNC) and a control group (standard care). Outcome measures included SSI incidence, length of hospital stay, and independent predictors of SSIs. Logistic regression analysis was used to identify significant factors.

Among the 360 included PLC patients, 180 received PNC while 180 did not. Patients in the PLC group had a significantly lower incidence of SSIs (28.3% vs 47.2%, P = 0.026) and shorter hospital stays (median: 8.2 vs 13.3 days, P = 0.049) compared to the control group. Multivariate logistic regression identified PNC as a significant protective factor against SSIs (OR = 2.01, 95% CI: 1.08-3.85, P = 0.031). Other significant predictors included education level (college or above: OR = 0.44, 95% CI: 0.24-0.79, P = 0.006) and comorbidities (more than two: OR = 2.21, 95% CI: 1.31-3.76, P = 0.003).

PNC emerged as an independent risk factor for SSIs in PLC patients undergoing LS. Thus, the provision of PNC is crucial for reducing the risk of SSIs and improving short-term outcomes in PLC patients undergoing LS.

Recurrence is of utmost importance for hepatocellular carcinoma (HCC) after ultrasound-guided microwave ablation (UGMWA) therapy. The fibrosis 4 (FIB-4) index is a valuable predictor of HCC recurrence after surgical resection. However, whether FIB-4 can predict the recurrence of HCC patients receiving UGMWA remains unclear. The FIB-4 index was detected in healthy controls, hepatitis patients, and HCC patients. The predictive value of FIB-4 in HCC occurrence and recurrence following UGMWA therapy was evaluated using receiver operating characteristic analysis. The associated factors of FIB-4 in HCC patients were compared between patients with high and low levels of FIB-4. A Kaplan-Meier plot was used to assess the impact of FIB-4 on overall survival (OS) and recurrence-free survival (RFS). FIB-4 levels were increased in HCC patients and could predict the occurrence of HCC. Meanwhile, it was associated with five factors, including recurrence. Furthermore, FIB-4 levels decreased in HCC patients after UGMWA therapy but increased in recurrent HCC patients following UGMWA therapy. Importantly, FIB-4 could predict recurrence after UGMWA. The HCC patients had shorter OS and RFS. FIB-4 was associated with HCC recurrence after UGMWA therapy. Specifically, it had a predictive value for HCC occurrence and recurrence following UGMWA therapy.

Reversible electroporation (EP) refers to the use of high-voltage electrical pulses on tissues to increase cell membrane permeability. It allows targeted delivery of high concentrations of chemotherapeutic agents including cisplatin and bleomycin, a process known as electrochemotherapy (ECT). It can also be used to deliver toxic concentrations of calcium and gene therapies that stimulate an anti-tumour immune response. ECT was validated for palliative treatment of cutaneous tumours. Evidence to date shows a mean objective response rate of ∼80% in these patients. Regression of non-treated lesions has also been demonstrated, theorized to be from an in situ vaccination effect. Advances in electrode development have also allowed treatment of deep-seated metastatic lesions and primary tumours, with safety demonstrated in vivo. Calcium EP and combination immunotherapy or immunogene electrotransfer is also feasible, but research is limited. Adverse events of ECT are minimal; however, general anaesthesia is often necessary, and improvements in modelling capabilities and electrode design are required to enable sufficient electrical coverage. International collaboration between preclinical researchers, oncologists, and interventionalists is required to identify the most effective combination therapies, to optimize procedural factors, and to expand use, indications and assessment of reversible EP. Registries with standardized data collection methods may facilitate this.

The 3-year mortality rate for hepatocellular carcinoma (HCC) in Indonesia was 94.4%. This underscores a significant health issue in Southeast Asia, particularly in Indonesia due to its large population. This study aimed to characterize the outcomes of liver resection for HCC at a National Referral Center in Indonesia.

Between 2010 and 2020, all patients with HCC undergoing liver resection were included as subjects. Variables collected included sex, age, hepatitis status, and tumor's characteristics. Mortality and survival were the primary outcomes of the study.

Among seventy patients, the mortality rate was 71.4%, with a median overall survival of 19.0 months (95% confidence interval [95%CI]: 6.831.2). Thirty-one patients (44.3%) had extra-large HCC tumors (> 10 cm). Those with extra-large tumors had a lower median survival of 8.0 months. Child-Pugh B and Edmonson-Steiner grade 4 were associated with an increased mortality risk, with unadjusted hazard ratios (HRs) of 2.2 (95%CI: 1.14.3, p = 0.026) and 3.2 (95%CI: 1.37.7, p = 0.011), respectively. Multivariate analysis indicated that Child-Pugh class B significantly increased the risk of mortality, with an adjusted HR of 2.3 (95%CI: 1.05.2, p = 0.046).

While surgical resection is feasible for tumors of any size, most clinical features are not statistically significantly associated with survival outcomes. The prevalence of extra-large tumors among Indonesian HCC patients highlights the importance of early diagnosis and intervention. Surgical intervention at an earlier stage and with better grade tumors could potentially enhance survival outcomes.

To investigate the mediating effect of financial toxicity on stigma and self-perceived burden in patients with liver cancer after surgery.

Using a convenience sampling method, 236 postoperative liver cancer patients treated at a tertiary hospital in Nanjing from April 2024 to July 2024 were selected for the study. Questionnaires were administered, including a general information survey, the Social Impact Scale (SIS), the Self-Perceived Burden Scale for Cancer Patients (SPBS-CP), and the Comprehensive Score for Financial Toxicity-Functional Assessment of Chronic Illness Therapy Version 2 (COST-FACIT-V2). Data were analyzed using SPSS 22.0 for descriptive statistics, correlation analysis, and regression analysis. MPlus 8.3 was employed to examine the mediating effect of financial toxicity between stigma and self-perceived burden, and the Bootstrap method was used to test the significance of the mediation effect.

