Minor hepatectomy combined with cholangioplasty and cholangiojejunostomy for Bismuth II hilar cholangiocarcinoma: A propensity score matching analysis.

BACKGROUND: The optimal surgical approach for Bismuth II hilar cholangiocarcinoma (HCCA) remains controversial. This study compared perioperative and oncological outcomes between minor and major hepatectomy. MATERIALS AND METHODS: One hundred and seventeen patients with Bismuth II HCCA who underwent hepatectomy and cholangiojejunostomy between January 2018 and December 2022 were retrospectively investigated. Propensity score matching created a cohort of 62 patients who underwent minor (n = 31) or major (n = 31) hepatectomy. Perioperative outcomes, complications, quality of life, and survival outcomes were compared between the groups. Continuous data are expressed as the mean ± standard deviation, categorical variables are presented as n (%). RESULTS: Minor hepatectomy had a significantly shorter operation time (245.42 ± 54.31 vs. 282.16 ± 66.65 min; P = 0.023), less intraoperative blood loss (194.19 ± 149.17 vs. 315.81 ± 256.80 mL; P = 0.022), a lower transfusion rate (4 vs. 11 patients; P = 0.038), more rapid bowel recovery (17.77 ± 10.00 vs. 24.94 ± 9.82 h; P = 0.005), and a lower incidence of liver failure (1 vs. 6 patients; P = 0.045). There were no significant between-group differences in wound infection, bile leak, bleeding, pulmonary infection, intra-abdominal fluid collection, and complication rates. Postoperative laboratory values, length of hospital stay, quality of life scores, 3-year overall survival (25.8 % vs. 22.6 %; P = 0.648), and 3-year disease-free survival (12.9 % vs. 16.1 %; P = 0.989) were comparable between the groups. CONCLUSION: In this propensity score-matched analysis, overall survival and disease-free survival were comparable between minor and major hepatectomy in selected patients with Bismuth II HCCA. Minor hepatectomy was associated with a shorter operation time, less intraoperative blood loss, less need for transfusion, more rapid bowel recovery, and a lower incidence of liver failure. Besides, this findings need confirmation in a large-scale, multicenter, prospective randomized controlled trial with longer-term follow-up.

LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression.

HCC is one of the most common malignant tumors worldwide. Although traditional treatment methods have been improved in recent years, the survival rate of HCC patients has not been significantly improved. Immunotherapy has shown extremely high clinical value in a variety of tumors. In this study, we found that TUG1 could regulate the expression of PD-L1 through JAK2/STAT3 to mediate immunosuppression. Here, The expression of TUG1 and PD-L1 in HCC tissues was evaluated through analysis of databases and verified in HCC tissue and HCC cancer cells by qRT-PCR. The effect of TUG1 on tumor immune escape was detected by coculture, and cell viability was detected with a CCK8 assay. The results demonstrated that TUG1 was closely associated with anticancer immunity. TUG1 and PD-L1 were highly expressed in HCC tissues and HCC cancer cells, and high expression of TUG1 and PD-L1 was related to the poor prognosis of HCC patients. In addition, knocking down TUG1 expression could reduce PD-L1 expression and enhance the cancer cell-killing capability of T cells. Downregulating TUG1 expression could also decrease the mRNA and protein expression of JAK2 and STAT3. To sum up, TUG1 and PD-L1 are overexpressed in patients with liver cancer and are related to the poor prognosis of these patients. Silencing TUG1 expression reduced the mRNA and protein expression of PD-L1 by affecting the JAK2/STAT3 pathway.

Epidemiology and outcome of individuals with intraductal papillary neoplasms of the bile duct.

