***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 Epidemiologic studies have suggested that hypertriglyceridemia and insulin resistance are related to the development of colon cancer . Nuclear peroxisome proliferator-activated receptors ( PPAR ) , which play a central role in lipid and glucose metabolism , had been hypothesized as being involved in colon cancerogenesis . In animal studies the lipid-lowering PPAR lig and bezafibrate suppressed colonic tumors . However , the effect of bezafibrate on colon cancer development in humans is unknown . Therefore , we proposed to investigate a possible preventive effect of bezafibrate on the development of colon cancer in patients with coronary artery disease during a 6-year follow-up . Methods Our population included 3011 patients without any cancer diagnosis who were enrolled in the r and omized , double blind Bezafibrate Infa rct ion Prevention ( BIP ) Study . The patients received either 400 mg of bezafibrate retard ( 1506 patients ) or placebo ( 1505 patients ) once a day . Cancer incidence data were obtained by matching a subject 's identification numbers with the National Cancer Registry . Each matched record was checked for correct identification . Results Development of new cancer ( all types ) was recorded in 177 patients : in 79 ( 5.25 % ) patients from the bezafibrate group vs. 98 ( 6.51 % ) from the placebo group . Development of colon cancer was recorded in 25 patients : in 8 ( 0.53 % ) patients from the bezafibrate group vs. 17 ( 1.13 % ) from the placebo group , ( Fisher 's exact test : one side p = 0.05 ; two side p = 0.07).A difference in the incidence of cancer was only detectable after a 4 year lag and progressively increased with continued follow-up . On multivariable analysis the colon cancer risk in patients who received bezafibrate tended to be lower with a hazard ratio of 0.47 and 95 % confidence interval 0.2–1.1 . Conclusion Our data , derived from patients with coronary artery disease , support the hypothesis regarding a possible preventive effect of bezafibrate on the development of colon cancer Lipid-lowering drugs are one of the most prescribed drugs worldwide . The aim was to compare 10-year all-cause mortality according to initial dyslipidemia status and lipid-lowering drug exposure . The PRIME study was a multicenter population -based prospect i ve cohort study of men recruited in 1991 to 1993 , aged 50 to 59 years at baseline , and followed up for 10 years . The 4 groups compared were  normolipidemic , untreated dyslipidemic , and dyslipidemic subjects on fibrate or statin therapy . Data were analyzed using multivariate Cox models . The cohort included 7,722 French men ( statin  group 4.0 % , fibrate group 7.9 % ,  untreated dyslipidemic  subjects 19.0 % , and normolipidemic subjects 69.1 % ) . After 10 years , 4.8 % of the sample was lost to follow-up and 416 deaths occurred ( cancers 53.1 % , cardiovascular diseases 17.1 % , and other 29.8 % ) . After adjustment for center , age , educational level , cardiovascular risk factors , lipids , alcohol intake , and history of cardiovascular and severe chronic diseases , hazard ratios ( HRs ) for all-cause mortality were 0.49 ( 95 % confidence interval [ CI ] 0.26 to 0.94 , p = 0.031 ) for subjects treated with a statin , 0.65 ( 95 % CI 0.42 to 0.99 , p = 0.046 ) for those on fibrate therapy , and 0.76 ( 95 % CI 0.56 to 1.03 , p = 0.080 ) for normolipidemic men compared with untreated dyslipidemic subjects . In the statin group , HRs for death from cardiovascular disease , cancer , and other causes were 0.55 ( p = 0.348 ) , 0.41 ( p = 0.067 ) , and 0.68 ( p = 0.546 ) compared with dyslipidemic subjects , respectively . In the fibrate group , HRs were 0.76 ( p = 0.499 ) , 0.52 ( p = 0.041 ) , and 0.87 ( p = 0.746 ) . In conclusion , in this cohort study carried out in a real-life setting , all-cause mortality was significantly lower in dyslipidemic subjects on fibrate or statin therapy than in untreated dyslipidemic patients . No excess risk of noncardiovascular death was observed