***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: BACKGROUND The effects of cholesterol-lowering treatment with statins on mortality and risk of cancer beyond the usual 5 - 6-year trial periods are unknown . We extended post-trial follow-up of participants in the Sc and inavian Simvastatin Survival Study ( 4S ) to investigate cause-specific mortality and incidence of cancer 5 years after closure of the trial . METHODS 4S was a r and omised double-blind trial of simvastatin or placebo in patients with coronary heart disease , serum total cholesterol 5.5 - 8.0 mmol/L , and serum triglycerides 2.5 mmol/L or lower . The double-blind period lasted for a median of 5.4 years ( range for survivors 4.9 - 6.3 ) and ended in 1994 . After the trial , most patients in both groups received open-label lipid-lowering treatment . National registers were used to assess mortality and causes of death and cancer incidence in the original treatment groups for a median total follow-up time of 10.4 years ( range for survivors 9.9 - 11.3 ) . Analysis was by intention to treat . FINDINGS 414 patients originally allocated simvastatin and 468 assigned placebo  died during the 10.4-year follow-up ( relative risk 0.85 [ 95 % CI 0.74 - 0.97 ] , p=0.02 ) , a difference largely attributable to lower coronary mortality in the simvastatin group ( 238 vs 300 deaths ; 0.76 [ 0.64 - 0.90 ] , p=0.0018 ) . 85 cancer deaths arose in the simvastatin group versus 100 in the placebo group ( 0.81 [ 0.60 - 1.08 ] , p=0.14 ) , and 227 incident cancers were reported in the simvastin group versus 248 in the placebo group ( 0.88 [ 0.73 - 1.05 ] , p=0.15 ) . Incidence of any specific type of cancer did not rise in the simvastatin group . INTERPRETATION Simvastatin treatment for 5 years in a placebo-controlled trial , followed by open-label statin therapy , was associated with survival benefit over 10 years of follow-up compared with open-label statin therapy for the past 5 years only . No difference was noted in mortality from and incidence of cancer between the original simvastatin group and placebo group Background —Therapeutic decisions regarding pharmacological therapy should be based on safety and tolerability as well as efficacy data . Clinical trials design ed to assess efficacy are often insufficiently powered to generate reliable safety data . Methods and Results —The West of Scotl and Coronary Prevention Study ( WOSCOPS ) , the Cholesterol and Recurrent Events ( CARE ) , and Long-term Intervention with Pravastatin in Ischemic Disease ( LIPID ) studies collectively accumulated > 112 000 person-years of exposure in double-blind r and omized trials comparing  placebo and pravastatin ( 40 mg once daily ) . During 5 years of exposure , the incidence of fatal and nonfatal cancers was similar between pravastatin and placebo groups . No differences in noncardiovascular serious adverse events were detected . With > 243 000 blood sample analyses , the percentage of patients with any abnormal liver function test after baseline sampling was similar ( > 3 × the upper limit of normal for alanine aminotransferase : 128 [ 1.4 % ] versus 131 [ 1.4 % ] patients for pravastatin versus placebo , respectively ) . Study medication was withdrawn in 3 pravastatin and 7 placebo patients due to creatine phosphokinase elevations ; no cases of mild or severe myopathy were reported . A Cox regression model considering treatment group , age , diabetes , smoking , whether primary or secondary prevention study , and cardiovascular serious adverse events indicates that the likelihood of discontinuing pravastatin was less than placebo . Conclusions —This prospect i ve analysis indicates that during prolonged exposure , 40 mg of pravastatin is well tolerated , with no excess of noncardiovascular serious adverse events , including liver function abnormalities and laboratory and clinical evidence for myositis . These extensive safety and tolerability data provide important information for therapeutic decisions regarding this pharmacological agent The Sc and inavian Simvastatin Survival Study ( 4S ) and