Results: The eradication rate of moxifloxacin based triple therapy
was 61.7%(95% CI 56.1–67.0) by ITT, and 73.6%(95% CI 67.8–78.6) by PP. ITT Neratinib manufacturer and PT according to first regimen were 63.5/77.0%(95% CI 56.4–70.2/69.6–82.9) in standard triple group, 62/69.2%(95% CI 44.0–77.3/50.0–83.5) in bisthmus containing quadruple group, 56.4/66.7%(95% CI 40.9–70.7/49.6–80.2) in concomitant group and 58.6/69.2%(95% CI 44.3–71.7/53.5–81.4) in sequential group. There was no significant difference between groups (p = 0.504). Conclusion: Two-week moxifloxacin based triple therapy as second line did not show expected level for the primary outcome. The group treated with moxifloxacin after failure of standard triple therapy had highest rate of eradication, but there was no statistical significance in the efficacy among the first line regimens. Key Word(s): 1. Helicobacter pylori; 2. Erradication rate; 3. Moxifloxacin; 4. second line; Presenting Author: TIANTIAN SUN Additional Authors: HSP assay WAN DU, JIE HONG, JINGYUAN FANG Corresponding Author: JIE HONG, JINGYUAN FANG Affiliations: Shanghai Jiaotong University School of Medicine Renji Hospital Objective: TMEFF2 desregulation is related to tumorigenesis. However, little is known about its regulations and functions in the H.pylori-associated gastric cancer. Here we investigate its biological
roles and bidirectional regulation between TMEFF2 and STAT3 in H.pylori -induced gastric carcinogenesis. Methods: Gene expression profiling Selleck Fludarabine studies were done to identify pivotal genes regulated by H.pylori and TMEFF2 was discovered. TMEFF2 expression in human gastric mucosas and gastric cancer tissues was examined by immunohistochemistry. Biological functions of this gene on tumor growth
were detected in vivo and vitro. Role of STAT3 in modulating TMEFF2 expression was examined by chromatin immunoprecipitation assay and luciferase assay, while the effects of TMEFF2 on STAT3 was detected by GST pull-down and co-immunoprecipitation. Results: We found that H.pylori infection activated STAT3 signaling and reduced STAT3-dependent TMEFF2 expression in vivo and vitro. STAT3 regulated the expression of TMEFF2 by binding to its promoter and decreased its transcription. Conversely, TMEFF2 appeared to modulate the phosphorylation of STAT3 by its intracellular domain binding to the SH2 domain of SHP-1, which may negatively regulate the activation of STAT3. Conclusion: TMEFF2 plays important roles in H.pylori induced gastric cancer and displayed predictive value for the aggressiveness of gastric cancer. The negative feedback loop between STAT3 and TMEFF2 may contribute to H.pylori-associated human gastric tumorigenesis. Key Word(s): 1. TMEFF2; 2. gastric cancer; 3. H.