***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 
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    Input: Oxidative stress may enhance prostatic carcinogenesis . A polymorphism [ valine ( V ) -- > alanine ( A ) ] of manganese superoxide dismutase ( MnSOD ) , the primary antioxidant enzyme in mitochondria , has been recently associated with prostate cancer . We examined the relationship between prostate cancer and the MnSOD polymorphism and its interactions with baseline plasma antioxidant levels ( selenium , lycopene , and alpha-tocopherol ) and beta-carotene treatment among 567 cases and 764 controls nested in the prospect i ve Physicians ' Health Study . We found little overall association between MnSOD polymorphism and prostate cancer risk ; however , this polymorphism significantly modified risk of prostate cancer associated with prediagnostic plasma antioxidants ( P(interaction ) > or = 0.05 ) . Among men with the AA genotype , high selenium level ( 4th versus 1st quartile ) was associated with a relative risk ( RR ) of 0.3 [ 95 % confidence interval ( CI ) , 0.2 - 0.7 ] for total prostate cancer ; for clinical ly aggressive prostate cancer , the RR was 0.2 ( 95 % CI , 0.1 - 0.5 ) . In contrast , among men with the VV/VA genotype , the RRs were 0.6 ( 0.4 - 1.0 ) and 0.7 ( 0.4 - 1.2 ) for total and clinical ly aggressive prostate cancer . These patterns were similar for lycopene and alpha-tocopherol and were particularly strong when these antioxidants and selenium were combined ; men with the AA genotype had a 10-fold gradient in risk for aggressive prostate cancer across quartiles of antioxidant status . Men with AA genotype who were r and omly assigned to beta-carotene treatment ( versus placebo ) had a RR of 0.6 ( 95 % CI , 0.2 - 0.9 ; P(interaction ) = 0.03 ) for fatal prostate cancer , but no significant association was observed in men with the VV/VA genotype . Both endogenous and exogenous antioxidants play an important and interdependent role in preventing clinical ly significant prostate cancer The association between plasma carotenoids and prostate cancer  risk was investigated in a case-control study nested within the prospect i ve Health Professionals Follow-up Study . We matched 450 incident prostate cancer cases diagnosed from 1993–1998 to 450 controls by age , time , month , and year of blood donation . Modest inverse , but not statistically significant , associations were observed among plasma α-carotene , β-carotene , and lycopene concentrations , and overall risk of prostate cancer diagnosis { odds ratio ( highest versus lowest quintile ; OR ) , α-carotene : OR , 0.67 [ 95 % confidence interval ( CI ) , −0.40–1.09 ] ; β-carotene : OR , 0.78 ( 95 % CI , 0.48–1.25 ) ; lycopene : OR , 0.66 ( 95 % CI , 0.38–1.13)}. The inverse association between plasma lycopene concentrations and prostate cancer risk was limited to participants who were 65 years or older ( OR , 0.47 ; 95 % CI , 0.23–0.98 ) and without a family history of prostate cancer ( OR , 0.48 ; 95 % CI , 0.26–0.89 ) . Combining , older age and a negative family history provided similar results ( OR , 0.43 ; 95 % CI , 0.18–1.02 ) . Inverse associations between β-carotene and prostate cancer risk were also found among younger participants ( < 65 years of age ; OR , 0.36 ; 95 % CI , 0.14–0.91 ; Ptrend = 0.03 ) . Combining dietary intake and plasma data confirmed our results . We found a statistically significant inverse association between higher plasma lycopene concentrations and lower risk of prostate cancer , which was restricted to older participants and those without a family history of prostate cancer . This observation suggests that tomato products may exhibit more potent protection against sporadic prostate cancer rather than those with a stronger familial or hereditary component . In addition , our findings also suggest that among younger men , diets rich in β-carotene may also play a protective role in prostate carcinogenesis BACKGROUND Several human studies have observed a direct association between retinol ( vitamin A ) intake and risk of prostate cancer ; other studies have found either an inverse association or no association of intake of beta-carotene ( the major provitamin A ) with risk of prostate cancer . Data regarding carotenoids other than beta-carotene in relation to prostate cancer risk are sparse . PURPOSE We concluded a prospect