Learning curve for a surgeon in robotic pancreaticoduodenectomy through a "G"-shaped approach: A cumulative sum analysis.

BACKGROUND: Robotic pancreaticoduodenectomy (RPD) can achieve similar surgical results to open and PD; however, RPD has a long learning curve and operation time (OT). To address this issue, we have summarized a surgical path to shorten the surgical learning curve and OT. AIM: To investigate the effective learning curve of a "G"-shaped surgical approach in RPD for patients. METHODS: A total of 60 patients, who received "G"-shaped RPD (GRPD) by a single surgeon in the First Hospital of Shanxi Medical University from May 2017 to April 2020, were included in this study. The OT, demographic data, intraoperative blood loss, complications, hospitalization time, and pathological results were recorded, and the cumulative sum (CUSUM) analysis was performed to evaluate the learning curve for GRPD. RESULTS: According to the CUSUM analysis, the learning curve for GRPD was grouped into two phases: The early and late phases. The OT was 480 ± 81.65 min vs 331 ± 76.54 min, hospitalization time was 22 ± 4.53 d vs 17 ± 6.08 d, and blood loss was 308 ± 54.78 mL vs 169.2 ± 35.33 mL in the respective groups. Complications, including pancreatic fistula, bile leakage, reoperation rate, postoperative death, and delayed gastric emptying, were significantly decreased after this surgical technique. CONCLUSION: GRPD can improve the learning curve and operative time, providing a new method for shortening the RPD learning curve.

XB130 Knockdown Inhibits the Proliferation, Invasiveness, and Metastasis of Hepatocellular Carcinoma Cells and Sensitizes them to TRAIL-Induced Apoptosis.

BACKGROUND: XB130 is a recently discovered adaptor protein that is highly expressed in many malignant tumors, but few studies have investigated its role in hepatocellular carcinoma (HCC). Therefore, this study explored the relationship between this protein and liver cancer and investigated its molecular mechanism of action. METHODS: The expression of XB130 between HCC tissues and adjacent nontumor tissues was compared by real-time polymerase chain reaction, immunochemistry, and Western blotting. XB130 silencing was performed using small hairpin RNA. The effect of silencing XB130 was examined using Cell Counting Kit-8, colony assay, wound healing assay, and cell cycle analysis. RESULTS: We found that XB130 was highly expressed in HCC tissues (cancer tissues vs. adjacent tissues: 0.23 ± 0.02 vs. 0.17 ± 0.02, P < 0.05) and liver cancer cell lines, particularly MHCC97H and HepG2 (MHCC97H and HepG2 vs. normal liver cell line LO-2: 2.35 ± 0.26 and 2.04 ± 0.04 vs. 1.00 ± 0.04, respectively, all P < 0.05). The Cell Counting Kit-8 assay, colony formation assay, and xenograft model in nude mice showed that silencing XB130 inhibited cell proliferative ability both in vivo and in vitro, with flow cytometry demonstrating that the cells were arrested in the G0/G1 phase in HepG2 (HepG2 XB130-silenced group [shA] vs. HepG2 scramble group [NA]: 74.32 ± 5.86% vs. 60.21 ± 3.07%, P < 0.05) and that the number of G2/M phase cells was decreased (HepG2 shA vs. HepG2 NA: 8.06 ± 2.41% vs. 18.36 ± 4.42%, P < 0.05). Furthermore, the cell invasion and migration abilities were impaired, and the levels of the epithelial-mesenchymal transition-related indicators vimentin and N-cadherin were decreased, although the level of E-cadherin was increased after silencing XB130. Western blotting showed that the levels of phosphorylated phosphoinositide 3-kinase (PI3K) and phospho-protein kinase B (p-Akt) also increased, although the level of phosphorylated phosphatase and tensin homolog increased, indicating that XB130 activated the PI3K/Akt pathway. Furthermore, we found that a reduction in XB130 increased liver cancer cell sensitivity to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis. CONCLUSIONS: Our findings suggest that XB130 might be used as a predictor of liver cancer as well as one of the targets for its treatment.

Anti-apoptosis Effect of Decoy Receptor 3 in Cholangiocarcinoma Cell Line TFK-1.