BACKGROUND Studies have shown that treatment of hyperlipidemia , especially lowering of plasma LDL levels , retards the progression of coronary atherosclerosis and prevents clinical cardiovascular events . No such studies have focused on subjects with low levels of HDL cholesterol . METHODS AND RESULTS We r and omly assigned 395 post-coronary bypass men , who had an HDL cholesterol concentration < or = 1.1 mmol/L and LDL cholesterol < or = 4.5 mmol/L , to receive gemfibrozil 1200 mg/d or placebo . Coronary angiography was performed at baseline and after , on average , 32 months of therapy . Changes in coronary dimensions were assessed by computer-assisted analysis . Average on-trial serum triglyceride concentrations were 1.69+/-0.68 and 1.02+/-0.37 , total cholesterol 5.48+/-0.68 and 4.83+/-0.63 , LDL cholesterol 3.84+/-0.59 and 3.39+/-0.56 , and HDL cholesterol 0.88+/-0.15 and 0.98+/-0.17 mmol/L in the placebo and gemfibrozil groups , respectively ( mean+/-SD , each P<.001 ) . The change in per-patient means of average diameters of native coronary segments was -0.04+/-0.11 mm in the placebo group and -0.01+/-0.10 mm in the gemfibrozil group ( P=.009 ) . The equivalent changes in minimum luminal diameters of stenoses were -0.09+/-0.18 and -0.04+/-0.15 mm , respectively ( P=.002 ) . A similar , albeit nonsignificant , trend toward treatment benefit was found in the predefined primary study end point , segments unaffected by grafts and those distal to graft insertions . In aortocoronary bypass grafts , 23 subjects ( 14 % ) assigned to placebo had new lesions in the follow-up angiogram , compared with 4 subjects ( 2 % ) assigned to gemfibrozil ( P<.001 ) . CONCLUSIONS Gemfibrozil therapy retarded the progression of coronary atherosclerosis and the formation of bypass-graft lesions after coronary bypass surgery in men with low HDL cholesterol as their main lipid abnormality Objective : To assess the effect of bezafibrate on the risk of coronary heart disease and stroke in men with lower extremity arterial disease . Design : Double blind placebo controlled r and omised trial . Setting : 85 general practice s and nine hospital vascular clinics . Participants : 1568 men , mean age 68.2 years ( range 35 to 92 ) at recruitment . Interventions : Bezafibrate 400 mg daily ( 783 men ) or placebo ( 785 men ) . Main outcome measures : Combination of coronary heart disease and of stroke . All coronary events , fatal and non-fatal coronary events separately , and strokes alone ( secondary end points ) . Results : Bezafibrate did not reduce the incidence of coronary heart disease and stroke . There were 150 and 160 events in the active and placebo groups respectively ( relative risk 0.96 , 95 % confidence interval 0.76 to 1.21 ) . There were 90 and 111 major coronary events in the active and placebo groups respectively ( 0.81 , 0.60 to 1.08 ) , of which 64 and 65 were fatal ( 0.95 , 0.66 to 1.37 ) and 26 and 46 non-fatal ( 0.60 , 0.36 to 0.99 ) . Beneficial effects on non-fatal events were greatest in men aged < 65 years at entry , in whom benefit was also seen for all coronary events ( 0.38 , 0.20 to 0.72 ) . There were no significant effects in older men . There were 60 strokes in those on active treatment and 49 in those on placebo ( 1.34 , 0.80 to 2.01 ) . There were 204 and 195 deaths from all causes in the two groups respectively ( 1.03 , 0.83 to 1.26 ) . Bezafibrate reduced the severity of intermittent claudication for up to three years . Conclusions : Bezafibrate has no effect on the incidence of coronary heart disease and of stroke combined but may reduce the incidence of non-fatal coronary events , particularly in those aged < 65 years at entry , in whom all coronary events may also be reduced OBJECTIVE To determine whether serum lipid intervention , in addition to conventional diabetes treatment , could alter cardiovascular outcomes in type 2 diabetes . RESEARCH DESIGN AND METHODS There were 164 type 2 diabetic subjects ( 117 men , 47 women ) without a history of clinical cardiovascular disease r and omized to