other r and omized clinical trials have demonstrated that cholesterol-lowering treatment with statins improves prognosis in patients with coronary atherosclerosis compared with placebo . The effect of therapy with statins beyond the typical 5 to 6 years ' duration of the trials , in particular regarding the risk of cancer , has not been investigated . This study examines the long-term effects of simvastatin for up to 8 years on cause-specific mortality in patients with coronary heart disease ( CHD ) . We performed an observational , government registry-based study of mortality in the groups originally r and omized to simvastatin or placebo in the 4S over an additional 2-year follow-up period , so that the median total follow-up period was 7.4 years ( range 6.9 to 8.3 in surviving patients ) . R and omization took place at outpatient clinics at 94 clinical centers in Denmark , Finl and , Icel and , Norway , and Sweden from 1988 to 1989 . Of 4,444 patients with CHD , 2,223 and 2,221 were r and omized to treatment with placebo or simvastatin therapy , respectively . Patients received treatment with simvastatin , starting at 20 mg/day , with titration to 40 mg/day at 12 or 24 weeks if total cholesterol was > 5.2 mmol/L ( 200 mg/dl ) , or placebo . After the double-blind period , most patients in both treatment groups received simvastatin as open-label prescription . Of the 1,967 patients originally treated with placebo and surviving the double-blind period , 97 ( 4.9 % ) died during the following 2 years . In the group r and omized to simvastatin the corresponding number was 74 of the 2 , 039 survivors ( 3.6 % ) . Adding these deaths to those occurring during the original trial , the total was 353 ( 15.9 % ) and 256 ( 11.5 % ) deaths in the groups originally r and omized to placebo and simvastatin , respectively . The relative risk was 0.70 ( 95 % confidence interval 0 . 60 to 0.82 , p = 0.00002 ) . The total number of cancer deaths was 68 ( 3.1 % ) in the placebo group and 52 ( 2.3 % ) in the simvastatin group ( relative risk 0.73 , 95 % confidence interval 0.51 to 0.05 , p = 0 . 087 ) , and the numbers of noncardiovascular and other deaths were similar in both groups . We therefore conclude that treatment with simvastatin for up to 8 years in patients with CHD is safe and yields continued survival benefit Effects of atorvastatin on  early recurrent ischemic events in acute coronary syndromes . The MIRACL study : A r and omized controlled trial CONTEXT Plasma levels of the inflammatory biomarker C-reactive protein ( CRP ) predict cardiovascular risk , and retrospective studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ( statins ) may lower CRP in a manner largely independent of low-density lipoprotein cholesterol ( LDL-C ) . However , prospect i ve trial data directly evaluating this anti-inflammatory effect of statins are not available . OBJECTIVE To test the hypothesis that pravastatin has anti-inflammatory effects as evidence d by CRP reduction . DESIGN , SETTING , AND PARTICIPANTS Community-based , prospect i ve , r and omized , double-blind trial including 1702 men and women with no prior history of cardiovascular disease ( primary prevention cohort ) and open-label study including 1182 patients with known cardiovascular disease ( secondary prevention cohort ) who provided at least baseline and 12-week blood sample s. The study was conducted in US office-based practice s from February to December 2000 . INTERVENTIONS Participants in the double-blind primary prevention trial were r and omly assigned to receive 40 mg/d of pravastatin ( n = 865 ) or placebo ( n = 837 ) for 24 weeks . Participants in the secondary prevention cohort received 40 mg/d of open-label pravastatin for 24 weeks . MAIN OUTCOME MEASURE Change in CRP levels from baseline to 24 weeks . RESULTS In the primary prevention trial , compared with placebo , pravastatin reduced median CRP levels by 16.9 % ( P<.001 ) at 24 weeks , reflecting a decrease of 0.02 mg/dL in the pravastatin group while no change in CRP levels was observed in the placebo group . This effect