The self-perceived burden score, stigma score, and financial toxicity score were (31.72 ± 7.52), (58.92 ± 8.69), and (18.62 ± 6.80), respectively. The financial toxicity and self-perceived burden were negatively correlated (r=-0.270,P=0.001). There was a positive correlation between stigma and self-perceived burden (r=0.586,P=0.000). Financial toxicity partially mediated the relationship between stigma and self-perceived burden, accounting for 4.84% of the total effect.

Stigma can influence the self-perceived burden of liver cancer patients through financial toxicity. Clinical nurses should prioritize alleviating patients' stigma while also paying close attention to their financial toxicity status, providing feasible assistance in a timely manner to reduce their self-perceived burden.

Compared to conventional polymer-based and biomaterial carriers, cells as vehicles for delivering bioactive molecules in the treatment of tumor diseases offer characteristics such as non-toxicity, biocompatibility, low immunogenicity, and prolonged in vivo circulation. However, the focus of current cell drug delivery systems predominantly lies on live cells, such as red blood cells, white blood cells and others. Here, a drug delivery strategy targeting liver cancer utilizing cryo-shocked liver cancer cells (HepG2) as carriers was presented, and non-proliferative HepG2 cells particles loaded with DOX (HepG2-DOX) was effectively prepared, which has good homologous targeting. Subsequent in vitro and in vivo experiments demonstrated the non-proliferative and non-pathogenic nature of this drug delivery system. The outcomes of in vitro experiments revealed that the inhibitory effect of HepG2-DOX on HepG2 was approximately five times higher than that of free DOX, with the IC50 value of HepG2-DOX being 0.0739 µg/mL and free DOX being 0.3606 µg/mL. Furthermore, in comparison to the positive DOX group, the HepG2-DOX group has a very significant advantage in tumor inhibition rate (91.34 % vs. 64.20 %). Cell uptake experiments indicated significant HepG2-DOX uptake by HepG2 cells compared to 4T1, LO2, and Raw cell groups, highlighting the excellent cell specificity of HepG2-DOX. Fluorescence imaging conducted in mice following the administration of HepG2-DOX demonstrated prompt drug localization within the tumor region, highlighting exceptional in vivo targeting precision. To sum up, this study introduced a novel strategy utilizing cryo-shocked liver cancer cells as a drug delivery system, effectively treating liver tumor by enhancing tumor targeting specificity.

One of the most common tumors is hepatocellular carcinoma (HCC), and the prognosis for late-stage HCC is still not good. It is anticipated that improved outcomes would result from a deeper comprehension of the pathophysiology of HCC. Ferroptosis as a new discovered cell death type is linked to the progression of HCC and may be crucial for its detection, prevention, therapy, and prognosis. Numerous studies suggest that epigenetic alterations mediated by non-coding RNAs (ncRNA) might influence cancer cell susceptibility to ferroptosis. This study elucidates the processes of ferroptosis and delineates the paths by which ncRNAs influence HCC by modulating ferroptosis. Furthermore, it offers significant insights into ferroptosis-associated ncRNAs, intending to discover novel therapeutic approaches for HCC. It also explores innovative concepts for the future use of ncRNA-based ferroptosis-targeted therapeutics.

Liver cancer is a leading cause of cancer-related deaths worldwide, highlighting the need for innovative approaches to understand its complex biology and develop effective treatments. While traditional in vivo animal models have played a vital role in liver cancer research, ethical concerns and the demand for more human-relevant systems have driven the development of advanced in vitro models. Spheroids and organoids have emerged as powerful tools due to their ability to replicate tumor microenvironment and facilitate preclinical drug development. Spheroids are simpler 3D culture models that partially recreate tumor structure and cell interactions. They can be used for drug penetration studies and high-throughput screening. Organoids derived from stem cells or patient tissues that accurately emulate the complexity and functionality of liver tissue. They can be generated from pluripotent and adult stem cells, as well as from liver tumor specimens, providing personalized models for studying tumor behavior and drug responses. Liver organoids retain the genetic variability of the original tumor and offer a robust platform for high-throughput drug screening and personalized treatment strategies. However, both organoids and spheroids have limitations, such as the absence of functional vasculature and immune components, which are essential for tumor growth and therapeutic responses. The field of preclinical modeling is evolving, with ongoing efforts to develop more predictive and personalized models that reflect the complexities of human liver cancer. By integrating these advanced in vitro tools, researchers can gain deeper insights into liver cancer biology and accelerate the development of novel treatments.

Diacylglycerol kinases (DGKs) phosphorylate diacylglycerol to generate phosphatidic acid, which plays important roles in intracellular signal transduction. DGKα is reportedly associated with progression of tumors, including hepatocellular carcinomas, but its relationship with liver regeneration has not been examined. The purpose of this research is to elucidate the role of DGKα in liver regeneration. Here, we provide a detailed examination of C57BL/6 wild-type and DGKα knockout (KO) mice subjected to 70% partial hepatectomy (70% PH) modeling, including survival rates, hematological marker and gene expression levels, and histological analyses of factors related to liver regeneration. Following 70% PH, DGKα KO mice produce higher levels of hepatobiliary enzymes and have a higher incidence of jaundice compared with wild-type mice, with a death rate of ~ 40%. Furthermore, they exhibit impaired glycogen and lipid consumption, low liver energy charge, and hepatocyte hypertrophy disorder, accompanied by significantly reduced liver expression of proliferating cell nuclear antigen and cyclin D. We conclude that DGKα is a key molecule in the post-PH liver regeneration process and may have potential as a therapeutic target for the acceleration of liver regeneration.

Ambient ionization mass spectrometry was proved to be a powerful tool for oncological surgery. Still, it remains a translational technique on the way from laboratory to clinic. Brain surgery is the most sensitive to resection accuracy field since the balance between completeness of resection and minimization of nerve fiber damage determines patient outcome and quality of life. In this review, we summarize efforts made to develop various intraoperative support techniques for oncological neurosurgery and discuss difficulties arising on the way to clinical implementation of mass spectrometry-guided brain surgery.

AMD1 is the gene encoding S-adenosylmethionine decarboxylase 1. How AMD1 affects the prognosis of hepatocellular carcinoma (HCC) patients is unclear.

