***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: In the Sh and ong Intervention Trial , 2 weeks of antibiotic treatment for Helicobacter pylori reduced the prevalence of precancerous gastric lesions , whereas 7.3 years of oral supplementation with garlic extract and oil ( garlic treatment ) or vitamin C , vitamin E , and selenium ( vitamin treatment ) did not . Here we report 14.7-year follow-up for gastric cancer incidence and cause-specific mortality among 3365 r and omly assigned subjects in this masked factorial placebo-controlled trial . Conditional logistic regression was used to estimate the odds of gastric cancer incidence , and the Cox proportional hazards model was used to estimate the relative hazard of cause-specific mortality . All statistical tests were two-sided . Gastric cancer was diagnosed in 3.0 % of subjects who received H pylori treatment and in 4.6 % of those who received placebo ( odds ratio = 0.61 , 95 % confidence interval = 0.38 to 0.96 , P = .032 ) . Gastric cancer deaths occurred among 1.5 % of subjects assigned H pylori treatment and among 2.1 % of those assigned placebo ( hazard ratio [ HR ] of death = 0.67 , 95 % CI = 0.36 to 1.28 ) . Garlic and vitamin treatments were associated with non-statistically significant reductions in gastric cancer incidence and mortality .  Vitamin treatment was associated with statistically significantly fewer deaths from gastric or esophageal cancer , a secondary endpoint ( HR = 0.51 , 95 % CI = 0.30 to 0.87 ; P = .014 ) AIM To investigate the effects of Helicobacter pylori ( H pylori ) eradication therapy for treatment of peptic ulcer on the incidence of gastric cancer . METHODS A multicenter prospect i ve cohort study was conducted between November 2000 and December 2007 in Yamagata Prefecture , Japan . The study included patients with H pylori-positive peptic ulcer who decided themselves whether to receive H pylori eradication ( eradication group ) or conventional antacid therapy ( non-eradication group ) . Incidence of gastric cancer in the two groups was determined based on the results of annual endoscopy and question naire surveys , as well as Yamagata Prefectural Cancer Registry data , and was compared between the two groups and by results of H pylori therapy . RESULTS A total of 4133 patients aged between 13 and 91 years ( mean 52.9 years ) were registered , and 56 cases of gastric cancer were identified over a mean follow-up of 5.6 years . The sex- and age-adjusted incidence ratio of gastric cancer in the eradication group , as compared with the non-eradication group , was 0.58 ( 95 % CI : 0.28 - 1.19 ) and ratios by follow-up period ( < 1 year , 1 - 3 years , > 3 years ) were 1.16 ( 0.27 - 5.00 ) , 0.50 ( 0.17 - 1.49 ) , and 0.34 ( 0.09 - 1.28 ) , respectively . Longer follow-up tended to be associated with better prevention of gastric cancer , although not to a significant extent . No significant difference in incidence of gastric cancer was observed between patients with successful eradication therapy ( 32/2451 patients , 1.31 % ) and those with treatment failure ( 11/639 patients , 1.72 % ) . Among patients with duodenal ulcer , which is known to be more prevalent in younger individuals , the incidence of gastric cancer was significantly less in those with successful eradication therapy ( 2/845 patients , 0.24 % ) than in those with treatment failure ( 3/216 patients , 1.39 % ) . CONCLUSION H pylori eradication therapy for peptic ulcer patients with a mean age of 52.9 years at registration did not significantly decrease the incidence of gastric cancer OBJECTIVE --To investigate the association between gastric cancer and prior infection with Helicobacter pylori . DESIGN --Case-control comparison of prevalence of IgG antibodies to H pylori in blood sample s collected prospect ively , before diagnosis of gastric cancer in the cases . Presence of H pylori antibody ( greater than 10 micrograms IgG/ml ) determined by enzyme linked immunosorbent assay ( ELISA ) . SUBJECTS--29 men with a subsequent diagnosis of gastric cancer and 116 aged matched controls selected from over 22,000 middle aged men participating in two ongoing cohort studies ( the British United Provident Association study and the Caerphilly collaborative heart disease study ) , who had provided blood sample s during 1975 - 1982 . RESULTS --20 of the 29 cases ( 69 % ) and 54 of the 116 controls ( 47 % ) were positive for H pylori specific antibody . The median specific IgG concentration was significantly higher in the cases than controls ( 90 micrograms/ml v 3.6 micrograms/ml , p less than 0.01 ) . The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 ( 95 % confidence interval 1.04 to 7.97 , 2p = 0.039 ) . CONCLUSIONS --H pylori infection may be an important cause of gastric cancer ; between 35 % and 55 % of all cases may be associated with such an infection Objective Helicobacter pylori infection and overexpression of cyclo-oxygenase-2 ( COX-2 ) are associated with gastric cancer and its precursors . To evaluate the effect of a selective COX-2 inhibitor alone and combined with H pylori eradication on the evolution of precancerous gastric lesions , a r and omised , placebo-controlled trial was conducted in Linqu County , Sh and ong Province , China . Methods A total of 1024 participants aged 35–64 years with H pylori infection and advanced gastric lesions were r and omly assigned in a factorial design to two interventions or placebo : anti-H pylori treatment for 7 days , and a COX-2 inhibitor ( celecoxib ) for 24 months . The effects of the interventions were evaluated by the regression or progression of advanced gastric lesions . Results Of the 1024 participants who received anti-H pylori treatment or placebo  , 919 completed a subsequent 24-month treatment with celecoxib or placebo .  