***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: PURPOSE A r and omized , double-blind , dose finding , placebo controlled , parallel group clinical study was done to determine the incidence of prostate cancer in men with high grade prostatic intraepithelial neoplasia treated with toremifene .  MATERIAL S AND METHODS A total of 514 patients with high grade prostatic intraepithelial neoplasia and no evidence of prostate cancer on screening biopsy were r and omized to 20 , 40 or 60 mg toremifene , or placebo daily for 12 months . Patients underwent re-biopsy at 6 and 12 months . RESULTS The number of evaluable patients , that is those with 1 on study biopsy who were compliant , was 447 . The cumulative risk of prostate cancer was decreased in patients on 20 mg toremifene compared with placebo ( 24.4 % vs 31.2 % , p < 0.05 ) . The annualized rate of prevention was 6.8 cancers per 100 men treated . In patients with no biopsy evidence of cancer at baseline and 6 months , the 12-month incidence of prostate cancer was decreased by 48.2 % with 20 mg toremifene compared with placebo ( 9.1 % vs 17.4 % , p < 0.05 ) . The 20 mg dose was most effective but cumulative and 12-month incidences of prostate cancer were lower for each toremifene dose vs placebo with a cumulative risk of 29.2 % and 28.1 % , and a 12-month incidence of 14.3 % and 13.0 % for 40 and 60 mg , respectively . Gleason scores were similar across treatments . The overall incidence of drug related and serious adverse events did not differ between any of the toremifene groups and the placebo group . CONCLUSIONS Toremifene decreased the incidence of prostate cancer by 1 year and had a tolerability profile comparable to that of placebo in a high risk population BACKGROUND Fish and seafood n-3 fatty acids may prevent or delay the progression of prostate cancer , but epidemiologic studies do not uniformly support this hypothesis . OBJECTIVE We examined the relation of fish and seafood n-3 fatty acid intakes with  prostate cancer incidence and mortality . DESIGN We conducted a prospect i ve cohort study among 20,167 men participating in the Physician 's Health Study who were free of cancer in 1983 . RESULTS During 382 144 person-years of follow-up , 2161 men were diagnosed with prostate cancer and 230 died of prostate cancer . Fish intake was unrelated to prostate cancer incidence . Survival analysis among the men diagnosed with prostate cancer revealed that those consuming fish > or=5 times/wk had a 48 % lower risk of prostate cancer death than did men consuming fish less than once weekly [ relative risk ( RR ) = 0.52 ; 95 % CI : 0.30 , 0.91 ; P for trend = 0.05 ] . A similar association was found between seafood n-3 fatty acid intake and prostate cancer mortality ( RR(Q5 versus Q1 ) = 0.64 ; 95 % CI : 0.42 , 0.99 ; P for trend = 0.02 ) . These associations became stronger when the analyses were restricted to clinical ly detected cases . CONCLUSION These results suggest that fish intake is unrelated to prostate cancer incidence but may improve prostate cancer survival BACKGROUND We conducted a study to determine whether dutasteride reduces the risk of incident prostate cancer , as detected on biopsy , among men who are at increased risk for the disease . METHODS In this 4-year , multicenter , r and omized , double-blind , placebo-controlled , parallel-group study , we compared dutasteride , at a dose of 0.5 mg daily , with placebo .  Men were eligible for inclusion in the study if they were 50 to 75 years of age , had a prostate-specific antigen ( PSA ) level of 2.5 to 10.0 ng per milliliter , and had had one negative prostate biopsy ( 6 to 12 cores ) within 6 months before enrollment . Subjects underwent a 10-core transrectal ultrasound-guided biopsy at 2 and 4 years . RESULTS Among 6729 men who underwent a biopsy or prostate surgery , cancer was detected in 659 of the 3305 men in the dutasteride group , as compared with 858 of the 3424 men in the placebo group , representing a relative risk reduction with dutasteride of 22.8 % ( 95 % confidence interval , 15.2 to 29.8 ) over the 4-year study period ( P<0.001 ) . Overall , in years 1 through 4 , among the 6706 men who underwent a needle biopsy , there were 220 tumors with a Gleason score of 7 to 10 among 3299 men in the dutasteride group and 233 among 3407 men in the placebo group ( P=0.81 ) . During years 3 and 4 , there were 12 tumors with a Gleason score of 8 to 10 in the dutasteride group , as compared with only 1 in the placebo group ( P=0.003 ) . Dutasteride therapy , as compared with placebo , result ed in a reduction in the rate of acute urinary retention ( 1.6 % vs. 6.7 % , a 77.3 % relative reduction ) . The incidence of adverse events was similar to that in studies of dutasteride therapy for benign prostatic hyperplasia , except that in our study , as compared with previous studies , the relative incidence of the composite category of cardiac failure was higher in the dutasteride group than in the placebo group ( 0.7 % [ 30 men ] vs. 0.4 % [ 16 men ] , P=0.03 ) . CONCLUSIONS Over the course of the 4-year study period , dutasteride reduced the risk of incident prostate cancer detected on biopsy and improved the outcomes related to benign prostatic hyperplasia . ( Clinical Trials.gov number , NCT00056407 . CONTEXT Secondary analyses of 2 r and omized controlled trials and supportive epidemiologic and pre clinical data indicated the potential of selenium and vitamin E for preventing prostate cancer . OBJECTIVE To determine whether selenium , vitamin E , or both could prevent prostate cancer and other diseases with little or no toxicity in relatively healthy men . DESIGN , SETTING , AND PARTICIPANTS A r and omized , placebo-controlled trial ( Selenium and Vitamin E Cancer Prevention Trial [ SELECT ] ) of 35,533 men from 427 participating sites in the United States , Canada , and