***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: Epidemiologic studies have failed to support the hypothesis that circulating and rogens are positively associated with prostate cancer risk and some recent studies have even suggested that high testosterone levels might be protective particularly against aggressive cancer . We tested this hypothesis by measuring  total testosterone , and rostanediol glucuronide , and rostenedione , DHEA sulfate , estradiol , and sex hormone – binding globulin in plasma  collected at baseline in a prospect i ve cohort study of 17,049 men . We used a case-cohort design , including 524 cases diagnosed during a mean 8.7 years follow-up and a r and omly sample d subcohort of 1,859 men . The association between each hormone level and prostate cancer risk was tested using Cox models adjusted for country of birth . The risk of prostate cancer was ∼30 % lower for a doubling of the concentration of estradiol but the evidence was weak ( Ptrend = 0.07 ) . None of the other hormones was associated with overall prostate cancer ( Ptrend ≥ 0.3 ) . None of the hormones was associated with nonaggressive prostate cancer ( all Ptrend ≥ 0.2 ) . The hazard ratio [ HR ; 95 % confidence interval ( 95 % CI ) ] for aggressive cancer almost halved for a doubling of the concentration of testosterone ( HR , 0.55 ; 95 % CI , 0.32 - 0.95 ) and and rostenedione ( HR , 0.51 ; 95 % CI , 0.31 - 0.83 ) , and was 37 % lower for a doubling of the concentration of DHEA sulfate ( HR , 0.63 ; 95 % CI , 0.46 - 0.87 ) . Similar negative but nonsignificant linear trends in risk for aggressive cancer were obtained for free testosterone , estradiol , and sex hormone – binding globulin ( Ptrend = 0.06 , 0.2 , and 0.1 , respectively ) . High levels of testosterone and adrenal and rogens are thus associated with reduced risk of aggressive prostate cancer but not with nonaggressive disease . ( Cancer Epidemiol Biomarkers Prev 2006;15(1):86–91 PURPOSE Several lines of evidence suggest that diet and weight gain may be important environmental factors implicated in prostate carcinogenesis , especially in tumor progression . The purpose of this study was to evaluate obesity at different ages in a well-characterized cohort of prostate cancer patients treated with prostatectomy  and to develop a prognostic model that incorporates body mass index ( BMI ) as a measure of obesity . EXPERIMENTAL DESIGN We carried out a prospect i ve study of 526 patients registered at the M.D. And erson Cancer Center from 1992 to 2001 . Kaplan-Meier and Cox proportional hazard analyses were done . RESULTS During an average follow-up of 54 months , 97 ( 18 % ) post-prostatectomy patients experienced biochemical failure . Patients who were obese ( BMI > or = 30 kg/m2 ) at diagnosis had a higher rate of biochemical failure than nonobese men ( P = 0.07 ) . Those obese at 40 years had an even greater rate of biochemical failure ( P = 0.001 ) . Higher BMI at diagnosis [ hazard ratio ( HR ) , 1.07 ; P = 0.01 ] and Gleason score = 7(4 + 3 ) and > or = 8 ( HR , 3.9 ; P = 0.03 and HR , 10.0 ; P < or = 0.001 , respectively ) remained significant independent predictors of biochemical failure in multivariate analysis . Men who gained weight at the greatest rate ( > 1.5 kg/y ) between 25 years and diagnosis progressed significantly sooner ( mean time , 17 months ) than those who exhibited a slower weight gain ( mean time , 39 months ; P(trend ) = 0.005 ) . The inclusion of obesity to the clinical nomogram improved performance . CONCLUSIONS Our findings vali date the importance for a role of obesity in prostate cancer progression and suggest a link to the biological basis of prostate cancer progression that can be therapeutically exploited Background : Prior prospect i ve cohort studies found that obesity was associated with increased risk of prostate cancer death . However , in the last 20 years dramatic changes in both the extent of obesity and prostate cancer screening and treatment have occurred . Whether the association between obesity and aggressive disease has changed as a result of these temporal changes is unclear . Methods : The study population consisted of 2,832 men treated by anatomic radical retropubic prostatectomy between 1985 and 2004 by a single surgeon . We evaluated the associations of obesity ( body mass index ≥30 kg/m2)with tumor stage and grade using logistic regression and with biochemical progression using Cox proportional hazards regression . We examined whether these associations have changed over the last 20 years . Results : On multivariable analysis , the strength of the positive association between obesity and high- grade disease increased over time whereas the strength of the positive association between obesity and positive surgical margins decreased over time . The strength of the positive association between obesity and extraprostatic extension fluctuated over time , although the strongest and only statistically significant association was among men treated since 2000 . The association between obesity and biochemical progression was strongest among men treated since 1995 ( relative risk , 1.90 ; 95 % confidence interval , 1.09 - 3.30 ; P = 0.02 ) . Conclusions : In the current study , with the exception of positive surgical margins , the positive association between obesity and high- grade disease , advanced stage , and biochemical progression after radical retropubic prostatectomy was in general strongest among men treated in the last 10 years . The reasons for these findings are not clear , although factors possibly related to prostate-specific antigen – based screening and /or other temporal changes in prostate cancer diagnosis and treatment may play a role PURPOSE Obesity has been proposed as an independent risk factor for patients undergoing surgery or radiotherapy ( RT ) for prostate cancer . Using body mass index ( BMI ) as a measure of obesity , we tested its role as a risk factor for patients receiving salvage RT after prostatectomy .  METHODS AND MATERIAL S Rates of subsequent biochemical relapse were examined in 90 patients who underwent salvage RT between 1984 and 2004 for biochemical failure after radical prostatectomy .  Median follow-up was 3.7 years . The BMI was tested as a continuous and categorical variable ( stratified as < 25 , 25-<30 , and > or=30 kg/m(2 ) ) . Univariate and multivariate proportional hazards regression analyses were performed for clinical , pathologic , and treatment factors associated with time to relapse after salvage RT . RESULTS There were 40 biochemical failures after salvage RT with a median time to failure of 1.2 years . The BMI was not associated with adverse clinical , pathologic , or treatment factors . On multivariate analysis , obesity was independently significant ( hazard ratio [ HR ] , 1.2 ; p = 0.01 ) , along with RT dose ( HR , 0.7 ; p = 0.003 ) and pre-RT prostate-specific antigen level ( HR , 1.2 ; p = 0.0003 ) . CONCLUSIONS This study is weakly suggestive that obesity may be a risk factor for salvage RT patients . Whether this results from greater biologic aggressiveness or technical inadequacies can not be answered by this study . Given the very high failure rate observed for severely obese patients , we propose that technical difficulties with RT are at play . This hypothesis is supported by the RT literature and could be prospect ively investigated . Techniques that optimize targeting , especially in obese patients , perhaps seem warranted at this time PURPOSE We examined the impact of obesity on disease specific and overall survival in patients with prostate cancer . MATERIAL S AND METHODS We identified 7,274 men from the Cancer of the Prostate Strategic Urological Research Endeavor data base with clinical ly localized prostate cancer , known body mass index and clinicopathological disease characteristics . Patients were classified by body mass index as normal ( less than 25 kg/m(2 ) ) , overweight ( 25 to 29.9 kg/m(2 ) ) , obese ( 30 to 34.9 kg/m(2 ) ) and severely obese ( 35 kg/m(2 ) or greater ) . Associations between body mass index and need for secondary treatment , disease specific survival and overall survival were analyzed using univariate and multivariate models . RESULTS Patients were classified by body mass index category as normal ( 28.8 % ) , overweight ( 50 % ) , obese ( 16.4 % ) and very obese ( 4.8 % ) . Mean followup was 51.3 + /- 38.5 months . During followup there were 1,044 deaths with 220 ( 21.1 % ) from prostate cancer . Stratified by body mass index category the groups