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BackgroundPancreatic cancer (PC) has the worst survival of all periampullary cancers. This may relate to histopathological differences between pancreatic cancers and other periampullary cancers. Our aim was to examine the distribution and histopathologic features of pancreatic, ampullary, biliary and duodenal cancers resected with a pancreaticoduodenectomy (PD) and to examine local trends of periampullary cancers resected with a PD.MethodsA retrospective review of PD between January 2000 and December 2012 at a public metropolitan database was performed. The institutional ethics committee approved this study.ResultsThere were 142 PDs during the study period, of which 70 cases were pre-2010 and 72 post-2010, corresponding to a recent increase in the number of cases. Of the 142 cases, 116 were for periampullary cancers. There were also proportionately more PD for PC (26/60, 43% pre-2010 vs 39/56, 70% post-2010, P = 0.005). There were 65/116 (56%) pancreatic, 29/116 (25%), ampullary, 17/116 (15%) biliary and 5/116 (4%) duodenal cancers. Nodal involvement occurred more frequently in PC (78%) compared to ampullary (59%), biliary (47%) and duodenal cancers (20%), P = 0.002. Perineural invasion was also more frequent in PC (74%) compared to ampullary (34%), biliary (59%) and duodenal cancers (20%), P = 0.002. Microvascular invasion was seen in 57% pancreatic, 38% ampullary, 41% biliary and 20% duodenal cancers, P = 0.222. Overall, clear margins (R0) were achieved in fewer PC 41/65 (63%) compared to ampullary 27/29 (93%; P = 0.003) and biliary cancers 16/17 (94%; P = 0.014).ConclusionsThis study highlights that almost half of PD was performed for cancers other than PC, mainly ampullary and biliary cancers. The volume of PD has increased in recent years with an increased proportion being for PC. PC had higher rates of nodal and perineural invasion compared to ampullary, biliary and duodenal cancers.

Background Hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancer type. This study was aimed to investigate the role of microRNA‐584‐5p (miR‐584‐5p) in regulating HCC progression. Methods The expression of miR‐584‐5p in HCC cell lines was analyzed by quantitative real‐time polymerase chain reaction. Effects of miR‐584‐5p depletion on HCC cell proliferation, migration, and invasion in vitro were analyzed by cell counting kit‐8 assay, wound‐healing assay, and transwell invasion assay. miR‐584‐5p targeting potassium voltage‐gated channel subfamily E regulatory subunit 2 (KCNE2) was identified using bioinformatics algorithm and dual‐luciferase activity reporter assay. Kaplan–Meier Plotter website was used to investigate the effect of miR‐584‐5p or KCNE2 expression on the overall survival of HCC patients. Results In vitro functional assays showed miR‐584‐5p depletion decreased HCC cell proliferation, cell migration, and cell invasion. Moreover, miR‐584‐5p functions by directly targeting KCNE2, and it in turn, mediates the effects of miR‐584‐5p on HCC cell behaviors. Conclusions These results demonstrated that miR‐584‐5p functions as an oncogenic miRNA in HCC.

Introduction In East Asia, hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancer types. Long noncoding RNA (lncRNA) prostate androgen-regulated transcript 1 ( PART1 ) was reported to play crucial roles in regulating cancer progression. However, roles and mechanisms of action of PART1 in hepatocellular carcinoma (HCC) still remain unknown. Methods Quantitative real-time polymerase chain reaction (RT-qPCR) method was used to detect the PART1 expression level in HCC cells. Cell proliferation, colony formation, and transwell invasion assays were performed to investigate the biological roles of PART1 on HCC cell behaviors. Bioinformatic analysis methods were performed to analyze connections of microRNA-590-3p (miR-590-3p) with PART1 or high mobility group box 2 ( HMGB2 ) in HCC. Moreover, expression levels of PART1 , miR-590-3p, and HMGB2 in HCC tissues and normal tissues were analyzed at ENCORI. Results PART1 expression was found to be significantly upregulated in HCC tissues and cells. Functionally, silencing of PART1 significantly suppressed HCC cell proliferation, colony formation and invasion in vitro, while forcing PART1 exerts opposite biological effects. Mechanically, miR-590-3p/ HMGB2 axis was downstream target of PART1 , and silencing of miR-590-3p or forcing of HMGB2 could rescue the stimulation effects of PART1 overexpression on HCC cell behaviors. Discussion Our results provided evidence that PART1 serves as oncogenic lncRNA through sponging miR-590-3p to upregulate HMGB2 expression in HCC.