Introduction:This retrospective observational study aimed to evaluate the safety and efficacy of Enhanced Recovery After Surgery (ERAS) protocols in older adult patients (≥65 years) with hepatocellular carcinoma (HCC) undergoing radical hepatectomy. Methods:In this retrospective observational study, 498 patients who underwent radical resection for HCC between January 2018 and December 2023 were included and divided into four groups: Older adult ERAS (OE Group, n=60), Younger adult ERAS (YE Group, n=148), Older adult non-ERAS (ONE Group, n=88), and Younger adult non-ERAS (YNE Group, n=202). Propensity score matching (PSM) was performed to balance baseline covariates, generating three pairwise matched cohorts: PSM-OE Group 1 vs PSM-YE Group (both n=37), PSM-OE Group 2 vs PSM-ONE Group (both n=53), and PSM-OE Group 3 vs PSM-YNE Group (both n=35). Short-term postoperative outcomes were compared across groups. Results:Results showed that postoperative pain control was significantly superior in PSM-OE Group 1 compared to PSM-YE Group (91.9% vs 70.3% pain-free, p=0.018) and in PSM-OE Group 2 compared to PSM-ONE Group (90.6% vs 69.8% pain-free, 7.328, p=0.013), with no significant difference between PSM-OE Group 3 and PSM-YNE Group (85.7% vs 74.3%, p=0.319). PSM-OE Group 2 had significantly shorter length of hospital stays (LOS: 13.17±4.71 vs 16.68±6.42 days, p=0.002) and length of postoperative stays (LPS: 6.94±3.26 vs 9.64±5.02 days, p=0.001) than PSM-ONE Group, while PSM-OE Group 3 also showed shorter LOS (13.31±4.74 vs 17.34±9.75 days, p=0.031) and LPS (7.26±3.53 vs 10.49±6.58 days, p=0.013) compared to PSM-YNE Group. The complication rate was notably lower in PSM-OE Group 2 than PSM-ONE Group (χ2=13.747, p=0.001), with no significant differences in complication rates between other matched pairs. Blood transfusion rates, average hospitalization costs, liver reserve function (assessed by PALBI score), and 30-day readmission rates (p=0.700) showed no significant differences across all matched cohorts. Multivariate regression analysis confirmed ERAS as an independent factor associated with reduced LOS (OR=1.733, p=0.038), LPS (OR=1.901, p=0.015), postoperative pain (OR=5.014, p=0.035), and complications (OR=5.235, p=0.021). Conclusion:ERAS protocols are safe and effective in enhancing postoperative recovery for older adult patients with HCC undergoing hepatectomy, supporting their adoption as standard perioperative care for this population.

This study evaluates the efficacy of pancreatic stump binding and ligation (PSBL) in reducing postoperative pancreatic fistula (POPF) after distal pancreatectomy (DP). A retrospective cohort analysis included 217 patients undergoing DP between 2015 and 2022. Patients were classified into two groups: those receiving PSBL (B-Group, n = 96) and those without (NB-Group, n = 121). The primary outcome was incidence of clinically relevant POPF (Grade B/C). The B-Group demonstrated lower POPF rates (11.5

Background: Liver cancer is a common malignant tumor with an increasing incidence in recent years. We aimed to develop a model by integrating clinical information and multi-omics profiles of genes to predict survival of patients with liver cancer.Methods: The multi-omics data were integrated to identify liver cancer survival-associated signal pathways. Then, a prognostic risk score model was established based on key genes in a specific pathway, followed by the analysis of the relationship between the risk score and clinical features as well as molecular and immunologic characterization of the key genes included in the prediction model. The function experiments were performed to further elucidate the undergoing molecular mechanism.Results: Totally, 4 pathways associated with liver cancer patients’ survival were identified. In the pathway of integrin cell surface interactions, low expression of COMP and SPP1, and low CNVs level of COL4A2 and ITGAV were significantly related to prognosis. Based on above 4 genes, the risk score model for prognosis was established. Risk score, ITGAV and SPP1 were the most significantly positively related to activated dendritic cell. COL4A2 and COMP were the most significantly positively associated with Type 1 T helper cell and regulatory T cell, respectively. The nomogram (involved T stage and risk score) may better predict short-term survival. The cell assay showed that overexpression of ITGAV promoted tumorigenesis.Conclusion: The risk score model constructed with four genes (COMP, SPP1, COL4A2, and ITGAV) may be used to predict survival in liver cancer patients.