BACKGROUND: Intraductal papillary neoplasm of the bile duct (IPNB) is a rare distinct subtype of precursor lesions of biliary carcinoma. IPNB is considered to originate from luminal biliary epithelial cells, typically displays mucin-hypersecretion or a papillary growth pattern, and results in cystic dilatation[1]. IPNB develops anywhere in the intrahepatic and extrahepatic biliary tracts, and can occur in various pathological stages from low-grade dysplasia to invasive carcinoma. IPNBs have similar phenotypic changes in the occurrence and development of all subtypes, and the prognosis is significantly better than that of traditional (non-papillary) cholangiocarcinoma. AIM: To evaluate the clinicopathological features of IPNB to provide evidence-based guidance for treatment. METHODS: Invasive IPNB, invasive intraductal papillary mucinous neoplasm of the pancreas (IPMN), and traditional cholangiocarcinoma data for affected individuals from 1975 to 2016 were obtained from the Surveillance, Epidemiology, and End Results (SEER) database. Annual percentage changes (APCs) in the incidence and incidence-based (IB) mortality were calculated. We identified the independent predictors of overall survival (OS) and cancer-specific survival (CSS) in individuals with invasive IPNB. RESULTS: The incidence and IB mortality of invasive IPNB showed sustained decreases, with an APC of -4.5% (95%CI: -5.1% to -3.8%) and -3.3% (95%CI: -4.1% to -2.6%) (P < 0.001), respectively. Similar decreases in incidence and IB mortality were seen for invasive IPMN but not for traditional cholangiocarcinoma. Both OS and CSS for invasive IPNB were better than for invasive IPMN and traditional cholangiocarcinoma. A total of 1635 individuals with invasive IPNB were included in our prognosis analysis. The most common tumor sites were the pancreaticobiliary ampulla (47.9%) and perihilar tract (36.7%), but the mucin-related subtype of invasive IPNB was the main type, intrahepatically (approximately 90%). In the univariate and multivariate Cox regression analysis, age, tumor site, grade and stage, subtype, surgery, and chemotherapy were associated with OS and CSS (P < 0.05). CONCLUSION: Incidence and IB mortality of invasive IPNB trended steadily downward. The heterogeneity of IPNB comprises site and the tumor's mucin-producing status.

Pancreatic adenosquamous carcinoma: A population level analysis of epidemiological trends and prognosis.

BACKGROUND: The incidence and mortality of pancreatic adenosquamous carcinoma (PASC) have received little attention. The goal of our study was to explore the overall epidemiological trend of PASC at the population level. METHODS: The Surveillance, Epidemiology, and End Results database was used to collect the incidence, incidence-based (IB) mortality, and patient details for PASC from 2000 to 2017. The Joinpoint regression tool was used to examine the trends in incidence and IB mortality. The Kaplan-Meier approach was used for survival analysis. Univariate and multivariate Cox regression analyses were used to determine the independent prognostic factors. RESULTS: We included 815 patients with PASC in the study. The incidence of PASC continuously increased from 2000 to 2017, with an annual percentage change (APC) of 3.9% (95% CI: 2.2%-5.7%, p < 0.05). IB mortality also increased continuously, with an APC of 5.0% (95% CI: 2.5%-7.6%, p < 0.05). Multivariate Cox regression analysis revealed that age, treatment, regional lymph node involvement, and tumor size were independent prognostic factors. Nomograms were created for PASC to predict 1- and 2-year survival probabilities, respectively. CONCLUSIONS: The incidence and IB mortality of PASC had a sustained and rapid increase, indicating that the preventive and treatment measures for PASC were not ideal. We must identify the significance of this condition as soon as possible, and commit greater attention and resources to PASC research.

Comprehensive analysis of the effects of KIF2C on prognosis, biological functions and immune infiltration in PAAD.

