Objective To investigate the therapeutic effects of endoscopy for palliative treatment of advanced pancreatic cancer. Methods A typical case of un-resectable advanced pancreatic cancer was reviewed, who underwent obstruction of upper gastrointestinal tract, obstructive jaundice and alimentary tract hemorrhage subsequently. The patient received multiple placement of intestinal tract stents, common bile duct stents and hemostatic treatment endoscopically. Because of the obstruction of upper gastrointestinal tract, jejunalostomy and retrograde endoscopy through the orificium fistulae were performed to place bile duct stents. Results The patient survived for 10 months with good life quality after diagnosis, obstruction of upper gastrointestinal tract, obstructive jaundice and alimentary tract hemorrhage were cured and didn't recur till death.Conclusion Therapeutic endoscopy, safe and effective, is the first choice for advanced pancreatic cancer complicated with obstruction of digestive tract (including gastrointestinal tract, bile duct and pancreatic duct).

Purpose: MicroRNAs play key regulatory roles in the tumorigenesis of hepatitis B virus-related hepatocellular carcinoma (HBVHCC). This study aimed to explore the regulatory effects of microRNA-98-5p (miR-98-5p) on the proliferation, migration, invasion, and apoptosis of HBV-HCC cells, as well as the underlying mechanisms involving nuclear factor-κB-inducing kinase (NIK). Materials and Methods: The expressions of miR-98-5p and NIK in HBV-HCC tissues and cells, and the level of HBV DNA in HBVHCC cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, migration, invasion, and apoptosis of HBV-HCC cells were analyzed by cell counting kit-8, wound healing, transwell, and flow cytometry assay, respectively. The targeting relationship between miR-98-5p and NIK was predicted by StarBase3.0 and verified by dual-luciferase reporter assay. HBV-HCC xenograft tumor model was constructed in mice to observe the tumor growth in vivo. Results: The expression of miR-98-5p was declined in HBV-HCC tissues and cells. Overexpression of miR-98-5p markedly reduced the level of HBV DNA; inhibited the proliferation, migration, and invasion; and promoted the apoptosis of HBV-HCC cells. NIK was a target of miR-98-5p. Overexpression of miR-98-5p markedly decreased the protein expression of NIK in MHCC97H-HBV cells. NIK reversed the tumor-suppressing effect of miR-98-5p on HBV-HCC cells. Furthermore, overexpression of miR-98-5p significantly inhibited the xenograft tumor growth and decreased the expression of NIK in mice. Conclusion MiR-98-5p inhibits the secretion of HBV, proliferation, migration, and invasion of HBV-HCC cells by targeting NIK.