***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 ) BACKGROUND To reduce cancer mortality , effective screening should be implemented properly . In Japan , the Research Group for Cancer Screening developed screening guidelines ; however , the development process was not well established . METHODS Based on the development processes of other guidelines , an original method , unique to Japan , was established to develop the Japanese cancer screening guidelines . RESULTS The guideline development process involved the following steps : topic selection , development of the analytic framework , systematic literature review , translation to recommendations , consultation and publication . Mortality reduction related to cancer screening was evaluated using both direct and indirect evidence . To select appropriate articles , an analytic framework for cancer screening program with key questions was developed . Direct evidence was defined as a single body of evidence that established the linkage between screening and health outcomes such as mortality and incidence . The use of indirect evidence to determine the level of evidence was limited to situations where test accuracy could be compared with that of a method whose evidence was supported by r and omized , controlled trials . Eight levels of evidence were defined based on the study design and quality . The benefits of each screening modality were determined based on the level of evidence according to the results of the systematic review . Balancing the benefits and harms , five grade s of recommendation were formulated for population -based and opportunistic screening . After organized consultations , three types of guidelines were published . CONCLUSION We developed a unique , st and ardized method for developing cancer screening guidelines in Japan . Based on this process , previously developed cancer screening guidelines have been revised BACKGROUND A causal relationship between Helicobacter pylori infection and gastric cancer has been established . A nonr and omized study has shown eradication of H. pylori after endoscopic resection ( ER ) of early gastric cancer inhibits development of new carcinomas . SUBJECTS AND METHODS Eligible subjects are patients with H. pylori infection who are newly diagnosed with early gastric cancer and plan to have ER or who are in the post-resection follow-up phase after ER time of enrollment . Patients are r and omly allocated to the eradication or the control arms ( no eradication and st and ard of care ) . Patients will be evaluated by endoscopy at 0.5 , 1 , 2 , and 3 years after r and omization . Diagnosis of a new carcinoma at another site of the stomach is defined as primary endpoint , and recurrence of tumors at the resection site as a secondary endpoint . In addition to intention-to-treat and per- protocol analyses using proportional hazards models , time to recurrence will be compared between treatment and control using multiple logistic regression analyses . In the latter two situations , the models will be adjusted for the factors exerting significant influences on the results . RESULTS Five hundred and forty-two subjects have been enrolled into the study and are being followed-up . CONCLUSIONS This study will have the statistical power to demonstrate whether H. pylori eradication therapy exerts any clinical ly relevant inhibitory effects on occurrence or recurrence of gastric cancer . In addition , it will be able to test the hypothesis that H. pylori infection is a promoter in gastric carcinogenesis 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 OBJECTIVES : Helicobacter pylori causes gastric adenocarcinoma . We assessed the success of H. pylori eradication therapy in a medically underserved population in Chiapas , Mexico , that is at high risk for gastric cancer risk . METHODS : Healthy volunteers with both antibodies to CagA and gastrin levels ≥25 ng/ml were r and omly assigned to receive either a combination of omeprazole , amoxicillin , and clarithromycin or matched placebo for 1 wk . Endoscopy with seven biopsies was performed at baseline , at 6 wk , and 1 yr after treatment . Treatment success was defined as loss of H. pylori by histological analysis . Cure was assessed using change in serology based on the st and ardized absorbance of a H. pylori ELISA . RESULTS : H. pylori eradication rates were high ( intent-to-treat analysis : 76.3 % [ 95 % CI = 68.7–84.0 % ] after 6 wk and 76.1 % [ 95 % CI = 67.7–84.6 % ] after 1 yr ; per protocol analysis : 77.8 % [ 95 % CI = 70.1–85.4 % ] after 6 wk and 75.2 % [ 95 % CI = 66.5–84.0 % ] after 1 yr ) . Nine subjects on active treatment and one subject on placebo who were without H. pylori at 6 wk were infected at 1 yr ( recurrence rates 10.7 % and 33.3 % , respectively , p = 0.31 ) . Median changes in st and ardized absorbance at 1 yr were 47 % and 1 % for successfully and unsuccessfully treated patients , respectively . A 10 % decline in st and ardized absorbance after 1 yr had 84 % sensitivity and 100 % specificity for H. pylori eradication . CONCLUSIONS : Even with a short course of treatment against H. pylori , a high rate of eradication rate can be achieved in population s at high risk for stomach cancer . Serum antibodies are useful in assessing efficacy of therapy 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 & AIMS : Helicobacter pylori eradication improves the prognosis of  peptic ulcer disease ( PUD ) , dyspepsia , and possibly gastric cancer . H pylori screening tests are accurate and eradication therapy is effective . H pylori population screening seems attractive . The aim of this study was to evaluate the long‐term effect of H pylori population screening and eradication on dyspepsia prevalence and the incidence of PUD , and as secondary outcomes to assess the effect on health care consumption and quality of life . METHODS : At baseline in 1998 to 1999 , 20,011 individuals aged 40 to 65 years were r and omized to H pylori screening and eradication or a control group with no screening .  Both groups received a question naire on dyspepsia and quality of life . Register data were obtained for all r and omized individuals . RESULTS : The baseline question naire response rate was 63 % . Of the 5749 individuals screened , 1007 ( 17.5 % ) were H pylori positive . Complete symptom data were obtained for 8658 ( 69 % ) individuals after 13 years . Dyspepsia prevalence decreased in both groups during the follow‐up period , but multivariate analysis showed no effect of H pylori screening and eradication ( adjusted odds ratio , 0.93 ; 95 % confidence interval , 0.82–1.04 ) ; compared with usual care . Intention‐to‐treat and per‐ protocol analyses of register data provided similar results .  H pylori screening  neither reduced PUD incidence significantly ( adjusted odds ratio , 0.88 ; 95 % confidence interval , 0.70−1 
    Output:
    
There is insufficient evidence to support or refute the effectiveness of eradication therapy in preventing gastric carcinoma in H. pylori-infected , high-risk population s. Rigorously conducted large RCTs of healthy infected adults only would provide evidence of the true efficacy of successful eradication .