Background and Objectives: The method of pancreatic reconstruction after pancreaticoduodenectomy (PD) is closely associated with postoperative morbidity, mortality, and patient's quality of life. The objective of this study is to evaluate which anastomosis approach - pancreaticogastrostomy (PG) or pancreaticojejunostomy (PJ) is a better option of choice in terms of postoperative complications. Methods: Articles comparing PG and PJ that were published by July 2011 were retrieved and subjected to a systematic review and meta-analysis. Results: Four randomized controlled trials (RCTs) and 22 observational clinical studies (OCSs) were included. RCTs showed that the PG group had significantly lower incidence rates of postoperative intra-abdominal fluid collection (p = 0.003, relative risk (RR) 0.50, 95% CI 0.31-0.79) and multiple intra-abdominal complications (p = 0.0007, RR 0.26, 95% CI 0.12-0.56) than the PJ group. OCSs demonstrated significant differences between PG and PJ in terms of frequencies of postoperative biliary fistula, intra-abdominal fluid collection, pancreatic fistula, morbidity, and mortality. The overall analysis revealed significant differences in frequencies of intra-luminal hemorrhage (p = 0.03, OR 2.82, 95% CI 1.08-7.33) and grade B/C pancreatic fistula (p = 0.002, OR 0.42, 95% CI 0.24-0.73) between the two groups. Conclusions: Current literature has no adequate evidence to prove that PG is superior to PJ for patients undergoing PD in terms of postoperative complications. A standardized classification of pancreatic fistula and other intra-abdominal complications may enable an objective, valid comparison between PG and PJ.

ObjectiveThe aim of this study was to present the therapeutic outcome of patients with locally advanced pancreatic cancer treated with pancreatoduodenectomy combined with vascular resection and reconstruction in addition to highlighting the mortality/morbidity and main prognostic factors associated with this treatment.Materials and MethodsWe retrospectively analyzed the clinical and pathological data of a total of 566 pancreatic cancer patients who were treated with PD from five teaching hospitals during the period of December 2006–December 2011. This study included 119 (21.0%) patients treated with PD combined with vascular resection and reconstruction. We performed a detailed statistical analysis of various factors, including postoperative complications, operative mortality, survival rate, operative time, pathological type, and lymph node metastasis.ResultsThe median survival time of the 119 cases that received PD combined with vascular resection was 13.3 months, and the 1-, 2-, and 3-year survival rates were 30.3%, 14.1%, and 8.1%, respectively. The postoperative complication incidence was 23.5%, and the mortality rate was 6.7%. For the combined vascular resection group, complications occurred in 28 cases (23.5%). For the group without vascular resection, complications occurred in 37 cases (8.2%). There was significant difference between the two groups (p = 0.001). The degree of tumor differentiation and the occurrence of complications after surgery were independent prognostic factors that determined the patients’ long-term survival.ConclusionsCompared with PD without vascular resection, PD combined with vascular resection and reconstruction increased the incidence of postoperative complications. However, PD combined with vascular resection and reconstruction could achieve the complete removal of tumors without significantly increasing the mortality rate, and the median survival time was higher than that of patients who underwent palliative treatment. In addition, the two independent factors affecting the postoperative survival time were the degree of tumor differentiation and the presence or absence of postoperative complications.