Using the Cancer Genome Atlas (TCGA) liver hepatocellular carcinoma datasets, gene enrichment and immunological traits were compared between groups with high and low AMD1 expression. After altering AMD1 expression in HCC cells, cell viability, the clonal formation rate, and migration and invasion ability were detected. Univariate Cox regression analysis and Pearson correlation were used to screen for AMD1-related genes (ARGs). Multidimensional bioinformatic algorithms were utilized to establish a risk score model for ARGs.

AMD1 expression was notably increased in the majority of cancer types. High AMD1 expression was associated with adverse outcomes and poorer immunotherapy response in HCC patients. AMD1 exhibited higher expression levels in HCC cell lines. The efficient inhibition of HCC cell proliferation, migration, and invasion in vitro can be achieved through the downregulation of AMD1. The AMD1-related risk score was constructed with the expression of 9 ARGs, and demonstrated high predictive efficacy in multiple validation cohorts. Patients with high risk scores exhibited greater resistance to classical chemotherapy drugs. The nomogram, which consists of age, stage, and the AMD1-related risk score, was used to calculate the probability of survival for each individual.

The present study indicates that AMD1 functions as a potential role in HCC progression and may serve as a therapeutic target in HCC. This study constructed a novel AMD1-related scoring system for predicting the prognosis and treatment responsiveness of patients with HCC, enabling the prediction of prognosis and identification of potential treatment targets.

Hepatocellular carcinoma (HCC) is one of the most common malignancies globally, particularly prevalent in China, where it accounts for nearly half of the world's new cases and deaths each year, but has limited therapeutic options. This study systematically investigated the impact of cucurbitacin I on HCC cell lines including SK-Hep-1, Huh-7, and HepG2. The results revealed that cucurbitacin I not only inhibited cell proliferation, cell migration and colony formation, but also induced apoptosis in HCC cells. The apoptotic induction was accompanied by a decrease in the expression of the anti-apoptotic factor B-cell lymphoma 2 (Bcl2), and an elevation in the expression levels of pro-apoptotic factors, including tumor protein p53 (P53), bcl2 associated X-apoptosis regulator (Bax), and caspase3 (Cas3). Additionally, cucurbitacin I caused cell cycle arrest by modulating the lysine acetyltransferase 2A (KAT2A)-E2F transcription factor 1 (E2F1)/Ubiquitin-conjugating enzyme E2 C (UBE2C) signaling axis. In terms of regulation on tumor microenvironment, cucurbitacin I was demonstrated the ability to inhibit HCC cell-induced M2 polarization of macrophages. This comprehensive study unveils the multifaceted anti-cancer mechanisms of cucurbitacin I, providing robust support for its potential application in the treatment of HCC, offering new avenues for the future development of HCC treatment strategies.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. Major treatments include liver transplantation, resection, and chemotherapy, but the 5-year recurrence rate remains high. Late diagnosis often prevents surgical intervention, contributing to poor patient survival rates. Carcinogenesis in HCC involves genetic alterations that drive the transformation of normal cells into malignant ones. Enhancer of zeste homolog 2 (EZH2), a key regulator of cell cycle progression, is frequently upregulated in HCC and is associated with advanced stages and poor prognosis, making it a potential biomarker. Additionally, signal transducer and activator of transcription 3, which binds to EZH2, affects disease staging and outcomes. Targeting EZH2 presents a promising therapeutic strategy. On the other hand, abnormal lipid metabolism is a hallmark of HCC and impacts prognosis. Fatty acid binding protein 5 is highly expressed in HCC tissues and correlates with key oncogenes, suggesting its potential as a biomarker. Other genes such as guanine monophosphate synthase, cell division cycle associated 5, and epidermal growth factor receptor provide insights into the molecular mechanisms of HCC, offering potential as biomarkers and therapeutic targets.

The role of IBA in regulating the recovery of liver cancer was investigated using a rat model of liver cancer and an intraoperative blood return model (IBA). SD rats were used to construct the IBA model. Kupffer cells were isolated from liver cancer tissues, and their biological characteristics were analyzed by flow cytometry. Comet assay was used to detect DNA damage in tumor cells; clone formation assay and transwell assay were used to detect tumor cell proliferation and migration ability. Western blot analysis was used to determine the changes in related signaling pathways. After the IBA treatment, the production of KCs was significantly promoted in rat liver cancer tissues, and the expression levels of cell cycle arrest proteins P53, AEN and CDKN1A were also significantly increased. In tumor cells, IBA induced cell cycle arrest and cellular DNA damage in a p53-mediated manner. In addition, the proliferation and migration of cancer cells were also significantly inhibited. Similar to the in vivo data, the expression of TP53, AEN and CDKN1A was also up-regulated. Our study showed that IBA can inhibit the malignant transformation of hepatocellular carcinoma by modulating the function-dependent p53-mediated pathway of tumor cells and KCs.

This study was designed to compare the efficacy of laparoscopic hepatectomy (LH) and radiofrequency ablation (RFA) in terms of their therapeutic effect on small hepatocellular carcinoma (SHCC). The SEER database was employed to integrate SHCC patients who had received treatment with either LH (n = 1132) or RFA (n = 797). The LH group (n = 623) and the RFA group (n = 623) were matched with 1:1 propensity score matching (PSM) in order to reduce the possibility of selection bias. The Kaplan-Meier method and Cox proportional hazards regression method were employed to ascertain the prognostic factors associated with overall survival (OS) and disease-specific survival (DSS). Both before and after PSM, the 1, 3 and 5-years OS and DSS were significantly higher in the LH groups compared to the RFA group. Besides, for SHCC with tumor size ≤ 2cm (n = 418), even P values not reaching statistical significance, the survival curves were compatible with a superiority of LH over RFA for OS and DSS in overall (P = 0.054 and P = 0.077), primary SHCC (P = 0.110 and P = 0.058) and recurrent SHCC (P = 0.068 and P = 1.000) cohorts. In contrast, for SHCC with tumor size between 2 and 3 cm (n = 828), LH group always had a better OS and DSS in the all cohorts (all P < 0.05). In addition, higher AFP level, poor differentiation grade, recurrent tumor and treatment type were independent prognostic factors for OS, while poor differentiation grade, larger tumor size and treatment type were the independent prognostic factors for DSS (all P < 0.05). LH was associated with better OS and DSS than RFA in SHCC patients. Even in tumor size ≤ 2 cm, LH still should be the first choice as its long-term survival benefits.

