Sa1896 The Human Gastric Pathogen Helicobacter pylori Alters Intracellular Signaling by Inducing Truncated Forms of p53 Tumor Suppressor

patients (218 without current HP infection and 49 with successful eradication of HP infection) were HP negative status (HP-negative group), 107 patients (19 with failed eradication and 88 with no treatment of HP infection) were HP positive status (HP-positive group). The incidence of metachronous gastric cancer was compared in both groups, and the risk factors associated with the development of metachronous gastric cancer after ER was analyzed. Results: Median follow-up duration after ER was 4.1 years (range 1.0 10.5 years). During the follow-up period, metachronous gastric cancer developed in 16 patients (15.0% [16/ 107]) in the HP-positive group and in 15 patients (5.6% [15/267]) in the HP-negative group. The cumulative incidence of metachronous gastic cancer was significantly different between HP-negative and HP-positive groups (P= .003 by Log-rank test). In a multivariate Coxproportional hazard model, age . 65 years (hazard ratio [HR], 2.88; 95% confidential interval [CI], 1.28 6.49; P= .011), family history of gastric cancer (HR, 2.48; 95% CI, 1.11 5.53; P= .026), and HP-positive status (HR, 2.52; 95% CI, 1.24 5.14; P= .011) were associated with the development ofmetachronous gastric cancer. Conclusions: Persistent H. pylori infection after ER for EGC seems be associated with the development of metachronous gastric cancer during long-term follow-up period.