receive either bezafibrate or placebo daily on a double-blind basis in addition to routine diabetes treatment and followed prospect ively for a minimum of 3 years . Serial biochemical and noninvasive vascular assessment s , carotid and femoral artery B-mode ultrasound measurements , and those pertaining to coronary heart disease (CHD)— clinical history , the World Health Organization ( WHO ) cardiovascular question naire , and resting and exercise electrocardiogram (ECG)—were recorded . RESULTS Bezafibrate treatment was associated with significantly greater reductions over 3 years in median serum triglyceride ( −32 vs. 4 % , P = 0.001 ) , total cholesterol ( −7 vs. −0.3 % , P = 0.004 ) , and total−to-HDL cholesterol ratio ( −12 vs. −0.0 % , P = 0.001 ) , and an increase in HDL cholesterol ( 6 vs. −2 % , P = 0.02 ) as compared with placebo . There was a trend toward a greater reduction of fibrinogen ( −18 vs. −6 % , P = 0.08 ) at 3 years . No significant differences between the two groups were found in the progress of ultrasonically measured arterial disease . In those treated with bezafibrate , there was a significant reduction ( P = 0.01 , log-rank test ) in the combined incidence of Minnesota-coded probable ischemic change on the resting ECG and of documented myocardial infa rct ion . CONCLUSIONS Improving dyslipidemia in type 2 diabetic subjects had no effect on the progress of ultrasonically measured arterial disease , although the lower rate of “ definite CHD events ” in the treated group suggests that this might result in a reduction in the incidence of coronary heart disease On 4 October 2002 , women who were moderate drinkers received good news : their risk of breast cancer was not raised , according to a report in the Lancet that was widely covered by the British media.1 The bad news was that smoking at an early age was now implicated as a risk factor for breast cancer . However , after they had enjoyed guilt-free drinks ( without cigarettes ) for only a few days , on 13 November the message was reversed : alcohol did increase the risk of breast cancer after all , but smoking was declared innocent.2 The press release procl aim ed “ Alcohol , tobacco and breast cancer : the definitive answer . ” A reader was driven to complain in the letters page of the Guardian ( 14 November 2002 ) : “ So let me get this right — alcohol 's no good anymore , and if you smoked within five years of getting your periods , that 's bad news too . Oh no , that was a couple of weeks ago ; smoking 's okay now … Do things stop being bad for us if we just forget about them for a bit , do you think ? ” This is a familiar story — so much so that in Bristol we set our medical students the exercise of examining the “ health scare of the week ” that appears each Friday , generally from a study reported in the BMJ or Lancet .w1 The widespread perception that epidemiological studies generate conflicting and often meaningless findings w2 has received support from recent r and omised controlled trials , which have failed to confirm even apparently robust findings from observational epidemiological studies . The most topical of these relates to hormone replacement therapy . In 1991 a meta- analysis of epidemiological results relating the use of hormone replacement therapy to the risk of coronary heart disease concluded that it halved the risk , and that the evidence was statistically robust ( relative risk 0.50 ; 95 % BACKGROUND Bezafibrate has effects on lipid metabolism and haemostatic function . We undertook a double-blind , placebo-control 
    Output:
    
When the analysis was restricted to major RCTs , the results did not substantially change .
Similarly , we found no evidence of differential effects by length of follow-up or type of fibrate .
Insignificant results were also obtained for the role of fibrates in cancers of the respiratory tract , breast , colon , gastrointestinal tract , prostate , genitourinary tract , or in melanoma .
Conclusion Our findings demonstrate that fibrates have a neutral effect on cancer outcomes .