In recent years several new techniques have emerged to induce hypertrophy of the future liver remnant prior to major hepatectomies. We aimed to summarize our initial experience with Double-vein Embolization as the first center in Hungary.

Between March 2023 and August 2024 a total of 16 Double-vein Embolization procedures were performed in Semmelweis University. Future liver remnant volume was calculated based on computed tomography scans obtained within 4 weeks prior and 2-3 weeks after the procedure. Tc-99m mebrofenin hepatobiliary scintigraphy results were available for 12/16 patients.

Technical success rate was 100 %. No major complication was observed. Successful resection rate was 93.8 %. One patient died due to post-hepatectomy liver failure. Future liver remnant volume and ratio increased significantly after the procedure compared to baseline (433.1 ± 163.8 cm3 vs. 603.5 ± 201.8 cm3, p < 0.0001 and 27.2 ± 6.5 % vs. 37 ± 8.8 %, p < 0.0001, respectively). Future liver remnant clearance improved significantly 1 and 2 weeks after the procedure (1.68 ± 0.58 %/min/m2 vs. 2.44 ± 0.64 %/min/m2 and 2.39 ± 0.31 %/min/m2, respectively). Mean function gain was 50.6 % after one week and 60.1% after two weeks, respectively.

Volumetric and functional outcomes in the present study are comparable with results reported in the literature. Our findings provide further evidence that Double-vein Embolization is a safe procedure that offers sufficient volumetric and functional gain in most candidates for liver resection. However, further studies are needed to define the exact place of this new technique in clinical practice.

Background  The AQP4-AS1/miR-4476-ALOX15 regulatory axis was discovered in previous studies. We aimed to investigate the regulatory mechanism of the ferroptosis-related regulator ALOX15 by AQP4-AS1 and miR-4476 in lung adenocarcinoma (LUAD) and find new targets for clinical treatment. Methods  After bioinformatics analysis, we contained one ferroptosis-related gene (FRG), namely ALOX15. MicroRNAs (miRNAs) and long noncoding RNAs were predicted by miRWalk. Furthermore, we constructed overexpressed LUAD cell lines. Real-time quantitative polymerase chain reaction and western blot were used to determine the expression of mRNA and protein, respectively. Cell Counting Kit-8 (CCK-8) and EdU assay were used to detect the cell proliferation. Double luciferase assay was used to detect the binding relationship between AQP4-AS1 and miR-4464. Results  ALOX15 was the most significantly downregulated FRG compared with normal tissues. Furthermore, protein-protein interaction network analysis indicated that the AQP4-AS1-miR-4476-ALOX15 regulatory axis might be involved in the occurrence and development of LUAD and there might be direct interaction between AQP4-AS1 and miR-4476, and miR-4476 and ALOX15. Furthermore, AQP4-AS1 and ALOX15 were significantly downregulated in the LUAD tissue and cell lines, whereas miR-4476 showed the opposite results ( p  < 0.001). AQP4-AS1 overexpression improved the ALOX15 expression in LUAD cell lines. CCK-8 and EdU assay revealed that overexpression of AQP4-AS1 and ALOX15 inhibited the LUAD cell proliferation. Double luciferase assay results indicated that there was a combination between AQP4-AS1 and miRNA-4476. In addition, we found that overexpressed AQP4-AS1 activates the ferroptosis in LUAD cell lines. Conclusions  AQP4-AS1 can regulate the expression of ALOX15 through competitive binding with miR-4476, further activate ferroptosis and inhibit the proliferation of LUAD cells.

Lack of efficient biomarkers and clinical translation of molecular typing impedes the implementation of targeted therapy for hepatocellular carcinoma (HCC). High-throughput sequencing techniques represented by next-generation sequencing (NGS) are tools for detecting targetable genes. The objective of this study is to explore the genetic alterations associated with clinicopathological features and the risk of recurrence/metastasis in HCC. NGS analysis was conducted on formalin-fixed paraffin-embedded tissues from 164 resected liver samples obtained from Chinese patients. Morphologic subtypes were reviewed based on hematoxylin-eosin and immunohistochemistry staining, Correlation to the acquired molecular features were analyzed with clinicopathological information. We also retrieved follow-up information of the 123 transplanted cases from 2017 to 2019 to screen recurrence/metastasis-associated factors by univariate analysis. Generally, the most frequently mutated genes include TP53 and CTNNB1 which showed a trend of mutually exclusive mutation. Copy-number variant with the highest frequency was detected in TAF1 and CCND1 in 11q13.3 loci. Correlation analysis showed that various genetic alterations were associated with morphologic subtypes and other pathologic features. While gene signatures of proliferation/nonproliferation class were correlated with differentiation, satellite foci and other invasive morphological features. Macrotrabecular-massive subtype, TSC2 (tuberous sclerosis complex 2) mutation, Ki-67 expression, and other six factors were found to be associated with recurrence/metastasis after liver transplantation. Genetic alterations detected by NGS show correlation with not only pathological and clinical features, but also with recurrence/metastasis after liver transplantation. Further gene-level molecular typing will be practical for targeted therapy and individual recurrence risk assessment in HCC patients.

