Diagnostic Performance of 18F-FDG PET(CT) in Bone-Bone Marrow Involvement in Pediatric Neuroblastoma: A Systemic Review and Meta-Analysis.

Objective: We sought to perform a systemic review and meta-analysis of the diagnostic performance of 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (computed tomography) (PET(CT)) in detection of bone and/or bone marrow involvement (BMI) in pediatric neuroblastoma (NB). Materials and Methods: We searched electronic databases Pubmed and Embase to retrieve relevant references. We calculated pooled sensitivity, specificity, positive and negative likelihood ratios (LR+ and LR-), diagnostic odds ratio (DOR), and the area under the curve (AUC). Moreover, a summary receiver operating characteristic (SROC) curve and likelihood ratio dot plot were plotted. Study-between statistical heterogeneity was evaluated via I-square index (I 2). Subgroup analyses were used to explore heterogeneity. Results: Seven studies including 127 patients were involved in this meta-analysis. The overall sensitivity and specificity were 0.87 (95% CI: 0.65-0.96) with heterogeneity I 2 = 88.1% (p < 0.001) and 0.96 (95% CI: 0.67-1.00) with heterogeneity I 2 = 77.8% (p < 0.001), respectively. The pooled LR+, LR-, and DOR were 21.3 (95% CI: 2.1-213.9), 0.14 (95% CI: 0.05-0.40), and 157 (95% CI: 16-1532), respectively. The area under the SROC curve was 0.97 (95% CI: 0.95-0.98). Conclusions: Through a meta-analysis, this study suggested that 18F-FDG PET(CT) has a good overall diagnostic accuracy in the detection of bone/BMI in pediatric neuroblastoma.

A transcriptome profile in gallbladder cancer based on annotation analysis of microarray studies.

The purpose of the present study was to identify aberrantly expressed genes for gallbladder cancer based on the annotation analysis of microarray studies and to explore their potential functions. Differential gene expression was investigated in cholesterol polyps, gallbladder adenoma and gallbladder cancer using microarrays. Subsequently, microarray results were comprehensively analyzed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to determine the affected biological processes or pathways. Differentially expressed genes (DEGs) of cholesterol polyps, gallbladder adenoma and gallbladder cancer were identified. Following comprehensive analysis, 14 genes were found to be differentially expressed in the gallbladder wall of both gallbladder cancer and gallbladder adenoma. The 20 most significantly upregulated genes were only upregulated in the gallbladder wall of gallbladder cancer, but not in the gallbladder wall of cholesterol polyps and gallbladder adenoma. In addition, 182 DEGs were upregulated in the gallbladder wall of gallbladder adenoma compared with the gallbladder wall of cholesterol polyps. A total of 20 most significant DEGs were found in both the tumor and gallbladder wall of gallbladder cancer. In addition, the most significant DEGs that were identified were only upregulated in the tumor of gallbladder cancer. GO and KEGG analysis indicated that the aforementioned DEGs could participate in numerous biological processes or pathways associated with the development of gallbladder cancer. The present findings will help improve the current understanding of tumorigenesis and the development of gallbladder cancer.

Effect of CEACAM6 silencing on the biological behavior of human gallbladder cancer cells.

Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is abnormally expressed in various malignant tumors and thus represents a potential biomarker, although information regarding its role in gallbladder cancer (GBC) is limited. This study aimed to evaluate the expression of CEACAM6 in GBC and the effect of CEACAM6 gene silencing on the proliferation, migration, invasion and apoptosis of human GBC cells. Immunochemistry was used to evaluate CEACAM6 expression in 95 GBC specimens and 40 peritumoral tissue specimens. GBC-SD and SGC-996 cell lines were used for in vitro experiments. CEACAM6 was knocked down by transfection of targeted small interfering RNA (siRNA), and reverse-transcription quantitative PCR and western blot analysis were used to detect knockdown efficiency. Cell Counting Kit-8 and colony formation assays were undertaken to evaluate cell proliferation. Variations in cell migration and invasion were detected by wound-healing and Transwell assays, respectively. Flow cytometry was applied to measure cell apoptosis and cell cycle distribution. CEACAM6 gene expression was significantly greater in GBC tissues than in peritumoral tissues, and its positive expression was associated with poor prognosis. CEACAM6 mRNA and protein expression in the CEACAM6 siRNA treatment group was significantly lower than that in the negative control group and the blank group. CEACAM6 knockdown inhibited GBC cell proliferation, migration and invasion but promoted cell apoptosis. Western blot analysis of invasion- and apoptosis-related proteins matrix metalloproteinase-2, Vimentin, BCL-2 and BAX further confirmed CEACAM6 mRNA depletion promoted cell apoptosis and inhibited invasion. Additionally, CEACAM6 mRNA depletion affected the progression of the GBC cell cycle to increase cell distribution in G0/G1 phase, and to reduce it in G2/M phase and S phase. These findings indicated that CEACAM6 overexpression may be related to the tumorigenesis and development of GBC. In summary, depletion of CEACAM6 mRNA suppressed the malignant biological behaviors of human gallbladder cancer cells.

