Surgical resection may provide better survival and lower recurrence rates than RFA for patients with HCC to the Milan criteria.

No abstract

When treating Childs A cirrhotic patients with solitary HCC larger than 3 cm but less than 5 cm, or with two or three lesions each less than 5 cm, surgical resection provides a better survival than RFA. When treating Childs A cirrhotics with solitary HCC ≤ 3 cm, RFA has a comparable RFS to surgical resection, but RFA is less invasive.

Hepatocellular carcinoma (HCC) is the most common malignant liver disease in the world. However, the mechanistic relationships among various genes and signaling pathways are still largely unclear. In this study, we aimed to elucidate potential core candidate genes and pathways in HCC. The expression profiles GSE14520, GSE25097, GSE29721, and GSE62232, which cover 606 tumor and 550 nontumour samples, were downloaded from the Gene Expression Omnibus (GEO) database. Furthermore, HCC RNA-seq datasets were also downloaded from the Cancer Genome Atlas (TCGA) database. The differentially expressed genes (DEGs) were filtered using R software, and we performed gene ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analysis using the online databases DAVID 6.8 and KOBAS 3.0. Furthermore, the protein-protein interaction (PPI) network complex of these DEGs was constructed by Cytoscape software, the molecular complex detection (MCODE) plug-in and the online database STRING. First, a total of 173 DEGs (41 upregulated and 132 downregulated) were identified that were aberrantly expressed in both the GEO and TCGA datasets. Second, GO analysis revealed that most of the DEGs were significantly enriched in extracellular exosomes, cytosol, extracellular region, and extracellular space. Signaling pathway analysis indicated that the DEGs had common pathways in metabolism-related pathways, cell cycle, and biological oxidations. Third, 146 nodes were identified from the DEG PPI network complex, and two important modules with a high degree were detected using the MCODE plug-in. In addition, 10 core genes were identified, TOP2A, NDC80, FOXM1, HMMR, KNTC1, PTTG1, FEN1, RFC4, SMC4, and PRC1. Finally, Kaplan-Meier analysis of overall survival and correlation analysis were applied to these genes. The abovementioned findings indicate that the identified core genes and pathways in this bioinformatics analysis could significantly enrich our understanding of the development and recurrence of HCC; furthermore, these candidate genes and pathways could be therapeutic targets for HCC treatment. K E Y W O R D S bioinformatical analysis, differentially expressed genes (DEGs), hepatocellular carcinoma (HCC), pathways J Cell Biochem. 2019;120:10069-10081.wileyonlinelibrary.com/journal/jcb

To investigate whether the platelets can improve liver function by mediating liver regeneration. Using a retrospective cohort with 234 consecutive adult-to-adult living donor liver transplantation recipients, we have discussed the relationship between immediate postoperative platelet count and outcome. Patients have been stratified into Low Platelet Group (106 patients) with platelet ≤68 × 109/L and High Platelet Group (128 patients) with platelet >68 × 109/L.Low Platelet Group has a higher rate of preoperative thrombocytopenia (90.6% vs. 32.8%, P < 0.001), higher model for end-stage liver disease score (15 vs. 11, P < 0.001), cirrhosis (86.8% vs. 76.6%, P = 0.046), hepatorenal syndrome (18.2% vs. 4.0%, P = 0.005) and fulminant hepatic failure (26.4% vs. 7.8%, P < 0.001). The packed red blood cells transfusion (7.5 vs. 5, P = 0.023) and plasma transfusion (1275 mL vs. 800 mL, P = 0.001) are more in patients with low platelet count. Low Platelet Group has a higher early allograft dysfunction (EAD) (22.6% vs. 7.0%, P = 0.001) and severe complications (22.6% vs. 10.9%, P = 0.016). The 90-day mortality between the 2 groups is similar. The multivariate analysis has found that postoperative platelet ≤68 × 109/L is an independent risk factor for EAD.Platelet maybe influences the functional status of the liver by promoting graft regeneration after liver transplantation.