Octamer-binding transcription factor 4 (OCT4) is one of the factors associated with self-renewal and differentiation in cancer stem cells, and is crucial for the progression of various types of human malignancy. However, the expression and function of OCT4 in human pancreatic cancer has not been fully elucidated. The purpose of the present study was to investigate the function and molecular mechanisms of OCT4 in pancreatic cancer cells. The clinical significance of OCT4 expression was assessed by an immunohistochemical assay using a tissue microarray procedure in pancreatic cancer tissues and cells with different degrees of differentiation. A loss-of-function approach was used to examine the effects of a lentivirus-mediated OCT4 small hairpin RNA vector on biological behaviors, including cell proliferative activity and invasive potential. The results demonstrated that the expression levels of OCT4 protein in cancer tissues were significantly elevated compared with those in adjacent non-cancerous tissues (65.0 vs. 42.5%; P=0.005), which was correlated with tumor differentiation (P=0.008). The knockdown of OCT4 inhibited the proliferation and invasion of pancreatic cancer cells (Panc-1) expressing high levels of OCT4, accompanied with decreased expression of AKT, proliferating cell nuclear antigen (PCNA) and matrix metalloproteinase-2 (MMP-2). In conclusion, the present study reveals that the increased expression of OCT4 is correlated with the differentiation of pancreatic cancer, while knockdown of OCT4 suppresses the growth and invasion of pancreatic cancer cells through inhibition of AKT pathway-mediated PCNA and MMP-2 expression, suggesting that OCT4 might serve as a potential therapeutic target for the treatment of pancreatic cancer.

MicroRNAs (miRNAs) act as a kind of small and noncoding RNA, which have been implicated in the regulation of various pathobiological processes in cancer, including progression in pancreatic cancer and in other human cancers. Previous reports demonstrate that pancreatic cancer has been reported as one of the leading causes of cancer-related death, and some factors including oncogenic genes and environments are involved in tumorigenesis. In our study, we found microRNA-146a (miR-146a) was evidently downregulated in pancreatic cancer tissues and cells. Overexpression of miR-146a obviously reduced cell proliferation and tumorigenesis in vitro, as determined by MTT analysis, colony formation analysis, EdU analysis, and cell cycle experiments. Here, we found tumor suppressor sex-determining region Y-box 7 (SOX7) was the direct target of miR-146a. Overexpression of miR-146a decidedly inhibited SOX7 expression, which promotes cell proliferation and tumorigenesis. Knockdown of miR-146a increased SOX7 expression. Depression of miR-146a and SOX7 promoted cell proliferation and tumorigenesis in vitro, confirming miR-146a regulated pancreatic cancer cell proliferation by inhibiting SOX7. In summary, we found miR-146a reduced the cell proliferation of pancreatic cancer through targeting SOX7. In the present study, we demonstrated the function of miR-146a in pancreatic cancer and might provide a new target in the treatment of pancreatic cancer.

Background: Pancreatic cancer (PC) presents a phenomenal disease burden worldwide. The GATA transcription factor family is associated with a variety of human malignancies. However, the relation between GATA family members (GATAs) and PC has not been elucidated. Methods: This study integrates large-scale bioinformatics database resources to analyze the expression patterns of GATAs in PC patients and explore their underlying function mechanism and relevance to immune infiltration and other different cell types in the tumor microenvironment in pancreatic cancer. First, the expression pattern of GATAs in pancreatic cancer was detected by the Oncomine database and the Gene Expression Profile Interaction Analysis (GEPIA2) database and verified through other datasets in the R2 platform. Then, we used the cBioPortal database and the Human Protein Atlas to assess the correlation between GATAs and clinicopathological features of PC. Then, survival analyses were performed to identify candidate prognostic factors in the GATA family in PC patients. Further, we performed gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, protein-protein interaction (PPI) network, immune-infiltration correlation analysis, and cell type analysis of the tumor microenvironment at the single-cell level to explain the function of GATAs in pancreatic cancer. Results: We found that GATA3 and GATA6 were highly expressed in pancreatic cancer, and the expression levels of GATA4 and GATA6 correlated with the pathological stage, differentiation grade, and molecular subtype of pancreatic cancer. The survival analysis revealed that lower GATA4 of PC patients was associated with better outcomes, and higher GATA6 might be associated with longer OS. In addition, GATA3 was associated with immune cell infiltration of PC, and GATA6 was mainly distributed in the epithelial cells with ductal phenotype. Conclusion: This work tentatively identified GATA3, GATA4, and GATA6 in the GATA family associated with pancreatic cancer. GATA4 may serve as a prognostic factor for PC patients, and GATA6 may act as a subtype marker for PC. In addition, GATA3 may reflect the immune-infiltration status of PC.