A cell-based fluorescent assay for FAP inhibitor discovery.

To facilitate the discovery of FAP inhibitors, a convenient cell-based fluorescent assay was developed by using a commonly available U87MG cell line and a FAP-specific substrate Suc-Gly-Pro-AMC. The assay enabled the fast determination of multiple IC50s by simply incubating a solution of phosphate-buffered saline in a 96-well plate within 30 min. The substrate specificity, cross-reaction and other related conditions were systematically optimized. This method was successfully applied to determine the IC50s of seven known inhibitors. The results are in consistence with the trend reported, which indicating that this practical assay is a valuable method to accelerate the discovery of FAP inhibitor.

Comprehensive analysis of DNA methylation and gene expression profiles in cholangiocarcinoma.

BACKGROUND: The incidence of cholangiocarcinoma (CCA) has risen in recent years, and it has become a significant health burden worldwide. However, the mechanisms underlying tumorigenesis and progression of this disease remain largely unknown. An increasing number of studies have demonstrated crucial biological functions of epigenetic modifications, especially DNA methylation, in CCA. The present study aimed to identify and analyze methylation-regulated differentially expressed genes (MeDEGs) involved in CCA tumorigenesis and progression by bioinformatics analysis. METHODS: The gene expression profiling dataset (GSE119336) and gene methylation profiling dataset (GSE38860) were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and differentially methylated genes (DMGs) were identified using the limma packages of R and GEO2R, respectively. The MeDEGs were obtained by overlapping the DEGs and DMGs. Functional enrichment analyses of these genes were then carried out. Protein-protein interaction (PPI) networks were constructed using STRING and visualized in Cytoscape to determine hub genes. Finally, the results were verified based on The Cancer Genome Atlas (TCGA) database. RESULTS: We identified 98 hypermethylated, downregulated genes and 93 hypomethylated, upregulated genes after overlapping the DEGs and DMGs. These genes were mainly enriched in the biological processes of the cell cycle, nuclear division, xenobiotic metabolism, drug catabolism, and negative regulation of proteolysis. The top nine hub genes of the PPI network were F2, AHSG, RRM2, AURKB, CCNA2, TOP2A, BIRC5, PLK1, and ASPM. Moreover, the expression and methylation status of the hub genes were significantly altered in TCGA. CONCLUSIONS: Our study identified novel methylation-regulated differentially expressed genes (MeDEGs) and explored their related pathways and functions in CCA, which may provide novel insights into a further understanding of methylation-mediated regulatory mechanisms in CCA.

Enhanced efficiency of Cu2ZnSn(S,Se)4 solar cells via anti-reflectance properties and surface passivation by atomic layer deposited aluminum oxide.

Reducing interface recombination losses is one of the major challenges in developing Cu2ZnSn(S,Se)4 (CZTSSe) solar cells. Here, we propose a CZTSSe solar cell with an atomic layer deposited Al2O3 thin film for surface passivation. The influence of passivation layer thickness on the power conversion efficiency (PCE), short-circuit current density (J sc), open-circuit voltage (V oc) and fill factor (FF) of the solar cell is systematically investigated. It is found that the Al2O3 film presents notable antireflection (AR) properties over a broad range of wavelengths (350-1000 nm) for CZTSSe solar cells. With increasing Al2O3 thickness (1-10 nm), the average reflectance of the CZTSSe film decreases from 12.9% to 9.6%, compared with the average reflectance of 13.6% for the CZTSSe film without Al2O3. The Al2O3 passivation layer also contributes to suppressed surface recombination and enhanced carrier separation. Passivation performance is related to chemical and field effect passivation, which is due to released H atoms from the Al-OH bonds and the formation of Al vacancies and O interstitials within Al2O3 films. Therefore, the J sc and V oc of the CZTSSe solar cell with 2 nm-Al2O3 were increased by 37.8% and 57.8%, respectively, in comparison with those of the unpassivated sample. An optimal CZTSSe solar cell was obtained with a V oc, J sc and η of 0.361 V, 33.78 mA and 5.66%. Our results indicate that Al2O3 films show the dual functions of AR and surface passivation for photovoltaic applications.