Background/Aims: To compare laparoscopic splenectomy and esophagogastric devascularization (LSED) with endoscopic variceal ligation (EVL) plus laparoscopic splenectomy (LS) in treating esophagogastric variceal bleeding (EGVB) caused by portal hypertension (PH). Methods: Between January 2015 and May 2022, 87 patients with PH caused by hepatitis B cirrhosis were included in the retrospective study (34 in LSED versus 53 in EVL + LS). Results: The clinical features of both groups were well-matched (P > .05). The EVL+LS group was associated with shorter operation time, lower operative blood loss, faster gastrointestinal (GI) recovery, lower C-reactive protein levels, and shorter hospital stays after operation (P < .05). Operative morbidity was more significant in the LSED group (19 55.9% versus 18 33.9%) (P < .05). On postoperative days 1 and 3, albumin levels were remarkably lower (P < .05) in the LSED group. The mean follow-up was 24.3 months for LSED and 26.5 for EVL+LS. Hematological parameters, hepatic functional status, hepatic hemodynamics, and endoscopy indicated a substantial improvement in both groups (P < .05), but no significant difference was identified (P > .05). There was no discernible difference in the incidence of GI bleeding between the two groups (P > .05). Conclusion: EVL+LS is a safer, simpler, and more minimally invasive treatment of EGVB secondary to PH.

Objective: To explore the correlation between hepatocellular carcinoma (HCC) gene variation profile and clinical characteristics in Han nationality with HBV infection in Sichuan province.Methods: The clinical data and HCC tissues were obtained from the enrolled patients. Whole exome sequencing and bioinformatics analysis were performed on formalin-fixed and paraffin-embedded samples from HCC. Tumor mutational burden (TMB) was measured by an algorithm developed in-house.Results: Sixteen high-frequency mutated genes with differential expressions were identified by WES. SMG1 gene variation could be positively correlated with satellite lesions. AMY2B and RGPD4 gene mutation seemed to have a greater chance of vascular invasion. The patients with TATDN1 variation have bigger diameters and greater chances of vascular and microvascular invasion (all P < 0.05). Univariate analysis indicated patients with gene TATDN1 variation had worse prognoses both in disease free survival (DFS) and overall survival (OS). In addition, the enrichment analysis showed many pathways, including the cell cycle pathway, viral oncogene pathway, MAPK pathway, PI3K-AKT pathway, etc., may be associated with HCC.Conclusion: This study explores the gene variation profile of HCC patients with HBV infection in Han nationality of Sichuan Province for the first time, which confirmed the existence of some high-frequency mutated genes and the possibility that the gene variations are involved in the tumorigenesis of HCC through multiple signal pathways. Also, patients with TATDN1 wild type showed a trend of better prognosis both in DFS and OS.(c) 2023 Asian Surgical Association and Taiwan Robotic Surgery Association. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).

Pancreatic follicular dendritic cell sarcoma (FDCS) is a rare neoplasm with unclear pathological characteristics. In this study, we report one case of pancreatic FDCS and review published cases to summarize the characteristics and treatment of pancreatic FDCS. A man in his early 30 s was admitted for jaundice, abdominal fullness, and weight loss for 15 days. Computed tomography revealed a large capsule solid mass in the pancreatic head together with a dilated bile duct and enlarged retroperitoneal lymph nodes. Serum biochemistry revealed high total bilirubin levels (313.9 μmol/L) and normal tumor marker levels. Pancreatoduodenectomy was performed, but no chemotherapy was administrated at the patient’s behest. The pathologic diagnosis was pancreatic FDCS infiltrating the duodenal seromuscular layer and common bile duct. The patient presented with liver metastasis 3 months after surgery and died 8 months after surgery from multiorgan failure. Pancreatic FDCS is a rare disease with high invasiveness. Our previous case exhibited paraneoplastic syndrome together with this disease, and further investigation is needed to confirm whether paraneoplastic syndrome is a typical syndrome of pancreatic FDCS.

At present, the role of lncRNA in different kinds of tumors has been widely reported, but its role with hypoxic environment and macrophage polarization is still unclear. Therefore, this study tried to clarify the role of exosomal lncRNA in tumor hypoxic environment and macrophage polarization in the process of hepatocellular carcinoma (HCC), and provide a basis for targeted therapy of HCC.Bioinformatics screening of differentially expressed lncRNA and mRNA was carried out through GEO database, and the expression of lncRNA HMMR-AS1 in tumor tissues was detected and verified in HCC tissues. The effects of HMMR-AS1 on proliferation, migration, apoptosis, and macrophage polarization were determined by in vitro and in vivo experiments. Perform luciferase reporter gene detection and RNA immunoprecipitation to reveal the interaction between HMMR-AS1, miR-147a, and ARID3A. At the same time, the JASPAR database and dual luciferase report were used to detect the relationship between HIF-1α and HMMR-AS1 transcription regulation. Finally, nanoparticle tracking technology, transmission electron microscopy, and western blot were used to detect the effect of hypoxic environment on exosome secretion.LncRNA HMMR-AS1 was significantly up-regulated in HCC tissues and HCC cells and was related to the poor prognosis. Inhibiting the expression of HMMR-AS1 could significantly inhibit tumor growth in vitro and in vivo. Further study of the mechanism showed that HMMR-AS1 could competitively bind to miR-147a to prevent the degradation of ARID3A. Exosomes carrying HMMR-AS1 could promote the M2 polarization of macrophages mediated by this pathway and further accelerate the progression of HCC. In addition, in the hypoxic environment, HIF-1α promotes its transcription by binding to the HMMR-AS1 promoter and induces an increase in the number of exosomes secreted.In summary, we first discovered and verified the role of lncRNA HMMR-AS1 in HCC. In terms of mechanism, the promotion of exosomal HMMR-AS1 competitive adsorption of miR-147a under hypoxic environment affects ARID3A-mediated macrophage polarization. These data provide a new direction for the research on the pathogenesis of HCC and the development of targeted therapy.