Kinesin family member 2 C (KIF2C), a modulator of microtubule depolymerization, bipolar spindle formation, and chromosome segregation, has been reported to play roles in cancer biology. Moreover, many articles have reported that KIF2C expression is closely associated with the progression and prognosis of a variety of tumors. However, the role of KIF2C in pancreatic cancer is unclear. In this study, we used various databases to investigate the correlation between KIF2C expression and pancreatic cancer. METHODS: First, we determined the location of KIF2C in tumour cell lines via The Human Protein Atlas and immunofluorescence staining. Then, we analysed the GEPIA2 and TISIDB databases to assess KIF2C expression in pancreatic cancer cells and its correlation with the prognosis of pancreatic cancer. Through the Linkdeomics database, we identified the mRNAs whose expression was correlated with KIF2C expression. Next, we used the miRDB, miRanda, miRTairBase, Targetscan and miRmap databases to predict miRNAs that interact with KIF2C. Furthermore, we performed PPI analysis of KIF2C using the STRING database and Cytoscape Mcode software. The TISIDB database was used to analyse the correlation between KIF2C expression and immunity in pancreatic cancer. Finally, datasets GSE62452 and PACA-UA(https://xenabrowser.net/datapages/?cohort=PACA-AU&removeHub=http%3 A%2 F%2F127.0.0.1%3A7222) were used to validate the results of survival analysis and immune analysis. RESULTS: It was revealed that KIF2C was mainly located in the nuclei of pancreatic cancer cells. We found that the KIF2C mRNA expression levels in pancreatic cancer tissues were higher than those in normal tissues. Notably, elevated KIF2C mRNA expression was significantly associated with decreased overall survival and disease-free survival in patients with pancreatic cancer. Furthermore, KIF2C expression was closely related to the expression of multiple proteins and miRNAs in pancreatic cancer tissues. In addition, KIF2C expression was closely related to CD4+T cells. These results indicated that the expression of KIF2C was closely related to the prognosis of pancreatic cancer. CONCLUSION: KIF2C expression is negatively correlated with the prognosis of pancreatic cancer patients, and one of the main mechanisms underlying this relationship may be related to the tumor immune microenvironment.

A novel prognostic model for diagnosing atypical bile duct hyperplasia in patients with intrahepatic lithiasis.

There is no specific method for the preoperative diagnosis of atypical bile duct hyperplasia, which is a precursor of cholangiocarcinoma. This study aimed to create a new model for diagnosing atypical bile duct hyperplasia based on routine laboratory tests in patients with intrahepatic lithiasis.The new diagnostic model was developed with a derivation cohort that included 375 patients with intrahepatic lithiasis. Clinical and pathological data were retrospectively collected. Prognostic factors were evaluated with univariate and logistic regression analyses. The validation cohort included 136 patients who were retrospectively screened to quantify the model's predictive value.Age and Carbohydrate Antigen 19-9 (CA-199) were revealed to be diagnostic indicators of atypical bile duct hyperplasia in patients with intrahepatic lithiasis. The new diagnostic model was created with the formula: -6.612 + (0.002 × CA-199) + (0.072 × Age). The area under the receiver operating curve of the model was 0.721. With 0.25 as the cutoff point, the sensitivity and specificity of this model in the derivation cohort were 13.9% and 95.9%, respectively. In the validation cohort, these values were 28.5% and 88.7%, respectively. The novel model has an acceptable and stable ability to predict atypical hyperplasia in the intrahepatic bile duct.This novel model provides a simple system for diagnosing atypical bile duct hyperplasia before surgery in patients with intrahepatic lithiasis.

[Interferon-induced transmembrane protein 3 knock-down inhibits proliferation and invasion of hepatocellular carcinoma HepG2 cells in vitro].

OBJECTIVE: To investigate the abnormal expression of interferon-induced transmembrane protein 3 (IFITM3) in hepatocellular carcinoma (HCC) and the effect of IFITM3 knock-down on the biological behaviors of hepatocellular carcinoma HepG2 cells. METHODS: Western blot analysis and immunohistochemical staining were used to determine the expression of IFITM3 protein in 60 HCC samples and paired adjacent tissues. A small interfering RNA fragments of IFITM3 (IFITM3 siRNA) was transiently transfected into HepG2 cells and expressions of IFITM3 at mRNA and protein levels were examined by qRT-PCR and Western blotting. The changes in the proliferation of the transfected cells were determined using cell counting kit 8 (CCK8) assay, and the cell invasion and migration were tested using Transwell assay and wound-healing assay. RESULTS: Compared with the adjacent tissues, HCC tissues expressed significantly higher levels of IFITM3. In HepG2 cells, transfection with IFITM3 siRNA resulted in significant down-regulation of IFITM3 expression at both the protein and mRNA levels and obviously suppressed cell proliferation, invasion, and migration ability as compared with the cells transfected with scrambled siRNA and control cells (P<0.05). CONCLUSIONS: IFITM3, which is overexpressed in HCC, plays a vital role in the proliferation and invasion of HCC cells and may serve as a potential target for gene therapy of HCC.