BACKGROUND: Decoy receptor 3 (DcR3) is a protein with anti-apoptotic effect that belongs to the tumor necrosis factor receptor superfamily. DcR3 is highly expressed in a variety of malignant tumors including cholangiocarcinoma and its expression was found to be related to the clinical stage, the invasion, and the metastasis of the tumor. This in vitro study aimed to investigate the effect of downregulated expression of DcR3 on cell viability, cell apoptosis, and cell cycle in cholangiocarcinoma cell line TFK-1. METHODS: Three different cell lines were cultured: human cholangiocarcinoma TFK-1, human biliary epithelial carcinoma HuCCT-1, and human cholangiocarcinoma RBE. The cholangiocarcinoma cell line with the highest expression of DcR3 was selected for further investigation. The expression of DcR3 was silenced/knocked down by transfection with DcR3-siRNA in the selected cell line. Various biological phenotype parameters such as cell viability, apoptosis, and cell cycle were observed. RESULTS: The mRNA and protein levels of DcR3 were measured in the three cell lines, and TFK-1 was selected. After the treatment with DcR3-siRNA for 48 h, DcR3 mRNA and protein expression in the treatment group were 38.45% (P < 0.01) and 48.03% (P < 0.05) of that of the control, respectively. It was found that the cell viability decreased to 61.87% of the control group (P < 0.01) after the downregulation of DcR3 in cholangiocarcinoma cell line TFK-1 by transfection with DcR3-siRNA, while the percentage of apoptotic cells was 2.98 times as compared with the control group (P < 0.05). Compared with the control group the ratio of G0/G1increased, and the ratio of G2/M decreased in the treatment group. However, the differences were not statistically significant. CONCLUSIONS: The effect of DcR3 on the growth and apoptosis of cholangiocarcinoma has been demonstrated. DcR3 is not only a predictive marker for malignant tumor but it is also likely to be a potential target for cancer gene therapy. Further studies should focus on exploring the binding ligand of DcR3, the signaling pathway involved, and the molecular mechanism for the regulation of DcR3 expression in cholangiocarcinoma.

LncSHRG promotes hepatocellular carcinoma progression by activating HES6.

Hepatocellular carcinoma, one of the most common cancers, leads to mass mortality worldwide currently. However, the underlying mechanism of its oncogenesis remains to be elucidated. Here we identified that a long noncoding RNA, lncSHRG, was greatly upregulated in human hepatocellular carcinoma samples. We found that lncSHRG was essential for liver cancer cell proliferation and tumor propagation in mice. In mechanism, lncSHRG recruits SATB1 to bind to HES6 promoter and initiates HES6 expression. HES6, which is highly expressed in hepatocellular carcinoma, promotes tumor cell proliferation. High expression level of HES6 is positively correlated with clinical severity and poor prognosis of people with hepatocellular carcinoma. Altogether, our research provides a new insight on the mechanism of hepatocellular carcinoma progression.

Preliminary study of a new pathological evolution-based clinical hepatolithiasis classification.

AIM: To investigate clinical features, treatment strategies and outcomes of patients with hepatolithiasis (HL) undergoing surgical treatment, using a new clinical classification. METHODS: Sixty-eight HL patients were hospitalized and treated surgically from August 2011 to December 2012 and they were classified into four HL types according to pathological evolution of the disease. These four HL types included type I primary type (defined as no previous biliary tract surgery), type II inflammatory type (with previous biliary tract surgery and cholangitis), type III mass-forming type (HL complicated by hepatic mass-forming lesion), and type IV terminal type (with secondary biliary cirrhosis and resultant portal hypertension). The perioperative data including general information, imaging data, postoperative complications, and immediate and final stone clearance rate were obtained and analyzed. RESULTS: In all 68 patients, the proportion of HL type I-IV was 50% (34/68), 36.8% (25/68), 10.3% (7/68) and 2.8% (2/68), respectively. Abdominal pain was the main clinical manifestation in type I (88.2%), fever was predominant in type II (52.0%), the malignancy rate in type III was high (71.4%), and portal hypertension and spleen enlargement were common in type IV (2/2, 100.0%). Liver resection rate for types I-III was 79.4%, 72.0% and 71.4%, respectively. The overall incidence of postoperative complications was 23.5% (16/68). There were no perioperative deaths. The average length of hospital stay was 12.7±7.3 d. Immediate and final stone clearance rate was 73.5% (50/68) and 89.7% (61/68), respectively. Fifty-nine of 68 patients (86.8%) were followed- up for >1 year after surgery, and 96.6% of these patients (57/59) had a good quality of life according to a criterion recommended for postoperative evaluation of quality of life. CONCLUSION: The pathological evolution-based clinical classification of HL has a role in optimizing treatment strategy, and patients can benefit from this classification when it is used properly.