differed with regard to the need for secondary treatment ( p = 0.05 ) and overall mortality ( p < 0.01 ) but there were no significant differences with regard to disease specific survival ( p = 0.09 ) . On multivariate analysis age 65 to 74 years ( HR 2.4 , p = 0.002 ) , age older than 75 years ( HR 3.2 , p = 0.0001 ) , high risk disease ( HR 1.6 , p < 0.0001 ) , conservative treatment ( HR 1.2 , p < 0.0001 ) and presence of diabetes ( HR 1.6 , p < 0.0001 ) were associated with decreased overall survival . Only conservative treatment ( HR 1.4 , p < 0.0001 ) , high risk disease ( HR 8.4 , p < 0.0001 ) and intermediate risk disease ( HR 2.5 , p = 0.004 ) were associated with decreased disease specific survival . CONCLUSIONS In a prospect i ve , community based cohort we were unable to establish a relationship between body mass index and prostate cancer disease specific survival or overall survival BACKGROUND The influence of excess body weight on the risk of death from  cancer  has not been fully characterized . METHODS In a prospect ively studied population of more than 900,000 U.S. adults ( 404,576 men and 495,477 women ) who were free of cancer at enrollment in 1982 , there were 57,145 deaths from cancer during 16 years of follow-up . We examined the relation in men and women between the body-mass index in 1982 and the risk of death from all cancers and from cancers at individual sites , while controlling for other risk factors in multivariate proportional-hazards models . We calculated the proportion of all deaths from cancer that was attributable to overweight and obesity in the U.S. population on the basis of risk estimates from the current study and national estimates of the prevalence of overweight and obesity in the U.S. adult population . RESULTS The heaviest members of this cohort ( those with a body-mass index [ the weight in kilograms divided by the square of the height in meters ] of at least 40 ) had death rates from all cancers combined that were 52 percent higher ( for men ) and 62 percent higher ( for women ) than the rates in men and women of normal weight . For men , the relative risk of death was 1.52 ( 95 percent confidence interval , 1.13 to 2.05 ) ; for women , the relative risk was 1.62 ( 95 percent confidence interval , 1.40 to 1.87 ) . In both men and women , body-mass index was also significantly associated with higher rates of death due to cancer of the esophagus , colon and rectum , liver , gallbladder , pancreas , and kidney ; the same was true for death due to non-Hodgkin 's lymphoma and multiple myeloma . Significant trends of increasing risk with higher body-mass-index values were observed for death from cancers of the stomach and prostate in men and for death from cancers of the breast , uterus , cervix , and ovary in women . On the basis of associations observed in this study , we estimate that current patterns of overweight and obesity in the United States could account for 14 percent of all deaths from cancer in men and 20 percent of those in women . CONCLUSIONS Increased body weight was associated with increased death rates for all cancers combined and for cancers at multiple specific sites Increasing body mass index ( BMI ) is associated with shorter time to prostate‐specific antigen ( PSA ) failure after radical prostatectomy . Whether BMI is associated with time to PSA failure was investigated in men treated with and rogen suppression therapy ( AST ) and radiation therapy ( RT ) for clinical ly localized prostate cancer Greater body mass index ( BMI ) is associated with shorter time to prostate‐specific antigen ( PSA ) failure following radical prostatectomy and radiation therapy ( RT ) . Whether BMI is associated with prostate cancer‐specific mortality ( PCSM ) was investigated in a large r and omized trial of men treated with RT and and rogen deprivation therapy ( ADT ) for locally advanced prostate cancer BACKGROUND In the European R and omized Study of Screening for Prostate Cancer ( ERSPC , Rotterdam region ) , men aged 55 - 74 years are screened for prostate cancer by prostate-specific antigen ( P 
    Output:
    
Elevated BMI is associated with risk of prostate cancer-specific mortality in prospect i ve cohort studies and biochemical recurrence in prostate cancer patients .