The long term complications including stent migration and restenosis were also analyzed. And survival of the patients was also analyzed. Results: In 150 patents, 55 cases undergoing I125 seeds stent and 95 cases

undergoing ordinary covered stent. After the operation, clinical symptoms such as dysphagia showed an obvious improvement in all patients. And no significant difference in the occurrence of complications such buy BGJ398 as infection, hemorrhage, severe chest pain, esophageal perforation, and radiation pneumonia between the two groups were observed (P>0.05). All patients were followed up for one year. The difference in the occurrence of stent migration between the two groups was not statistically significant (P&gt0.05). While the rate of esophageal restenosis in patients implanted with I125 seeds stent was significant lower than that in patients with traditional stent. And the rate of esophageal restenosis in patients I-BET-762 solubility dmso implanted with I125 seeds stent was significant lower than that in patients with traditional stent (P<0.05). And the appearance of restenosis in I125 seeds stent group was much later than that in conventional stent group (P<0.05). Furthermore, the survival of the patients with I125 seeds stent implantation

was 7.63±4.28 months compared to 4.09±3.85 months for patents with traditional stent (P<0.05). Conclusion: The implantation of I125 seeds stent is a feasible and safe treatment for the patients with advanced esophageal cancer. Key Word(s): 1. I125 seed; 2. stent; 3. esophageal carcinoma; 4. comparison; Presenting Author: MINGLI SU Additional Authors: MINHU CHEN, JIE CHEN Corresponding Author: JIE CHEN Affiliations: Department of Gastroenterology,The first affiliated

hospital of Sun Yat-sen University Objective: Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor which plays a role in the development, invasion and metastasis of gastric cancer. We have reported previously that 3,3′-Diindolylmethane (DIM), an AhR modulator, could inhibit gastric cancer cell proliferation by inducing apoptosis and click here cell cycle arrest in G1 phase. This study was to further explore the inhibitory effect of DIM on gastric cancer in an animal model. Methods: Female athymic nude mice, 4 weeks old, were treated with DIM by gavage at different dose (0, 5, 10, 20 mg/kg/day, 8 mice/group) 2 weeks before gastric cancer cells SGC7901 were injected subcutaneously into left wings. Animals were treated for six more weeks until sacrificed. Tumor sizes were measured biweekly. At the end of the experiment, mice were sacrificed, and tumors were excised, weighed, and tested using western blot and immunohistochemical studies. In addition blood samples were collected for biochemical analysis.