was seen as early as 12 weeks ( median reduction in CRP with pravastatin , 14.7 % ; P<.001 ) and was present among all prespecified subgroups according to sex , age , smoking status , body mass index , baseline lipid levels , presence of diabetes , and use of aspirin or hormone replacement therapy . No significant association was observed between baseline CRP and baseline LDL-C levels , end-of- study CRP and end-of- study LDL-C levels , or change in CRP and change in LDL-C levels over time . In linear regression analyses , the only significant predictors of change in CRP on a log scale were r and omized pravastatin allocation and baseline CRP levels ( P<.001 for both ) . Similar reductions in CRP levels were observed at 12 weeks ( -14.3 % ) and 24 weeks ( -13.1 % ) in the secondary prevention cohort treated with pravastatin ( P<.005 for both ) . CONCLUSIONS In this prospect i ve trial , pravastatin reduced CRP levels at both 12 and 24 weeks in a largely LDL-C-independent manner . These data provide evidence that statins may have anti-inflammatory effects in addition to lipid-lowering effects BACKGROUND Although statins reduce coronary and cerebrovascular morbidity and mortality in middle-aged individuals , their efficacy and safety in elderly people is not fully established . Our aim was to test the benefits of pravastatin treatment in an elderly cohort of men and women with , or at high risk of developing , cardiovascular disease and stroke . METHODS We did a r and omised controlled trial in which we assigned 5804 men ( n=2804 ) and women ( n=3000 ) aged 70 - 82 years with a history of , or risk factors for , vascular disease to pravastatin ( 40 mg per day ; n=2891 ) or placebo ( n=2913 ) . Baseline cholesterol concentrations ranged from 4.0 mmol/L to 9.0 mmol/L. Follow-up was 3.2 years on average and our primary endpoint was a composite of coronary death , non-fatal myocardial infa rct ion , and fatal or non-fatal stroke . Analysis was by intention-to-treat . FINDINGS Pravastatin lowered LDL cholesterol concentrations by 34 % and reduced the incidence of the primary endpoint to 408 events compared with 473 on placebo ( hazard ratio 0.85 , 95 % CI 0.74 - 0.97 , p=0.014 ) . Coronary heart disease death and non-fatal myocardial infa rct ion risk was also reduced ( 0.81 , 0.69 - 0.94 , p=0.006 ) . Stroke risk was unaffected ( 1.03 , 0.81 - 1.31 , p=0.8 ) , but the hazard ratio for transient ischaemic attack was 0.75 ( 0.55 - 1.00 , p=0.051 ) . New cancer diagnoses were more frequent on pravastatin than on placebo ( 1.25 , 1.04 - 1.51 , p=0.020 ) . However , incorporation of this finding in a meta- analysis of all pravastatin and all statin trials showed no overall increase in risk . Mortality from coronary disease fell by 24 % ( p=0.043 ) in the pravastatin group . Pravastatin had no significant effect on cognitive function or disability . INTERPRETATION Pravastatin given for 3 years reduced the risk of coronary disease in elderly individuals . PROSPER therefore extends to elderly individuals the treatment strategy currently used in middle aged people OBJECTIVES To investigate the mechanisms by which bezafibrate retarded the progression of coronary lesions in the Bezafibrate Coronary Atherosclerosis Intervention Trial ( BECAIT ) , we examined the relationships of on-trial lipoproteins and lipoprotein subfractions to the angiographic outcome measurements . BACKGROUND BECAIT , the first double-blind , placebo-controlled , r and omized serial angiographic trial of a fibrate compound , showed that progression of focal coronary atherosclerosis in young survivors of myocardial infa rct ion could be retarded by bezafibrate treatment . METHODS A total of 92 dyslipoproteinemic men who had survived a 
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The melanoma outcomes data collected in this review of RCTs of statins and fibrates does not exclude the possibility that these drugs prevent melanoma .
Until further evidence is established , limiting exposure to ultraviolet radiation remains the most effective way to reduce the risk of melanoma