Hepatocellular carcinoma (HCC) ranks the sixth most common malignancy but the third leading cause of cancer-related mortality in the world. Significant breakthroughs have been made in systemic treatment for HCC over the past two decades, which have improved treatment outcomes. In addition to multiple tyrosine kinase inhibitors (mTKIs), immune checkpoint inhibitors (ICIs) and antiangiogenic drugs are increasingly being applied. The combination of ICI and antiangiogenic or dual ICIs has become the new standard of care due to remarkable response rates. However, currently available systemic regimens are primarily reserved for certain patients in the intermediate and advanced stages who will not benefit from locoregional treatments. Evidence supporting the use of systemic treatment as neoadjuvant or adjuvant therapies in patients with early-stage HCC, especially the high risk of recurrence after curative treatments, remains limited. This review identified recent developments in systemic therapy, including mTKIs and ICIs, considering results on first- and second-line treatment, role of neoadjuvant and adjuvant settings, and combination with loco-regional therapy. Various ongoing clinical trials regarding the role of systemic therapies and potential novel targets in patients with early-, intermediate-, and advanced-stage HCC were also summarized and revealed that systemic therapy is no longer limited to advanced-stage HCC. Moreover, the introduction of T-cell redirecting strategies, including bispecific antibodies and chimeric antigen receptor T cells, has revolutionized the treatment landscape for HCC. Future research should focus on an in-depth exploration of the mechanisms governing the establishment of tumor barriers.

Bone mineral density (BMD) and monocyte-to-lymphocyte ratio (MLR) were recently identified as novel risk factors for patients with several malignancies. The objective of this study was to validate the role of preoperative BMD/MLR as a potential prognostic biomarker in patients with hepatocellular carcinoma (HCC) undergoing liver resection.

This investigation enrolled 442 adult patients diagnosed with HCC who underwent liver resection. The patients were classified into high- and low-BMD/MLR groups based on the median, and forward stepwise logistic regression was employed to identify independent predictors for early HCC recurrence. To mitigate the impact of confounding factors, a propensity score matching (PSM) analysis was conducted between patients in the high- and low-BMD/MLR groups. The Kaplan-Meier method was employed to assess and compare the disease-free survival (DFS) and overall survival (OS) between the two cohorts.

The study categorized patients into high-BMD/MLR and low-BMD/MLR groups. Forward stepwise logistic regression analysis revealed that low BMD/MLR (P < 0.001), tumor size > 50 mm (P < 0.001), and AFP > 200 ug/L (P = 0.001) were significantly associated with the early recurrence of HCC. Moreover, the results suggested that DFS and OS were significantly shorter in the low-BMD/MLR group compared to the high-BMD/MLR group, both before and after PSM (P < 0.05).

Preoperative BMD/MLR held promise as a prognostic biomarker for early recurrence and prognosis in patients with HCC who underwent liver resection. Furthermore, the integration of tumor size, AFP level, and BMD/MLR demonstrated a robust predictive capacity for early recurrence within this patient population.

Precise Couinaud segmentation from preoperative liver computed tomography (CT) is crucial for surgical planning and lesion examination. However, this task is challenging as it is defined based on vessel structures, and there is no intensity contrast between adjacent Couinaud segments in CT images. To solve this challenge, we design a multi-scale point-voxel fusion framework, which can more effectively model the spatial relationship of points and the semantic information of the image, producing robust and smooth Couinaud segmentations. Specifically, we first segment the liver and vessels from the CT image and generate 3D liver point clouds and voxel grids embedded with the vessel structure. Then, our method with two input-specific branches extracts complementary feature representations from points and voxels, respectively. The local attention module adaptively fuses features from the two branches at different scales to balance the contribution of different branches in learning more discriminative features. Furthermore, we propose a novel distance loss at the feature level to make the features in the segment more compact, thereby improving the certainty of segmentation between segments. Our experimental results on three public liver datasets demonstrate that our proposed method outperforms several state-of-the-art methods by large margins. Specifically, in out-of-distribution (OOD) testing of LiTS dataset, our method exceeded the voxel-based 3D UNet by approximately 20% in Dice score, and outperformed the point-based PointNet2Plus by approximately 8% in Dice score. Our code and manual annotations of the public datasets presented in this paper are available online: https://github.com/xukun-zhang/Couinaud-Segmentation.

Sini decoction (SND), a popular formula from traditional Chinese medicine (TCM), plays a critical role in the treatment of liver disease. Its protective effect for the heart against cardiovascular diseases is well documented. However, its effects and pharmacological mechanisms for the liver remain unclear. This study aimed to clarify the effect and mechanism of the SND-polysaccharide compound (SNDPC) on hepatocellular carcinoma (HCC).

Different genes affected by SNDPC in HCC were analyzed via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Databases including Multi-Experiment Matrix (MEM), HCCDB, LinkedOmics, and Gene Expression Profiling Interactive Analysis (GEPIA) were used to determine the correlation between PHLDA2 and ANXA2. Cell proliferation and viability were identified using Cell Counting Kit-8 (CCK-8). Cell apoptosis was estimated using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and Western blotting. Glycolysis was determined by measuring glucose uptake, lactate concentration, extracellular acidification rate (ECAR), and the expressions of LHDA, HK2, and PKM2. The binding between PHLDA2 and ANXA2 was identified by coimmunoprecipitation.

SNDPC significantly weakened cell proliferation, facilitated cell apoptosis, and suppressed glycolysis by reducing glucose uptake, lactate concentration, ECAR, and the expressions of LDHA, HK2, and PKM2 in HCC cells. Furthermore, PHLDA2 was predicted to bind to ANXA2, which was confirmed by coimmunoprecipitation. SNDPC reduced the expressions of PHLDA2 and ANXA2 in HCCLM3 cells, and PHLDA2 silencing decreased the proliferation of cells, promoted cell apoptosis, and inhibited glycolysis of HCCLM3 cells while reversing the overexpression of PHLDA2.

SNDPC suppressed proliferation and glycolysis while accelerating the apoptosis of HCC cells through PHLDA2/ANXA2.