The H pylori eradication rate by per- protocol analysis was 78.2 % . Compared with placebo , the proportions of regression of gastric lesions significantly increased in the celecoxib treatment ( 52.8 % vs 41.2 % ) and anti-H pylori treatment ( 59.3 % vs 41.2 % ) group , and OR by per- protocol analysis was 1.72 ( 95 % CI 1.07 to 2.76 ) for celecoxib and 2.19 ( 95 % CI 1.32 to 3.64 ) for H pylori eradication . No statistically significant effect was found for H pylori eradication followed by celecoxib on the regression of advanced gastric lesions ( OR 1.48 , 95 % CI 0.91 to 2.40 ) . Conclusion This population -based intervention trial revealed that celecoxib treatment or H pylori eradication alone had beneficial effects on the regression of advanced gastric lesions . No favourable effects were seen for H pylori eradication followed by celecoxib treatment . Trial registration HARECCTR0500053 in accordance with WHO ICTRP requirements CONTEXT Although chronic Helicobacter pylori infection is associated with gastric cancer , the effect of H pylori treatment on prevention of gastric cancer development in chronic carriers is unknown . OBJECTIVE To determine whether treatment of H pylori infection reduces the incidence of gastric cancer . DESIGN , SETTING , AND PARTICIPANTS Prospect i ve , r and omized , placebo-controlled , population -based primary prevention study of 1630 healthy carriers of H pylori infection from Fujian Province , China , recruited in July 1994 and followed up until January 2002 . A total of 988 participants did not have precancerous lesions ( gastric atrophy , intestinal metaplasia , or gastric dysplasia ) on study entry . INTERVENTION Patients were r and omly assigned to receive H pylori eradication treatment : a 2-week course of omeprazole , 20 mg , a combination product of amoxicillin and clavulanate potassium , 750 mg , and metronidazole , 400 mg , all twice daily ( n = 817 ) ; or placebo ( n = 813 ) . MAIN OUTCOME MEASURES The primary outcome measure was incidence of gastric cancer during follow-up , compared between H pylori eradication and placebo groups . The secondary outcome measure was incidence of gastric cancer in patients with or without precancerous lesions , compared between the 2 groups . RESULTS Among the 18 new cases of gastric cancers that developed , no overall reduction was observed in participants who received H pylori eradication treatment ( n = 7 ) compared with those who did not ( n = 11 ) ( P = .33 ) . In a subgroup of patients with no precancerous lesions on presentation , no patient developed gastric cancer during a follow-up of 7.5 years after H pylori eradication treatment compared with those who received placebo ( 0 vs 6 ; P = .02 ) . Smoking ( hazard ratio [ HR ] , 6.2 ; 95 % confidence interval [ CI ] , 2.3 - 16.5 ; P<.001 ) and older age ( HR , 1.10 ; 95 % CI , 1.05 - 1.15 ; P<.001 ) were independent risk factors for the development of gastric cancer in this cohort . CONCLUSIONS We found that the incidence of gastric cancer development at the population level was similar between participants receiving H pylori eradication treatment and those receiving placebo during a period of 7.5 years in a high-risk region of China . In the subgroup of H pylori carriers without precancerous lesions , eradication of H pylori significantly decreased the development of gastric cancer . Further studies to investigate the role of H pylori eradication in participants with precancerous lesions are warranted Background We previously reported that eradication of Helicobacter pylori could reduce the risk of developing gastric cancer in patients with peptic ulcer diseases . In the present study , we further followed up our patient groups to identify factors associated with the development of gastric cancer . Methods Prospect i ve posteradication evaluations were conducted in 1342 consecutive patients ( 1191 men and 151 women ; mean age , 50 years ) with peptic ulcer disease who had received H. pylori eradication therapy . The patients had undergone endoscopic examination before eradication therapy  to evaluate peptic ulcers , background gastric mucosa , and H. pylori infection . After confirmation of eradication , follow-up endoscopy was performed yearly . Results A total of 1131 patients were followed for up to 9.5 years ( mean , 3.9 years ) . Gastric cancer developed in 9 of 953 patients cured of infection and in 4 of 178 who had persistent infection ( P = 0.04 ) . The risk of developing gastric cancer after receiving H. pylori eradication therapy was increased according to the grade of baseline gastric mucosal atrophy ( P = 0.01 ) . In patients with peptic ulcer diseases , persistent infection of H. pylori ( hazard ratio , 3.9 ; P = 0.03 ) , the grade of baseline gastric mucosal atrophy ( 3.3 , P = 0.01 ) and age ( 2.0 , P = 0.04 ) were identified as significant risk factors for developing gastric cancer . Conclusions The grade of gastric atrophy was closely related to the development of gastric cancer after receiving H. pylori eradication therapy . Thus , eradication of H. pylori before the significant expansion of atrophy is most beneficial to prevent gastric cancer Among 2258 Helicobacter pylori-seropositive subjects r and omly assigned to receive one-time  H. pylori treatment with amoxicillin-omeprazole or its placebo , we evaluated the 15-year effect of treatment on gastric cancer incidence  and mortality  in subgroups defined by age , baseline gastric histopathology , and post-treatment infection status . We used conditional logistic and Cox regressions for covariable adjustments in incidence and mortality analyses , respectively . Treatment was associated with a statistically significant decrease in gastric cancer incidence ( odds ratio = 0.36 ; 95 % confidence interval [ CI ] = 0.17 to 0.79 ) and mortality ( hazard ratio = 0.26 ; 95 % CI = 0.09 to 0.79 ) at ages 55 years and older and a statistically significant decrease in incidence among those with intestinal metaplasia or dysplasia at baseline ( odds ratio = 0.56 ; 95 % CI = 0.34 to 0.91 ) . Treatment benefits for incidence and mortality among 
    Output:
    
H. pylori eradication is associated with a significantly lower risk of GC ; this finding has significant implication s for the prevention of this cancer .
The benefit is maximized when H. pylori eradication is applied at early stages of the infection