i ve cohort study to examine the relationship between the intake of various carotenoids , retinol , fruits , and vegetables and the risk of prostate cancer . METHODS Using responses to a vali date d , semiquantitative food-frequency question naire mailed to participants in the Health Professionals Follow-up Study in 1986 , we assessed dietary intake for a 1-year period for a cohort of 47,894 eligible subjects initially free of diagnosed cancer . Follow-up question naires were sent to the entire cohort in 1988 , 1990 , and 1992 . We calculated the relative risk ( RR ) for each of the upper categories of intake of a specific food or nutrient by dividing the incidence rate of prostate cancer among men in each of these categories by the rate among men in the lowest intake level . All P values result ed from two-sided tests . RESULTS Between 1986 and 1992 , 812 new cases of prostate cancer , including 773 non-stage A1 cases , were documented . Intakes of the carotenoids beta-carotene , alpha-carotene , lutein , and beta-cryptoxanthin were not associated with risk of non-stage A1 prostate cancer ; only lycopene intake was related to lower risk ( age- and energy-adjusted RR = 0.79 ; 95 % confidence interval [ CI ] = 0.64 - 0.99 for high versus low quintile of intake ; P for trend = .04 ) . Of 46 vegetables and fruits or related products , four were significantly associated with lower prostate cancer risk ; of the four -- tomato sauce ( P for trend = .001 ) , tomatoes ( P for trend = .03 ) , and pizza ( P for trend = .05 ) , but not strawberries -- were primary sources of lycopene . Combined intake of tomatoes , tomato sauce , tomato juice , and pizza ( which accounted for 82 % of lycopene intake ) was inversely associated with risk of prostate cancer ( multivariate RR = 0.65 ; 95 % CI = 0.44 - 0.95 , for consumption frequency greater than 10 versus less than 1.5 servings per week ; P for trend = .01 ) and advanced ( stages C and D ) prostate cancers ( multivariate RR = 0.47 ; 95 % CI = 0.22 - 1.00 ; P for trend = .03 ) . No consistent association was observed for dietary retinol and risk of prostate cancer . CONCLUSIONS These findings suggest that intake of lycopene or other compounds in tomatoes may reduce prostate cancer risk , but other measured carotenoids are unrelated to risk . IMPLICATION S Our findings support recommendations to increase vegetable and fruit consumption to reduce cancer incidence but suggest that tomato-based foods may be especially beneficial regarding prostate cancer risk Dietary consumption of the carotenoid lycopene ( mostly from tomato products ) has been associated with a lower risk of  prostate cancer . Evidence relating other carotenoids , tocopherols , and retinol to prostate cancer risk has been equivocal . This prospect i ve study was design ed to examine the relationship between plasma concentrations of several major antioxidants and risk of prostate cancer . We conducted a nested case-control study using plasma sample s obtained in 1982 from healthy men enrolled in the Physicians ' Health Study , a r and omized , placebo-controlled trial of aspirin and beta-carotene .  Subjects included 578 men who developed prostate cancer within 13 years of follow-up and 1294 age- and smoking status-matched controls . We quantified the five major plasma carotenoid peaks ( alpha- and beta-carotene , beta-cryptoxanthin , lutein , and lycopene ) plus alpha- and gamma-tocopherol and retinol using high-performance liquid chromatography . Results for plasma beta-carotene are reported separately . Odds ratios ( ORs ) , 95 % confidence intervals ( Cls ) , and Ps for trend were calculated for each quintile of plasma antioxidant using logistic regression models that allowed for adjustment of potential confounders and estimation of effect modification by assignment to either active beta-carotene or placebo in the trial . Lycopene was the only antioxidant found at significantly lower mean levels in cases than in matched controls ( P = 0.04 for all cases ) . The ORs for all prostate cancers declined slightly with increasing quintile of plasma lycopene ( 5th quintile OR = 0.75 , 95 % CI = 0.54 - 1.06 ; P , trend = 0.12 ) ; there was a stronger inverse association for aggressive prostate cancers ( 5th quintile OR = 0.56 , 95 % CI = 0.34 - 0.91 ; P , trend = 0.05 ) . In the placebo group , plasma lycopene was very strongly related to lower