Hepatocellular carcinoma (HCC) is a leading contributor to cancer-related deaths worldwide and presents significant challenges in diagnosis and treatment due to its heterogeneous nature. The discovery of biomarkers has become crucial in addressing these challenges, promising early detection, precise diagnosis, and personalized treatment plans. Key biomarkers, such as alpha fetoprotein (AFP) glypican 3 (GPC3) and des gamma carboxy prothrombin (DCP) have shown potential in improving clinical results. Progress in proteomic technologies, including next-generation sequencing (NGS), mass spectrometry, and liquid biopsies detecting circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA), has deepened our understanding of HCC's molecular landscape. Immunological markers, like PD-L1 expression and tumor-infiltrating lymphocytes (TILs), also play a crucial role in guiding immunotherapy decisions. Despite these advancements, challenges remain in biomarker validation, standardization, integration into clinical practice, and cost-related barriers. Emerging technologies like single-cell sequencing and machine learning offer promising avenues for further exploration. Continued investment in research and collaboration among researchers, healthcare providers, and policymakers is vital to harness the potential of biomarkers fully, ultimately revolutionizing HCC management and improving patient outcomes through personalized treatment approaches.

After major liver resections, anatomical shifts due to liver parenchymal hypertrophy and organ displacement can happen. The aim of this study was to evaluate the impact of these anatomical changes on the main abdominal arteries (coeliac trunk and superior mesenteric artery) and on patient outcomes.

All patients who underwent major liver resections (between January 2010 and July 2021) and who underwent preoperative and postoperative arterial-phase contrast-enhanced abdominal CT imaging were studied. Observed arterial position changes were classified into three groups: no position changes; class I position changes (vessel displacement with or without kinking with a vessel angle greater than 105°); and class II position changes (kinking less than or equal to 105°). The Mann-Whitney test and the Kruskal-Wallis test were used to compare continuous variables and the chi-squared test and Fisher's exact test were used to compare categorical variables. Univariable and multivariable logistic regression analyses were used to identify the risk factors for morbidity and mortality.

A total of 265 patients (149 men and median age of 59 years) were enrolled. Arterial position changes were detected in a total of 145 patients (54.7%) (99 patients (37%) with class I position changes and 46 patients (18%) with class II position changes) and were observed more often after extended resection and right-sided resection (P < 0.001). Major complications were seen in 94 patients (35%) and the rate of mortality was 15% (40 patients died). Post-hepatectomy liver failure (P = 0.030), major complications (P < 0.001), and mortality (P = 0.004) occurred more frequently in patients with class II position changes. In multivariable analysis, arterial position change was an independent risk factor for post-hepatectomy liver failure (OR 2.86 (95% c.i. 1.06 to 7.72); P = 0.038), major complications (OR 2.10 (95% c.i. 1.12 to 3.93); P = 0.020), and mortality (OR 2.39 (95% c.i. 1.03 to 5.56); P = 0.042).

Arterial position changes post-hepatectomy are observed in the majority of patients and are significantly related to postoperative morbidities and mortality.

Background: Eosinophils, a type of white blood cell originating from the bone marrow, are widely believed to play a crucial role in inflammatory processes, including allergic reactions and parasitic infections. However, the relationship between eosinophils and liver cancer is not well understood. Methods: Tumor immune infiltration scores were calculated using single-sample Gene Set Enrichment Analysis (ssGSEA). Key modules and hub genes associated with eosinophils were screened using Weighted Gene Co-expression Network Analysis (WGCNA). Univariate and multivariate Cox analyses, along with LASSO regression, were used to identify prognostic genes and create a risk model. The Tumor Immune Dysfunction and Exclusion (TIDE) score was used to evaluate the immunotherapeutic significance of the eosinophil-associated gene risk score (ERS) model. Experiments such as flow cytometry, immunohistochemical analysis, real-time quantitative PCR (RT-qPCR), and Western blotting were used to determine gene expression levels and the status of eosinophil infiltration in tumors. Results: A risk trait model including 4 eosinophil-associated genes (RAMP3, G6PD, SSRP1, PLOD2) was developed by univariate Cox analysis and Lasso screening. Pathologic grading (p < 0.001) and model risk scores (p < 0.001) were found to be independent predictors of hepatocellular carcinoma (HCC) patient survival. Western blotting revealed higher levels of eosinophil peroxidase (EPX) in HCC tissues compared to adjacent normal tissues. Immunohistochemistry showed that eosinophils mainly infiltrated the connective tissue around HCC. The HCC samples showed low expression of RAMP3 and high expression of G6PD, SSRP1, and PLOD2, as detected by IHC and RT-qPCR analysis. The in vivo mouse experiments showed that IL-33 treatment induced the recruitment of eosinophils and reduced the number of intrahepatic tumor nodules. Conclusion: Overall, eosinophil infiltration in HCC is significantly correlated with patient survival. The risk assessment model based on eosinophil-related genes serves as a reliable clinical prognostic indicator and provides insights for precise treatment of HCC.

Associating liver partition with portal vein ligation for staged liver resection (ALPPS) has been used in the treatment of patients with advanced or massive liver cancer without sufficient future liver remnant, but concerns remain regarding tumor outcomes and surgical safety. This study aims to evaluate the efficacy and safety of a new procedure, hepatic artery restriction operation combined with ALPPS (HARO-ALPPS), in the treatment of hepatocellular carcinoma (HCC) patients especially with severe fibrosis.

This retrospective study analyzed 8 patients who underwent HARO-ALPPS for HCC and compared their outcomes with 64 patients who underwent conventional ALPPS. The primary outcomes assessed were liver regeneration ability (measured by relative and absolute kinetic growth rates), postoperative complications, and mortality. The secondary outcomes included overall survival and disease-free survival.

HARO-ALPPS significantly restricted the blood supply of the hepatic artery. One week after surgery, the blood flow of the right hepatic artery dropped to 62.1%. At the same time, HARO-ALPPS shows superior liver regeneration ability, which is particularly prominent in the background of liver fibrosis. No serious complications occurred after HARO-ALPPS. The overall survival rate of HARO-ALPPS was 75%, which was higher than that of ALPPS (64%, P =0.816).

Compared to conventional ALPPS, HARO-ALPPS exhibits a better liver regeneration ability, and favorable long-term outcomes. Further prospective studies are needed to validate these findings and evaluate the long-term oncologic outcomes of this novel procedure.

