Pure laparoscopic versus open left lateral sectionectomy for hepatocellular carcinoma: A propensity score matching analysis.

Backgrounds/Aims: Anatomical resection has superior oncologic outcomes over non-anatomical resection in hepatocellular carcinoma, and left lateral sectionectomy is the simplest and easiest perform anatomical resection procedure among liver resections. The purpose of this study was to find out the safety and feasibility of pure laparoscopic left lateral sectionectomy (PLLLS) for hepatocellular carcinoma. Methods: Patients who underwent left lateral sectionectomy at a tertiary referral hospital, from August 2007 to April 2019 were enrolled in this retrospective study. After matching the 1 : 3 propensity score, 17 open and 51 pure laparoscopic cases were selected out of 102 cases of total left lateral resection for hepatocellular carcinoma. The group was analyzed in terms of patient demographics, preoperative data, and postoperative outcomes. Results: During the study period, there was no open conversion case. The mean operative time and complication were not statistically significant different between the two groups. There was no statistically significant difference in disease-free survival and overall survival had no statistical between the two groups. There were no mortality cases, and postoperative hospital stay was significantly shorter in the PLLLS group than in the open left lateral sectionectomy (OLLS) group. Conclusions: The oncologic outcomes and complication rate were the same in the PLLLS and OLLS groups. However, the hospital stay was shorter in the PLLLS group than in the OLLS group. The present study findings demonstrate that the PLLLS is a safe and feasible procedure for hepatocellular carcinoma.

Integrative meta-analysis of multiple gene expression profiles in acquired gemcitabine-resistant cancer cell lines to identify novel therapeutic biomarkers.

In molecular-targeted cancer therapy, acquired resistance to gemcitabine is a major clinical problem that reduces its effectiveness, resulting in recurrence and metastasis of cancers. In spite of great efforts to reveal the overall mechanism of acquired gemcitabine resistance, no definitive genetic factors have been identified that are absolutely responsible for the resistance process. Therefore, we performed a cross-platform meta-analysis of three publically available microarray datasets for cancer cell lines with acquired gemcitabine resistance, using the R-based RankProd algorithm, and were able to identify a total of 158 differentially expressed genes (DEGs; 76 up- and 82 down-regulated) that are potentially involved in acquired resistance to gemcitabine. Indeed, the top 20 up- and down-regulated DEGs are largely associated with a common process of carcinogenesis in many cells. For the top 50 up- and down-regulated DEGs, we conducted integrated analyses of a gene regulatory network, a gene co-expression network, and a protein-protein interaction network. The identified DEGs were functionally enriched via Gene Ontology hierarchy and Kyoto Encyclopedia of Genes and Genomes pathway analyses. By systemic combinational analysis of the three molecular networks, we could condense the total number of DEGs to final seven genes. Notably, GJA1, LEF1, and CCND2 were contained within the lists of the top 20 up- or down-regulated DEGs. Our study represents a comprehensive overview of the gene expression patterns associated with acquired gemcitabine resistance and theoretical support for further clinical therapeutic studies.

Cross-platform meta-analysis of multiple gene expression profiles identifies novel expression signatures in acquired anthracycline-resistant breast cancer.

Anthracyclines are among the most effective and commonly used chemotherapeutic agents. However, the development of acquired anthracycline resistance is a major limitation to their clinical application. The aim of the present study was to identify differentially expressed genes (DEGs) and biological processes associated with the acquisition of anthracycline resistance in human breast cancer cells. We performed a meta-analysis of publically available microarray datasets containing data on stepwise-selected, anthracycline­resistant breast cancer cell lines using the RankProd package in R. Additionally, the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were used to analyze GO term enrichment and pathways, respectively. A protein-protein interaction (PPI) network was also generated using Cytoscape software. The meta-analysis yielded 413 DEGs related to anthracycline resistance in human breast cancer cells, and 374 of these were not involved in individual DEGs. GO analyses showed the 413 genes were enriched with terms such as 'response to steroid metabolic process', 'chemical stimulus', 'external stimulus', 'hormone stimulus', 'multicellular organismal process', and 'system development'. Pathway analysis revealed significant pathways including steroid hormone biosynthesis, cytokine-cytokine receptor interaction, drug metabolism-cytochrome P450, metabolism of xenobiotics by cytochrome P450, and arachidonic acid metabolism. The PPI network indicated that proteins encoded by TRIM29, VTN, CCNA1, and karyopherin α 5 (KPNA5) participated in a significant number of interactions. In conclusion, our meta-analysis provides a comprehensive view of gene expression patterns associated with acquired resistance to anthracycline in breast cancer cells, and constitutes the basis for additional functional studies.