Puerto Rico r and omly assigned to 4 groups ( selenium , vitamin E , selenium + vitamin E , and placebo ) in a double-blind fashion between August 22 , 2001 , and June 24 , 2004 . Baseline eligibility included age 50 years or older ( African American men ) or 55 years or older ( all other men ) , a serum prostate-specific antigen level of 4 ng/mL or less , and a digital rectal examination not suspicious for prostate cancer . INTERVENTIONS Oral selenium ( 200 microg/d from L-selenomethionine ) and matched vitamin E placebo , vitamin E ( 400 IU/d of all rac-alpha-tocopheryl acetate ) and matched selenium placebo , selenium + vitamin E , or placebo + placebo for a planned follow-up of minimum of 7 years and a maximum of 12 years . MAIN OUTCOME MEASURES Prostate cancer and prespecified secondary outcomes , including lung , colorectal , and overall primary cancer . RESULTS As of October 23 , 2008 , median overall follow-up was 5.46 years ( range , 4.17 - 7.33 years ) . Hazard ratios ( 99 % confidence intervals [ CIs ] ) for prostate cancer were 1.13 ( 99 % CI , 0.95 - 1.35 ; n = 473 ) for vitamin E , 1.04 ( 99 % CI , 0.87 - 1.24 ; n = 432 ) for selenium , and 1.05 ( 99 % CI , 0.88 - 1.25 ; n = 437 ) for selenium + vitamin E vs 1.00 ( n = 416 ) for placebo . There were no significant differences ( all P>.15 ) in any other prespecified cancer end points . There were statistically nonsignificant increased risks of prostate cancer in the vitamin E group ( P = .06 ) and type 2 diabetes mellitus in the selenium group ( relative risk , 1.07 ; 99 % CI , 0.94 - 1.22 ; P = .16 ) but not in the selenium + vitamin E group . CONCLUSION Selenium or vitamin E , alone or in combination at the doses and formulations used , did not prevent prostate cancer in this population of relatively healthy men . TRIAL REGISTRATION clinical trials.gov identifier : NCT00006392 CONTEXT Many individuals take vitamins in the hopes of preventing chronic diseases such as cancer , and vitamins E and C are among the most common individual supplements . A large-scale r and omized trial suggested that vitamin E may reduce risk of prostate cancer ; however , few trials have been powered to address this relationship . No previous trial in men at usual risk has examined vitamin C alone in the prevention of cancer . OBJECTIVE To evaluate whether long-term vitamin E or C supplementation decreases risk of prostate and total cancer events among men . DESIGN , SETTING , AND PARTICIPANTS The Physicians ' Health Study II is a r and omized , double-blind , placebo-controlled factorial trial of vitamins E and C that began in 1997 and continued until its scheduled completion on August 31 , 2007 . A total of 14,641 male physicians in the United States initially aged 50 years or older , including 1307 men with a history of prior cancer at r and omization , were enrolled . INTERVENTION Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily . MAIN OUTCOME MEASURES Prostate and total cancer . RESULTS During a mean follow-up of 8.0 years , there were 1008 confirmed incident cases of prostate cancer and 1943 total cancers . Compared with placebo , vitamin E had no effect on the incidence of prostate cancer ( active and placebo vitamin E groups , 9.1 and 9.5 events per 1000 person-years ; hazard ratio [ HR ] , 0.97 ; 95 % confidence interval [ CI ] , 0.85 - 1.09 ; P = .58 ) or total cancer ( active and placebo vitamin E groups , 17.8 and 17.3 cases per 1000 person-years ; HR , 1.04 ; 95 % CI , 0.95 - 1.13 ; P = .41 ) . There was also no significant effect of vitamin C on total cancer ( active and placebo vitamin C groups , 17.6 and 17.5 events per 1000 person-years ; HR , 1.01 ; 95 % CI , 0.92 - 1.10 ; P = .86 ) or prostate cancer ( active and placebo vitamin C groups , 9.4 and 9.2 cases per 1000 person-years ; HR , 1.02 ; 95 % CI , 0.90 - 1.15 ; P = .80 ) . Neither vitamin E nor vitamin C had a significant effect on colorectal , lung , or other site-specific cancers . Adjustment for adherence and exclusion of the first 4 or 6 years of follow-up did not alter the results . Stratification by various cancer risk factors demonstrated no significant modification of the effect of vitamin E on prostate cancer risk or either agent on total cancer risk . CONCLUSIONS In this large , long-term trial of male physicians , neither vitamin E nor C supplementation reduced the risk of prostate or total cancer . These data provide no support for the use of these supplements for the prevention of cancer in middle-aged and older men . TRIAL REGISTRATION clinical trials.gov Identifier : NCT00270647 BACKGROUND In 2008 , we reported that radical prostatectomy , as compared with watchful waiting , reduces the rate of death from prostate cancer . After an additional 3 years of follow-up , we now report estimated 15-year results . METHODS From October 1989 through February 1999 , we r and omly assigned 695 men with early prostate cancer to watchful waiting or radical prostatectomy .  Follow-up was complete through December 2009 , with histopathological review of biopsy and radical-prostatectomy specimens and blinded evaluation of causes of death . Relative risks , with 95 % confidence intervals , were estimated with the use of a Cox proportional-hazards model . RESULTS During a median of 12.8 years , 166 of the 347 men in the radical-prostatectomy group and 201 of the 348 in the watchful-waiting group died ( P=0.007 ) . In the case of 55 men assigned to surgery and 81 men assigned to watchful waiting , death was due 
    Output:
    
The strongest evidence exists to support the use of 5 α-reductase inhibitors ( 5-ARIs ) for prevention of prostate cancer .
However , the evidence is insufficient to recommend that these agents be used routinely among all men .
At present there is no suitable evidence to recommend using any specific nutritional supplement or diet to prevent prostate cancer .