The limited response of hepatocellular carcinoma (HCC) to chemotherapy drugs has always been a bottleneck in therapy. DNA damage repair is a major reason for chemoresistance. Previous studies have confirmed that KIN17 affects chemosensitivity. In this study, we examined the impact of KIN17 on chemotherapy response and DNA repair in HCC cells treated with oxaliplatin (L-OHP). We evaluated the expression and biological roles of KIN17 in HCC using bioinformatic analysis. The correlation between KIN17 and RAD51, particularly their nuclear expression levels, was evaluated using immunofluorescence, immunoblotting after nucleocytoplasmic separation in HCC cells, and immunohistochemistry of mouse xenograft tumors and human HCC tissues. The results indicated a significant increase in KIN17 expression in HCC tissues compared to normal tissues. The GSEA analysis revealed that upregulation of KIN17 was significantly associated with DNA damage repair. Knockdown of KIN17 led to increased DNA damage and reduced cellular survival after exposure to L-OHP. On the other hand, overexpression of KIN17 was linked to decreased DNA damage and improved cell survival following L-OHP treatment. Further experiments indicated that KIN17 affects the expression of RAD51, particularly in the nucleus. KIN17 plays a crucial role in influencing the sensitivity of HCC to chemotherapy by triggering the DNA repair response. Increased expression of KIN17 is associated with a poor prognosis for HCC patients, indicating that KIN17 could serve as a prognostic marker and therapeutic target for HCC.

Radiofrequency ablation (RFA) is a local treatment modality for primary liver cancers. Although various input parameters of the RF generator have been adjusted to improve the ablation ranges, the limited ablation ranges remain an obstacle to RFA. This study aimed to compare the ablation ranges and efficacy of sine and square electrical waveforms in a mouse tumor model. An RF generator with an adjustable electrical waveform was developed, and its ablation range in the porcine liver was compared. For all RF parameters, the square electrical waveform ablation range was greater than that of the sine electrical waveform (all p < 0.001) in the porcine liver. The 45 BALB/c nude mice were used to evaluate the efficacy of the two electrical waveforms after the RFA. The mean tumor volume in the square group was significantly lower than that in the sine group (p < 0.001), indicating a higher survival rate (60%). The cellular coagulative necrosis, inflammatory cell infiltration, heat shock proteins, cellular necrosis, and tumor necrosis were significantly greater in square electrical waveform than in sine electrical waveform (all; p < 0.05). RFA with square electrical waveforms has therapeutic potential for tumor management with an enhanced ablation range.

Double Primary Hepatic Cancer (DPHC) which refers to synchronous hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) coexisting in the same liver, has rarely been reported. Here we discussed the clinical characteristics, diagnosis, treatment, and prognosis of DPHC based on an analysis of 12 DPHC cases. Meanwhile, data of 60 HCC cases and 60 ICC cases were collected at a ratio of 5:1 and with matched age and gender to DPHC in the same period. A total of 4,626 cases of primary liver cancer were screened, and the proportion of DPHC was approximately 0.26%. Hepatitis B Virus prevalence in the DPHC group (83.3%) was higher than that in the ICC group (38.3%). Lymph node metastasis was more common in the DPHC group (16.7%) compared to the HCC group (1.7%). The median disease-free survival (DFS) and overall survival (OS) for DPHC were 6.0±2.6 months and 15.0±1.7 months, respectively. Pathological diagnosis indicated a significant effect of preoperative adjuvant transarterial chemoembolization (TACE) on HCC, but limited efficacy on ICC. Both alpha fetoprotein and carbohydrate antigen 19-9 levels were elevated in the DPHC group. In conclusion, the preferred treatment for DPHC is radical resection and regional lymphadenectomy. Preoperative TACE is effective for DPHC with large HCC components. The prognosis for DPHC is marked by high recurrence and high mortality.

Background: Cancer-associated fibroblasts (CAFs) are the key components of the immune barrier in liver cancer. Therefore, gaining a deeper understanding of the heterogeneity and intercellular communication of CAFs holds utmost importance in boosting immunotherapy effectiveness and improving clinical outcomes. Methods: A comprehensive analysis by combing single-cell, bulk, and spatial transcriptome profiling with multiplexed immunofluorescence was conducted to unravel the complexities of CAFs in liver cancer. Results: Through an integrated approach involving 235 liver cancer scRNA-seq samples encompassing over 1.2 million cells, we found that CAFs were particularly increased in hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC). FAP + fibroblasts were identified as the dominant subtype of CAFs, and which were mainly involved in extracellular matrix organization and angiogenesis. These CAFs were enriched in the tumor boundary of HCC, but diffusely scattered within ICC. The DAB2 + and SPP1 + tumor-associated macrophages (TAMs) reinforce the function of FAP + CAFs through signals such as TGF-β, PDGF, and ADM. Notably, the interaction between DAB2 + TAMs and FAP + CAFs promoted the formation of immune barrier and correlated with poorer patient survival, non-response to immunotherapy in HCC. High FAP and DAB2 immunohistochemical scores predicted shorter survival and higher serum AFP concentration in a local clinical cohort of 90 HCC patients. Furthermore, this communication pattern might be applicable to other solid malignancies as well. Conclusions: The interaction between DAB2 + TAMs and FAP + CAFs appears crucial in shaping the immune barrier. Strategies aimed at disrupting this communication or inhibiting the functions of FAP + CAFs could potentially enhance immunotherapy effectiveness and improve clinical outcomes.