prostate cancer risk ( 5th quintile OR = 0.40 ; P , trend = 0.006 for aggressive cancer ) , whereas there was no evidence for a trend among those assigned to beta-carotene supplements . However , in the beta-carotene group , prostate cancer risk was reduced in each lycopene quintile relative to men with low lycopene and placebo . The only other notable association was a reduced risk of aggressive cancer with higher alpha-tocopherol levels that was not statistically significant . None of the associations for lycopene were confounded by age , smoking , body mass index , exercise , alcohol , multivitamin use , or plasma total cholesterol level . These results concur with a recent prospect i ve dietary analysis , which identified lycopene as the carotenoid with the clearest inverse relation to the development of prostate cancer . The inverse association was particularly apparent for aggressive cancer and for men not consuming beta-carotene supplements . For men with low lycopene , beta-carotene supplements were associated with risk reductions comparable to those observed with high lycopene . These data provide further evidence that increased consumption of tomato products and other lycopene-containing foods might reduce the occurrence or progression of prostate cancer BACKGROUND Evidence has accumulated from observational studies that people eating more fruits and vegetables , which are rich in beta-carotene ( a violet to yellow plant pigment that acts as an antioxidant and can be converted to vitamin A by enzymes in the intestinal wall and liver ) and retinol ( an alcohol chemical form of vitamin A ) , and people having higher serum beta-carotene concentrations had lower rates of lung cancer . The Beta-Carotene and Retinol Efficacy Trial ( CARET ) tested the combination of 30 mg beta-carotene and 25,000 IU retinyl palmitate ( vitamin A ) taken daily against placebo in 18314 men and women at high risk of developing lung cancer . The CARET intervention was stopped 21 months early because of clear evidence of no benefit and substantial evidence of possible harm ; there were 28 % more lung cancers and 17 % more deaths in the active intervention group ( active = the daily combination of 30 mg beta-carotene and 25,000 IU retinyl palmitate ) . Promptly after the January 18 , 1996 , announcement that the CARET active intervention had been stopped , we published preliminary findings from CARET regarding cancer , heart disease , and total mortality . PURPOSE We present for the first time results based on the pre-specified analytic method , details about risk factors for lung cancer , and analyses of subgroups and of factors that possibly influence response to the intervention . METHODS CARET was a r and omized , double-blinded , placebo-controlled chemoprevention trial , initiated with a pilot phase and then exp and ed 10-fold at six study centers . Cigarette smoking history and status and alcohol intake were assessed through participant self-report . Serum was collected from the participants at base line and periodically after r and omization and was analyzed for beta-carotene concentration . An Endpoints Review Committee evaluated endpoint reports , including pathologic review of tissue specimens . The primary analysis is a stratified logrank test for intervention arm differences in lung cancer incidence , with weighting linearly to hypothesized full effect at 24 months after r and omization . Relative risks ( RRs ) were estimated by use of Cox regression models ; tests were performed for quantitative and qualitative interactions between the intervention and smoking status or alcohol intake . O'Brien-Fleming boundaries were used for stopping criteria at interim analyses . Statistical significance was set at the .05 alpha value , and all P values were derived from two-sided statistical tests . RESULTS According to CARET 's pre-specified analysis , there was an RR of 1.36 ( 95 % confidence interval [ CI ] = 1.07 - 1.73 ; P = .01 ) for weighted lung cancer incidence for the active intervention group compared with the placebo group , and 
    Output:
    
Conclusions : Our data demonstrate that higher dietary and circulating lycopene concentrations are inversely associated with PCa risk .
This was accompanied by dose-response relationships for dietary and circulating lycopene .
However , lycopene was not associated with a reduced risk of advanced PCa .