Prognostic Value of Postoperative Complication for Gastric Cancer.

Background: The incidence of complications in gastric cancer (GC) patients after surgery was increasing, and it was not clear whether postoperative complications would have an impact on prognosis. The current study attempted to investigate the role of postoperative complication for prognosis on GC patients undergoing radical resection. Materials and Methods: Eligible studies were searched in three databases, including PubMed, Embase, and the Cochrane Library, in accordance with the searching strategy on September 4th, 2022. The survival values were most concerned; then, hazard ratios (HRs) and 95% confidence intervals (CIs) were pooled up. All prognostic values, including overall survival (OS), disease-free survival (DFS), disease-specific survival (DSS), and recurrence-free survival (RFS), were allowed. Subgroup analysis based on complication types was used for further in-depth research. Results: A total of 29 studies involving 33,858 patients were included in this study. Intra-abdominal abscess (19.4%) was the most common complications in the included studies, followed by anastomotic leakage (17.0%) and pneumonia (16.4%). There were 23, 4, 6, and 10 studies that reported OS, DFS, DSS, and RFS, respectively. After analysis, postoperative complication was found to be an independent prognostic factor for OS (HR = 1.52, I2 = 1.14%, 95% CI = 1.42-1.61, P = .00), DFS (HR = 1.71, I2 = 0.00%,95% CI = 1.44-1.98, P < .05), DSS (HR = 1.60, I2 = 54.58%, 95% CI = 1.26-1.93, P < .1), and RFS (HR = 1.26, I2 = 0.00%, 95% CI = 1.11-1.41, P < .05). Subgroup analysis found that noninfectious complication was not significantly associated with OS (HR = 1.39, I2 = 0.00%, 95% CI = 0.96-1.82, P > .05). Conclusion: Surgeons needed to pay more attention to GC patients who developed postoperative complications, especially infectious complications, and take proactive management to improve the prognosis.

Activation of UBEC2 by transcription factor MYBL2 affects DNA damage and promotes gastric cancer progression and cisplatin resistance.

Ubiquitin-conjugating enzyme E2 C (UBE2C) plays a carcinogenic role in gastric cancer (GC); yet, its role in cisplatin (DDP) resistance in GC is enigmatic. This study sought to probe into the impact of UBE2C on DDP resistance in GC and its concrete molecular mechanism in GC progression. Bioinformatics analysis was used to analyze differentially expressed mRNAs and predict upstream regulatory molecules in GC. Real-time quantitative reverse transcriptase polymerase chain reaction and western blot were used to detect the expression of UBE2C and MYB proto-oncogene like 2 (MYBL2). Dual luciferase and chromatin immunoprecipitation (ChIP) assays were used to verify the binding relationship. Cell counting kit-8 was used to detect cell viability and calculate IC50 values. Flow cytometry was used to detect the cell cycle. Comet assay was used to detect DNA damage. Western blot was used to detect the expression of DNA loss-related proteins (γ-H2AX, ATM/p-ATM). The knockdown of highly expressed UBE2C in GC cell lines could reduce cell viability, induce G2/M arrest, induce apoptosis, and promote DNA damage and DDP sensitivity. Bioinformatics analysis predicted that the substantially upregulated MYBL2 was an upstream transcription factor in UBE2C. The binding relationship between the UBE2C promoter region and MYBL2 was verified by dual luciferase and ChIP. Overexpression of UBE2C in the rescue experiment was found to reverse the inhibited GC progression and promoted DDP sensitivity brought by the knockdown of MYBL2. In conclusion, the MYBL2/UBE2C regulatory axis may be a potential way to overcome DDP resistance in GC.

Sigmoid colon perforation caused by migrated plastic biliary stents: a case report.

INTRODUCTION: Endoscopic migration of plastic biliary stents is performed by endoscopic retrograde cholangiopancreatography (ERCP) for biliary and pancreatic diseases. This plays an increasingly important role. Intestinal perforation caused by stent migration is one of the complications. Although sigmoid colon perforation caused by stent migration is rare, it can be life-threatening. This case shows us that we should increase awareness of sudden abdominal pain after ERCP. METHOD: We provide a review of the clinical manifestations, imaging data of this case, and the literature related to the perforation caused by stent migration. RESULTS: A male patient had a history of choledocholithiasis, cholecystolithiasis, and biliary pancreatitis treated with ERCP and a pancreatic stent. After the operation, the patient developed cholangitis and was treated with ERCP and a plastic biliary stent. This patient was admitted to the emergency department with sudden lower abdominal pain. A CT scan showed sigmoid colon perforation by a foreign body and infra-diaphragmatic free air. An emergency surgery confirmed that the stent had caused the perforation. The patient was then treated with sigmoid colectomy and sigmoidostomy. DISCUSSION: Biliary stent migration after ERCP is rare, but intestinal perforation caused by migration should be considered in cases of abdominal pain of unknown cause.

RNAi-mediated inhibition of PDGF-D leads to decreased cell growth, invasion and angiogenesis in the SGC-7901 gastric cancer xenograft model.

Platelet-derived growth factor-D (PDGF-D) plays an important role in many types of human cancer. However, little is known about the function of this gene in gastric cancer. Here we demonstrated that PDGF-D is commonly overexpressed in gastric cancer. Silencing of PDGF-D using RNA interference significantly attenuated the proliferation and invasion potentials of SGC-7901 gastric cancer cells in which PDGF-D is overexpressed. Moreover, suppression of PDGF-D expression resulted in less activation of beta-catenin and its downstream effector genes, cyclin D1 and matrix metalloproteinases, which are known to be involved in cell proliferation and invasion, respectively. Further, downregulation of PDGF-D remarkably reduced VEGF expression and secretion and proangiogenic activities of SGC-7901 cells in vitro. Most importantly, PDGF-D downregulation caused a significant decrease in tumor growth and angiogenesis in a SGC-7901 xenograft model. Together these findings suggest that PDGF-D is involved in the promotion of gastric cancer growth, invasion and angiogenesis, and RNAi-mediated silencing of this gene may thus offer a promising therapeutic strategy for PDGF-D-overexpressing gastric cancer.