Minimally invasive liver surgery, particularly hepatectomy, has evolved significantly with the advent of laparoscopic and robotic techniques. These approaches offer potential benefits over traditional open surgery, including reduced postoperative pain, shorter hospital stays, faster recovery, and improved cosmetic outcomes. This comprehensive review aims to compare the operative efficiency and postoperative recovery outcomes of robotic and laparoscopic hepatectomy. It seeks to provide an in-depth analysis of the advantages and limitations of each technique, assess their cost-effectiveness, and explore emerging trends and future directions in minimally invasive liver surgery. A comprehensive literature search was conducted to identify studies comparing robotic and laparoscopic hepatectomy. The review includes an analysis of operative time, intraoperative blood loss, conversion rates, postoperative pain, length of hospital stay, complication rates, oncological outcomes, and overall cost. Additionally, advancements in technology and future research directions were explored to provide a comprehensive overview of the current landscape and future potential of these surgical techniques. Both robotic and laparoscopic hepatectomy have demonstrated comparable outcomes in terms of oncological safety and effectiveness. However, robotic hepatectomy offers advantages in terms of precision and dexterity, particularly in complex cases, due to its advanced visualization and instrumentation. Laparoscopic hepatectomy, while associated with shorter operative times and lower costs, is limited by technical challenges, especially in major liver resections. The review also highlights the increasing adoption of robotic systems, despite their higher costs and the need for specialized training. Robotic and laparoscopic hepatectomy are both viable options for minimally invasive liver surgery, each with distinct advantages and limitations. The choice between the two should be based on patient-specific factors, the complexity of the procedure, and the surgeon's expertise. Ongoing advancements in technology, including the integration of artificial intelligence and augmented reality, are expected to further refine these techniques, enhancing their efficacy and accessibility. Future research should focus on large-scale, multicenter trials to provide more definitive comparisons and guide clinical decision-making.

General anesthesia is commonly used in the surgical management of gastrointestinal tumors; however, it can lead to emergence agitation (EA). EA is a common complication associated with general anesthesia, often characterized by behaviors, such as crying, struggling, and involuntary limb movements in patients. If treatment is delayed, there is a risk of incision cracking and bleeding, which can significantly affect surgical outcomes. Therefore, having a proper understanding of the factors influencing the occurrence of EA and implementing early preventive measures may reduce the incidence of agitation during the recovery phase from general anesthesia, which is beneficial for improving patient prognosis.

To analyze influencing factors and develop a risk prediction model for EA occurrence following general anesthesia for primary liver cancer.

Retrospective analysis of clinical data from 200 patients who underwent hepatoma resection under general anesthesia at Wenzhou Central Hospital (January 2020 to December 2023) was conducted. Post-surgery, the Richmond Agitation-Sedation Scale was used to evaluate EA presence, noting EA incidence after general anesthesia. Patients were categorized by EA presence postoperatively, and the influencing factors were analyzed using logistic regression. A nomogram-based risk prediction model was constructed and evaluated for differentiation and fit using receiver operating characteristics and calibration curves.

EA occurred in 51 (25.5%) patients. Multivariate analysis identified advanced age, American Society of Anesthesiologists (ASA) grade III, indwelling catheter use, and postoperative pain as risk factors for EA (P < 0.05). Conversely, postoperative analgesia was a protective factor against EA (P < 0.05). The area under the curve of the nomogram was 0.972 [95% confidence interval (CI): 0.947-0.997] for the training set and 0.979 (95%CI: 0.951-1.000) for the test set. Hosmer-Lemeshow test showed a good fit (χ 2 = 5.483, P = 0.705), and calibration curves showed agreement between predicted and actual EA incidence.

Age, ASA grade, catheter use, postoperative pain, and analgesia significantly influence EA occurrence. A nomogram constructed using these factors demonstrates strong predictive accuracy.

Liver cancer, which is well-known to us as one of human most prevalent malignancies across the globe, poses a significant risk to live condition and life safety of individuals in every region of the planet. It has been shown that immune checkpoint treatment may enhance survival benefits and make a significant contribution to patient prognosis, which makes it a promising and popular therapeutic option for treating liver cancer at the current time. However, there are only a very few numbers of patients who can benefit from the treatment and there also exist adverse events such as toxic effects and so on, which is still required further research and discussion. Fortunately, the clustered regularly interspaced short palindromic repeat/CRISPR-associated nuclease 9 (CRISPR/Cas9) provides a potential strategy for immunotherapy and immune checkpoint therapy of liver cancer. In this review, we focus on elucidating the fundamentals of the recently developed CRISPR/Cas9 technology as well as the present-day landscape of immune checkpoint treatment which pertains to liver cancer. What's more, we aim to explore the molecular mechanism of immune checkpoint treatment in liver cancer based on CRISPR/Cas9 technology. At last, its encouraging and powerful potential in the future application of the clinic is discussed, along with the issues that already exist and the difficulties that must be overcome. To sum up, our ultimate goal is to create a fresh knowledge that we can utilize this new CRISPR/Cas9 technology for the current popular immune checkpoint therapy to overcome the treatment issues of liver cancer.

Precision surgery for liver tumors favors laparoscopic anatomical liver resection (LALR), involving the removal of specific liver segments or subsegments. Indocyanine green (ICG)-negative staining is a commonly used method for defining resection boundaries but may be prone to failure. The challenge arises when ICG staining fails, as it cannot be repeated during surgery. In this study, we employed the virtual liver segment projection (VLSP) technology as a salvage approach for precise boundary determination. Our aim was to assess the feasibility of the VLSP to be used for the determination of the boundaries of the liver resection in this situation.

Between January 2021 and June 2023, 12 consecutive patients undergoing subsegment-oriented LALR were included in this pilot series. The VLSP technology was utilized to define the resection boundaries at the time of ICG-negative staining failure. Routine surgical parameters and short-term outcomes were evaluated to assess the safety of VLSP in this procedure. In addition, its feasibility was assessed by analyzing the accuracy between the predicted resected liver volume (PRLV) and actual resected liver volume (ARLV).

Of the 12 enrolled patients, the mean operation time was 444.58 ± 101.70 min (range 290-570 min), with a mean blood loss of 125.00 ± 96.53 ml (range 50-400 mL). One patient (8.3%) was converted to laparotomy for subsequent parenchymal transection, four (33.3%) received blood transfusions and four (33.3%) had postoperative complications. All patients received an R0 resection. The Pearson correlation coefficient (r) between PRLV and ARLV was 0.98 (R2 = 0.96, p < 0.05), and the relative error (RE) was 8.62 ± 6.66% in the 12 patients, indicating agreement.

Failure of intraoperative ICG-negative staining during subsegment-oriented LALR is possible, and VLSP may be an alternative to define the resection boundaries in such cases.