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Pancreatic cancer remains as one of the most lethal malignancies. Resistance to conventional therapies has led to little improvement in the survival of pancreatic cancer patients over the past few decades. Immune-based treatment strategies for pancreatic cancer, such as immune-checkpoint inhibitors, therapeutic vaccines, and combination immunotherapies show promise. Many immunotherapies have been explored in clinical trials, but they have yet to show significant therapeutic effects. Nevertheless, immunotherapy is inevitably the future of pancreatic cancer cure. This article introduces the current research progress and bottlenecks of immunotherapy for pancreatic cancer and puts forward further optimization directions and solutions. We hope to provide a reference for the future use of immunotherapy for pancreatic cancer.

Objective To explore the value of preoperative LAR combined with AFP in evaluating the prognosis of patients with HCC. Methods We retrospectively analyzed the clinical data of 106 patients with HCC. Kaplan-Meier method was used to draw the survival curve. Univariate analysis was used to analyze possible variables affecting LAR. Cox risk regression model was used to evaluate the clinical value of preoperative LAR and AFP on the prognosis of HCC patients. Results The DFS and OS of the high LAR group and the high AFP group were shorter than those of the low LAR group and the low AFP group (P < 0.05). LAR≥4.58, AFP≥400μg/L and T3-T4 were independent risk factors affecting DFS and OS of HCC patients (P < 0.05). Postoperative interventional surgery was an independent factor influencing OS prolongation (P < 0.05). The DFS and OS were the shortest in the high LAR and high AFP group, and the DFS and OS were the longest in the low LAR and low AFP group (P < 0.05). Conclusion Preoperative LAR and AFP are independent poor prognostic factors of HCC. Preoperative LAR combined with AFP has a certain value in judging the prognosis of HCC patients.

Acute pancreatitis remains a serious public health problem, and the burden of acute pancreatitis is increasing. With significant morbidity and serious complications, appropriate and effective therapies are critical. Great progress has been made in understanding the pathophysiology of acute pancreatitis over the past two decades. However, specific drugs targeting key molecules and pathways involved in acute pancreatitis still require further study. Natural compounds extracted from plants have a variety of biological activities and can inhibit inflammation and oxidative stress in acute pancreatitis by blocking several signaling pathways, such as the nuclear factor kappa-B and mitogen-activated protein kinase pathways. In this article, we review the therapeutic effects of various types of phytochemicals on acute pancreatitis and discuss the mechanism of action of these natural compounds in acute pancreatitis, aiming to provide clearer insights into the treatment of acute pancreatitis. [ABSTRACT FROM AUTHOR]

Objective To investigate the expression of LncRNA LINC00857 in pancreatic cells and the effect of lncRNA LINC00857 down-regulation on proliferation, migration and apoptosis of pancreatic cancer PANC-1 cells and possible mechanism. Methods The lentiviral vector GV112 was constructed and infected PANC-1 cells to obtain experimental group, while the blank plasmid was transfected as a negative control group and the cells without intervention were taken as normal control group. CCK-8 assay, Transwell assay, scratch test, flow cytometry, Western blot were used to detect the effect of LINC00857 down-regulation on cell proliferation, migration, apoptosis, cell cycle and EMT-related proteins. Results LINC00857 expression in pancreatic cancer cells were significantly higher than that in normal pancreatic epithelial cells (P < 0.001). Knockdown of LINC00857 could significantly inhibit the proliferation and migration of PANC-1 cells (P < 0.0001); compared with the negative control group, the apoptosis rates of cells in the experimental groups were significantly increased (P < 0.05), the number of cells in G0/G1 phase increased (P < 0.01), the number of cells in S phase decreased (P < 0.05), and the cells were blocked in the G1 phase, E-cadherin expression was significantly up-regulated (P < 0.05) and N-cadherin and Vimentin expression were significantly down-regulated (N-cadherin: P < 0.01, Vimentin: P < 0.05). Conclusion LINC00857 can promote proliferation and migration of PANC-1 cells and inhibit its apoptosis by regulating G1/S phase transition and EMT signaling pathway.

Objective To investigate the expression of MYEOV in human pancreatic cancer cells and its effect on the proliferation and migration of pancreatic cancer SW1990 cells after knockdown. Methods The lentiviral vector GV248 was constructed and infected SW1990 cells to obtain two experimental groups (SW1990-sh1 and SW1990-sh2), while the blank plasmid was transfected as a negative control group and the untreated cells were taken as blank control group. MYEOV mRNA and protein expression were detected by qPCR and Western blot before and after transfection. The cells proliferation was determined by CCK-8 assay; the cell migration ability was analyzed by scratch test; The mRNA expression of SMADs in the TGF-β/SMAD signaling pathway was detected by qPCR. Results Compared with the pancreatic ductal epithelium cell line HPDE6, the mRNA expression of MYEOV in six pancreatic cancer cells were significantly increased (P < 0.01). However, low expression of MYEOV protein was detected only in PANC-1 and SW1990 cells. The mRNA and protein expression of MYEOV in the experimental groups were significantly downregulated. The proliferation and migration of SW1990 cells were lower than the control group (P < 0.001). MYEOV knockdown could reduce the mRNA expression of SMAD1, SMAD4, SMAD5 and SMAD9 in TGF-β pathway, while the expression of SMAD2, SMAD3 and SMAD7 mRNA were only down-regulated in the SW1990-sh2 group (P < 0.001). Conclusion MYEOV mRNA is overexpressed in pancreatic cancer cells. MYEOV could promote the proliferation and migration of pancreatic cancer cells via TGF-β/SMAD pathway.