Patients with early gastric cancers that are limited to gastric mucosa or submucosa usually have an advanced loss of mucosal glandular tissue (glandular atrophy) and are at high risk for subsequent (metachronous) development of new gastric cancer. The long-term effects of treatment to eradicate Helicobacter pylori on histologic improvement and the prevention of metachronous gastric cancer remain unclear.

Statins, HMG‐CoA reductase inhibitors could be associated with the risk reduction of colorectal cancer. We previously demonstrated that simvastatin inhibits NF‐κB signaling in human intestinal epithelial cells and ameliorates acute murine colitis. The aim of our study was to evaluate the effects of simvastatin on the apoptotic pathways related to NF‐κB signaling in colon cancer cells, and on anticancer effects in 2 different animal models. We treated cell lines (COLO 205 and HCT 116) with simvastatin or vehicle and determined apoptosis by cell cycle analysis, Annexin V‐FITC staining, caspase‐3 activity assay and confocal microscopy. We assessed the expression of antiapoptotic factors by RT‐PCR and Western blotting. In the colitis‐associated colon cancer (CAC) model, we induced colonic tumors in C57/BL6 mice by azoxymethane and dextran sulfate sodium administration, and evaluated simvastatin's effect on tumor growth. In the xenograft model, we evaluated its effect on the inoculated tumor growth. In both cell lines, simvastatin caused dose‐ and time‐dependent cell death. Annexin V staining significantly increased after simvastatin treatment. It augmented caspase‐3 activity and downregulated the expression of Bcl‐2, Bcl‐xL, cIAP1 and cFLIP. In the CAC model, simvastatin significantly reduced tumor development. In the xenograft model, tumors from animals treated with simvastatin had smaller volumes, larger necrotic areas, lower expression of VEGF and higher apoptotic scores. In conclusion, simvastatin inhibited colon cancer development by induction of apoptosis and suppression of angiogenesis. These results suggest that simvastatin could be a potential chemopreventive and therapeutic agent of CAC as well as de novo colon cancer.

Introduction: The eradication rates for Helicobacter pylori have decreased in Korea although the prevalence of this bacterium has also decreased. Antibiotic resistance is likely to be a crucial factor in H. pylori eradication success, and we therefore mapped these resistance patterns nationwide in Korea.Materials and Methods: Five hundred and ninety adult subjects were prospectively enrolled from 2017 to 2018 from 15 centers across six geographic areas of Korea. A total of 580 biopsy tissues had been sampled from these patients during an upper endoscopy and were frozen at −80°C and delivered to a central laboratory. The agar dilution method was used to determine the minimum inhibitory concentration of amoxicillin, clarithromycin, metronidazole, tetracycline, ciprofloxacin, and levofloxacin for each H. pylori isolate.Results: The culture success rate was 60.2% (349/580). Resistance rates against clarithromycin, metronidazole, amoxicillin, tetracycline, levofloxacin, and ciprofloxacin were 17.8%, 29.5%, 9.5%, 0%, 37.0%, and 37.0%, respectively. The geographic distribution of metronidazole and quinolone resistance was highly variable. Some subjects had multiple H. pylori strains in the antrum and body of the stomach and showed a heterogeneous resistance profile between these anatomic areas. The H. pylori multidrug resistance (MDR) rate was 25.2% (88/349) among amoxicillin, clarithromycin, metronidazole, tetracycline, and quinolone and 11.2% (39/349) among four of these major antibiotics except for quinolone. The Seoul and Chungcheong areas showed a relatively lower MDR rate.Conclusion: The antibiotic resistance of H. pylori differs by drug and geographic area in Korea. Detailed nationwide antibiotic resistance mapping is needed to develop an effective H. pylori eradication strategy.

Background and study aim: Endoscopic resection for early gastric cancers that meet the expanded indication is considered to be an investigational treatment. The study aim was to evaluate long-term outcomes of endoscopic resection compared with surgery for early gastric cancers meeting the expanded indication. Methods: We retrospectively reviewed data from patients who underwent endoscopic resection or surgery for gastric cancers meeting the expanded indication between 2001 and 2009. Overall survival rate was the primary outcome; gastric cancer recurrence rates and complication rates were secondary outcomes. Results: Among 457 patients included, 165 underwent endoscopic resection and 292 surgery, with median follow-up duration of 58.6 months. The 5-year overall survival rates were 97.5 % and 97.0 % for endoscopic resection and surgery, respectively; Kaplan–Meier analysis showed no significant difference (P = 0.425). The 5-year gastric cancer recurrence rate was higher for endoscopic resection than for surgery (4.8 % vs. 0.3 %; P < 0.001) mainly because of metachronous cancers which developed only in the endoscopic resection group (9/165, 5.5 %). Most of the metachronous cancers (88.9 %) were curatively treated with endoscopic resection. Early complication rates were similar between the groups (P = 0.557), but the endoscopic resection group had more grade III or higher complications according to the Clavien–Dindo classification compared with the surgery group (4.8 % vs. 1.4 %, P = 0.026). Late complications occurred only following surgery (4.8 %, P = 0.004), and most (92.9 %) were grade III or higher. Conclusions: Endoscopic resection may be an optimal alternative to surgery for gastric cancers that meet the expanded indication criteria, because of a comparable long-term overall survival rate. ^* These two authors contributed equally to this work.