Pancreatic stellate cells (PSCs) are the primary cell components of pancreatic cancer (PC) and are involved in tumor growth, metastasis and resistance. However, the role and the mechanism of PSCs in gemcitabine (GEM) resistance to PC still need more investigation. We found that CXCL12 mRNA and secreted CXCL12 protein were higher in PSCs after GEM treatment. The conditioned medium (CM) from GEM-treated PSCs reduced the GEM sensitivity of PC cells. Blocking of CXCL12 in CM by anti-CXCL12 antibody partly restored the GEM sensitivity of PC cells. Blocking of CXCL12 decreased glucose consumption, lactate production, ECAR, and glycolysis-related gene expression in PC cells. The PI3K/AKT/mTOR pathway was activated by the binding of CXCL12 and CXCR4. Moreover, CXCR4 mRNA and protein expressions in PC cells were increased after GEM treatment. Our results indicated the cross-talk between PSCs and PC cells during GEM chemotherapy. CXCL12 secreted by PSCs reduces GEM sensitivity of PC cells by binding to CXCR4 and activating PI3K/AKT/mTOR-glycolysis pathway in PC. Our findings would lay the foundation for solving GEM resistance in PC.

Hepatocellular carcinoma (HCC) is a rapidly growing tumor characterized by a high potential for vascular invasion and metastasis. The purpose of our study is to explore the regulation mechanism of long noncoding RNA (lncRNA) LINC01419 on cell-cycle distribution and metastasis in hepatocellular carcinoma (HCC) by regulating zinc finger of the cerebellum (ZIC1) through PI3K/Akt signaling pathway. Bioinformatics analysis and dual-luciferase reporter assay were used to analyze LINC01419 and related genes in HCC, and their expression in HCC tissues and adjacent normal tissues were determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot. Then, HCC cell lines were subjected to the construction of LINC01419/ZIC1 overexpression/knockdown cells utilizing lentiviral vectors. RIP and ChIP assays were applied to identify the LINC01419-binding protein. BSP and MSP assays were used to determine gene methylation. According to the results, LINC01419 was highly expressed in HCC tissues and cells, while ZIC1 was poorly expressed. LINC01419 targeted and downregulated ZIC1 expression. Furthermore, LINC01419 increased the methylation of ZIC1 promoter and repressed ZIC1 expression. PI3K/Akt signaling pathway was activated by LINC01419 overexpression and ZIC1 knockdown, under which conditions, the HCC cell self-renewal and proliferation were promoted while cell apoptosis was attenuated, accompanied by accelerated formation and metastasis of xenografted tumors in mice. In conclusion, LINC01419 enhances the methylation of ZIC1 promoter, inhibits ZIC1 expression, and activates the PI3K/Akt signaling pathway, thereby enhancing the malignant phenotypes of HCC cells in vitro as well as tumor formation and metastasis in vivo.

Emerging evidence suggests that long noncoding RNAs (lncRNAs) function as competitive endogenous RNA (ceRNA) targeting proteins and genes; however, the role of lncRNAs in hepatocellular carcinoma (HCC) is not well understood. We investigated the mechanism by which lncRNA SNHG6 promotes the development of HCC. RT-qPCR revealed upregulated lncRNA SNHG6 in the HCC setting. Elevated SNHG6 expression was indicative of poor prognosis in patients with HCC. SNHG6 overexpression resulted in increased cyclin D1, cyclin E1, and E2F1 expression both in vitro and in vivo. SNHG6 also promoted HCC cell proliferation by enhancing G1-S phase transition in vitro. Dual luciferase reporter assays, RIP, and RNA pull-down assays demonstrated SNHG6 competitively bound to miR-204-5p and inhibited its expression preventing miR-204-5p from targeting E2F1. Overexpression of miR-204-5p abolished the effect of SNHG6. Our data suggest that SNHG6 functions as a ceRNA that targets miR-204-5p resulting in an increased E2F1 expression and enhanced G1-S phase transition, thereby promoting the tumorigenesis of HCC.