***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: Background : Nutrients in the one-carbon metabolism pathway may be involved in carcinogenesis . Few cohort studies have investigated the intakes of folate and related nutrients in relation to gastric and esophageal cancer . Methods : We prospect ively examined the association between self-reported intakes of folate , methionine , vitamin B6 , and vitamin B12 and gastric and esophageal cancer in 492 293 men and women . Results : We observed an elevated risk of esophageal squamous cell carcinoma with low intake of folate ( relative risk ( 95 % confidence interval ) : Q1 vs Q3 , 1.91 ( 1.17 , 3.10 ) ) , but no association with high intake .  Folate intake was not associated with esophageal adenocarcinoma , gastric cardia adenocarcinoma , or non-cardia gastric adenocarcinoma . The intakes of methionine , vitamin B6 , and vitamin B12  were not associated with esophageal and gastric cancer . Conclusion : Low intake of folate was associated with increased risk of esophageal squamous cell carcinoma Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately following acute stroke and that endogenous antioxidant defences are rapidly depleted , thus permitting further tissue damage . Several studies point to an antioxidant effect of B-group vitamins and a pro-oxidant effect of elevated plasma tHcy ( total homocysteine ) . In the present study , we assessed whether supplementary B-group vitamins during this critical period will enhance antioxidant capacity and mitigate oxidative damage .  Forty-eight patients with acute ischaemic stroke within 12 h of symptom onset were assigned to receive daily oral supplements of B-group vitamins comprising 5 mg of folate , 5 mg of vitamin B2 , 50 mg of vitamin B6 and 0.4 mg of vitamin B12 ( n=24 ) or no supplements ( n=24 ) for 14 days . The treatment group and controls were matched for stroke subtype and age . Blood sample s were obtained before intervention and also at 7 and 14 days post-recruitment for measurement of the following biomarkers : red cell folate ( whole blood folate corrected with haematocrit ) , erythrocyte glutathione reductase activity coefficient ( EGRAC ; measure of vitamin B2 status ) , plasma pyridoxal phosphate ( vitamin B6 status ) , plasma vitamin B12 , plasma alpha-tocopherol , plasma ascorbic acid , plasma TAOC ( total antioxidant capacity ) , plasma MDA ( malondialdehyde ) , plasma tHcy and CRP ( C-reactive protein ) . Supplementation for 14 days with B-group vitamins significantly increased the plasma concentrations of pyridoxal phosphate and red blood cell folate and improved a measure of B2 status compared with the control group ( P<0.05 ) . Plasma tHcy decreased in both groups albeit less in the control group , but differences in cumulative changes were not significant . There was , however , a decrease in plasma MDA concentration in the treatment group , in contrast with the increase seen in the control group and these differences were significant ( P=0.05 ) . CRP concentration , a marker of tissue inflammation , was significantly lower in the treatment group compared with controls ( P<0.05 ) . In conclusion , B-group vitamin supplementation immediately post-infa rct may have antioxidant and anti-inflammatory effects in stroke disease independent of a homocysteine-lowering effect BACKGROUND Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately after acute ischemic stroke and that endogenous antioxidant defenses are rapidly depleted , thus permitting further tissue damage . Several studies point to an antioxidant effect of B-group vitamins and a pro-oxidant effect of elevated total plasma homocysteine ( tHcy ) . METHODS To test whether supplementary antioxidants with or without B-group vitamins during this critical period enhance antioxidant capacity or mitigate oxidative damage , ninety-six acute ischemic stroke patients within 12 hours of symptom onset were r and omly assigned to receive either daily oral 800 IU ( 727 mg ) vitamin E and 500 mg vitamin C ( n = 24 ) , or B-group vitamins ( 5 mg folic acid , 5 mg vitamin B(2 ) , 50 mg vitamin B(6 ) , and 0.4 mg of vitamin B(12 ) ; n = 24 ) , both vitamins together ( n = 24 ) , or no supplementation ( n = 24 ) for 14 days . Treatment groups and controls were matched for stroke subtype and age . Blood was obtained before treatment , at day 7 , and day 14 for measurements of plasma or blood vitamin status , plasma total antioxidant capacity ( TAOC ) , malondialdehyde ( MDA ) , tHcy and C-reactive protein ( CRP ) . RESULTS Supplementation with antioxidant vitamins and B-group vitamins separately or together significantly increased the plasma concentration of vitamin C , E , pyridoxal phosphate ( B(6 ) status ) , red blood cell folate , and improved a measure of B(2 ) status ( red cell glutathione reductase activation coefficient [ EGRAC ] ) , compared with the control group . Plasma TAOC increased significantly in the antioxidant treatment groups compared with the nonsignificant decline seen in the control group . tHcy concentrations decreased in subjects who received B-group vitamins and the control group compared with the rise seen in those who received antioxidants alone . There was a significant reduction in plasma MDA concentration in the 3 treatment groups , in contrast to the increase seen in the control group ; however , the changes were most evident in antioxidant groups . CRP concentrations ( a marker of tissue inflammation ) were significantly lower in the 3 treatment groups compared with the control group . There were no additive or synergistic effects of antioxidants and B-group vitamins together on any outcome measure . CONCLUSIONS Antioxidants supplementation with or without B-group vitamins enhances antioxidant capacity , mitigates oxidative damage , and may have an anti-inflammatory effect immediately postinfa rct in stroke disease CONTEXT Recently , concern has been raised about the safety of folic acid , particularly in relation to cancer risk . OBJECTIVE To evaluate effects of treatment with B vitamins on cancer outcomes and all-cause mortality in 2 r and omized controlled trials . DESIGN , SETTING , AND PARTICIPANTS Combined analysis and extended follow-up of participants from 2 r and omized , double-blind , placebo-controlled clinical trials ( Norwegian Vitamin Trial and Western Norway B Vitamin Intervention Trial ) . A total of 6837 patients with ischemic heart disease were treated with B vitamins or placebo between 1998 and 2005 , and were followed up through December 31 , 2007 . INTERVENTIONS Oral treatment with folic acid ( 0.8 mg/d ) plus vitamin B(12 ) ( 0.4 mg/d ) and vitamin B(6 ) ( 40 mg/d ) ( n = 1708 ) ; folic acid ( 0.8 mg/d ) plus vitamin B(12 ) ( 0.4 mg/d ) ( n = 1703 ) ; vitamin B(6 ) alone ( 40 mg/d ) ( n = 1705 ) ; or placebo ( n = 1721 ) . MAIN OUTCOME MEASURES Cancer incidence , cancer mortality , and all-cause mortality . RESULTS During study treatment , median serum folate concentration increased more than 6-fold among participants given folic acid . After a median 39 months of treatment and an additional 38 months of posttrial observational follow-up , 341 participants ( 10.0 % ) who received folic acid plus vitamin B(12 ) vs 288 participants ( 8.4 % ) who did not receive such treatment were diagnosed with cancer ( hazard ratio [ HR ] , 1.21 ; 95 % confidence interval [ CI ] , 1.03 - 1.41 ; P = .02 ) . A total of 136 ( 4.0 % ) who received folic acid plus vitamin B(12 ) vs 100 ( 2.9 % ) who did not receive such treatment died from cancer ( HR , 1.38 ; 95 % CI , 1.07 - 1.79 ; P = .01 ) . A total of 548 patients ( 16.1 % ) who received folic acid plus vitamin B(12 ) vs 473 ( 13.8 % ) who did not receive such treatment died from any cause ( HR , 1.18 ; 95 % CI , 1.04 - 1.33 ; P = .01 ) . Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B(12 ) . Vitamin B(6 ) treatment was not associated with any significant effects . CONCLUSION Treatment with folic acid plus vitamin B(12 ) was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease in Norway , where there is no folic acid fortification of foods . TRIAL REGISTRATION clinical trials.gov Identifier : NCT00671346 Abstract Purpose . The incidence of adenocarcinoma of the esophagus is increasing in most Western industrialized nations especially in white males . The impact of vitamins on the development of squamous cell carcinoma ( SCC ) and adenocarcinoma ( AC ) of the esophagus has not been eluci date d. The goal of this pilot- study was to analyze the influence of daily vitamin consumption on the frequency of esophageal carcinoma in Germany . Methods . Ninety-nine patients ( males ) with esophageal carcinoma ( 52 with SCC and 47 with AC ) were compared to a control group of 50 r and omly selected males from the Cologne area . Using a computer program to record the data , patients and controls were question ed in detail about their dietary habits . The interaction between known risk factors and the influence of vitamins on esophageal tumor risk were analyzed using logistic regression analysis . Results . The univariate analysis showed a significant risk reduction with increased intake  of β-carotene , vitamin C , vitamin E , and folic acid for both AC and for SCC . The results of logistic regression analysis were compatible with the known risk factors for SCC ( alcohol and tobacco ) and for AC ( obesity , tobacco , and alcohol ) and showed a significant risk reduction with an intake of vitamin E greater than 13 mg/day ( RR=0.13 , 95 % CI=0.1–0.5 , P=0.0004 ) and vitamin C greater than 100 mg/day ( RR=0.33 , 95 % CI=0.11–0.92 , P=0.034 ) for patients with SCC and similar results for patients with AC . Conclusion . Our data showed that low intake of vitamin C and E correlates significantly with the development of squamous cell carcinoma as well as adenocarcinoma of the esophagus in males . The relevance of interaction of vitamins with other dietary factors , alcohol , and tobacco are topics of current research Objective This study aims to investigate the risk of esophageal squamous cell carcinoma  in relation to exogenous factors in a rural area of China with a high incidence of esophageal squamous cell carcinoma . Methods A population -based case – control study was conducted in Yangzhong County , Jiangsu Province , China , with 355 histologically confirmed esophageal squamous cell carcinoma cases recruited between 1 January 2004 and 28 February 2006 and 408 controls matched by sex and age , r and omly selected from the local population . Results Stratified logistic regression analysis by sex revealed that hot-temperature food items , pork braised in brown sauce and old stocked rice intake could increase the risk of esophageal squamous cell carcinoma with odds ratio of 2.127 ( 95 % confidence interval : 1.394–3.245 ) , 2.059 ( 95 % confidence interval : 1.417–2.993 ) and 9.059 ( 95 % confidence interval : 5.930–13.840 ) , respectively , in men and 3.048 ( 95 % confidence interval : 1.733–5.364 ) , 1.914 ( 95 % confidence interval : 1.159–3.162 ) and 14.532 ( 95 % confidence interval : 7.816–27.019 ) , respectively , in women , whereas diet high in salt and chili , tobacco smoking and alcohol drinking only showed possible risk effects in men with odds ratio 2.338 ( 95 % confidence interval : 1.568–3.485 ) , 3.378 ( 95 % confidence interval : 2.117–5.389 ) , 1.976 ( 95 % confidence interval : 1.337–2.921 ) and 2.197 ( 95 % confidence interval : 1.510–3.195 ) , respectively . Green tea drinking showed a protective effect in women ( odds ratio=0.257 ; 95 % confidence interval : 0.070–0.94 
    Output:
    
Conclusion These findings support that vitamin B may have an influence on carcinogenesis of the esophagus .
Vitamin B1 , B3 , B6 , B9 showed a decreased risk of EC , and vitamin B12 showed an increased risk of EC