***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 To further clarify the relationship between total cholesterol and cancer , which remains unclear . METHODS We prospect ively examined the association between total cholesterol and site-specific and all-cancer incidence among 1,189,719 Korean adults enrolled in the National Health Insurance Corporation who underwent a st and ardized biennial medical examination in 1992 to 1995 and were observed for 14 years until cancer diagnosis or death . RESULTS Over follow-up , 53,944 men and 24,475 women were diagnosed with a primary cancer . Compared with levels less than 160 mg/dL , high  total  cholesterol ( ≥ 240 mg/dL ) was positively associated with prostate cancer ( hazard ratio [ HR ] , 1.24 ; 95 % CI , 1.07 to 1.44 ; P trend = .001 ) and colon cancer ( HR , 1.12 ; 95 % CI , 1.00 to 1.25 ; P trend = .05 ) in men and breast cancer in women ( HR , 1.17 ; 95 % CI , 1.03 to 1.33 ; P trend = .03 ) . Higher total cholesterol was associated with a lower incidence of liver cancer ( men : HR , 0.42 ; 95 % CI , 0.38 to 0.45 ; P trend < .001 ; women : HR , 0.32 ; 95 % CI , 0.27 to 0.39 ; P trend < .001 ) , stomach cancer ( men : HR , 0.87 ; 95 % CI , 0.82 to 0.93 ; P trend ≤ .001 ; women : HR , 0.86 ; 95 % CI , 0.77 to 0.97 ; P trend = .06 ) , and , in men , lung cancer ( HR , 0.89 ; 95 % CI , 0.82 to 0.96 ; P trend < .001 ) . Results for liver cancer were slightly attenuated after additional adjustment for liver enzyme levels and hepatitis B surface antigen status ( men : HR , 0.60 ; P trend < .001 ; women : HR , 0.46 ; P trend = .003 ) and exclusion of the first 10 years of follow-up ( men : HR , 0.59 ; P trend < .001 ; women : HR , 0.44 ; P trend < .001 ) . Total cholesterol was inversely associated with all-cancer incidence in both men ( HR , 0.84 ; 95 % CI , 0.81 to 0.86 ; P trend < .001 ) and women ( HR , 0.91 ; 95 % CI , 0.87 to 0.95 ; P trend < .001 ) , but these associations were attenuated after excluding incident liver cancers ( men : HR , 0.95 ; P trend < .001 ; women : HR , 0.98 ; P trend = .32 ) . CONCLUSION In this large prospect i ve study , we found that total cholesterol was associated with the risk of several different cancers , although these relationships differed markedly by cancer site Background Observational studies have indicated that high calcium intake may prevent colorectal cancer , but as for r and omized trials the results are inconclusive . Meanwhile , limited data on the link between serum calcium and cancer risk is available . We investigated the relation between serum calcium and risk of different gastrointestinal cancers in a prospect i ve study . Methods A cohort based on 492,044 subjects with baseline information on calcium ( mmol/L ) and albumin ( g/L ) was selected from the Swedish Apolipoprotein MOrtality RISk ( AMORIS ) study . Multivariable Cox proportional hazard models were used to analyse associations between st and ardised levels , quartiles and age/sex-specific categories of serum calcium and risk of oesophageal , stomach , colon , rectal cancer and also colorectal cancer combined , while taking into account serum albumin and other comorbidities . Results During 12 years of follow-up , we identified 323 incident oesophageal cancers , 782 stomach cancers , 2519 colon cancers , and 1495 rectal cancers . A positive association was found between albumin-adjusted serum calcium and risk of oesophageal [ HR : 4.82 ( 95 % CI : 2.07 – 11.19 ) for high compared to normal age-specific calcium levels ] and colon cancer [ e.g. HR : 1.07 ( 95 % CI : 1.00 – 1.14 ) for every SD increase of calcium ] as well as colorectal cancer [ e.g. HR : 1.06 ( 95 % CI : 1.02 - 1.11 ) for every SD increase of calcium ] in women . In men there were similar but weaker non-statistically significant trends . Conclusion The positive relation between serum calcium , oesophageal cancer and colorectal cancer calls for further studies including calcium regulators to evaluate whether there is a true link between calcium metabolism and development of gastrointestinal cancer Purpose : Leukocyte telomere length has gained attention as a marker of oxidative damage and age-related diseases , including cancer . We hypothesize that leukocyte telomere length might be able to predict future risk of cancer and examined this in a cohort of patients with Barrett 's esophagus , who are at increased risk of esophageal adenocarcinoma and thus were enrolled in a long-term cancer surveillance program . Patients and Methods : In this prospect i ve study ,  telomere length  was measured by quantitative PCR in baseline blood sample s in a cohort of 300 patients with Barrett 's esophagus followed for a mean of 5.8 years .  Leukocyte telomere length hazard ratios ( HR ) for risk of esophageal adenocarcinoma were calculated using multivariate Cox models . Results : Shorter telomeres were associated with increased esophageal adenocarcinoma risk ( age-adjusted HR between top and bottom quartiles of telomere length , 3.45 ; 95 % confidence interval , 1.35 - 8.78 ; P = 0.009 ) . This association was still significant when individually or simultaneously adjusted for age , gender , nonsteroidal anti-inflammatory drug ( NSAID ) use , cigarette smoking , and waist-to-hip ratio ( HR , 4.18 ; 95 % confidence interval , 1.60 - 10.94 ; P = 0.004 ) . The relationship between telomere length and cancer risk was particularly strong among NSAID nonusers , ever smokers , and patients with low waist-to-hip ratio . Conclusion : Leukocyte telomere length predicts risk of esophageal adenocarcinoma in patients with Barrett 's esophagus independently of smoking , obesity , and NSAID use . These results show the ability of leukocyte telomere length to predict the risk of future cancer and suggest that it might also have predictive value in other cancers arising in a setting of chronic inflammation . ( Cancer Epidemiol Biomarkers Prev 2007;16(12):2649–55 BACKGROUND From March 1986 through May 1991 , we conducted a r and omized nutritional intervention trial , the General Population Trial , in Linxian , China , a region with epidemic rates of squamous esophageal and adenomatous gastric cardia cancers . We found that participants who received selenium , beta-carotene , and vitamin E  had significantly lower cancer mortality rates than those who did not . In the current study , we examined the relationship between selenium levels measured in pretrial ( 1985 ) sera from participants and the subsequent risk of developing squamous esophageal , gastric cardia , and gastric non-cardia cancers during the trial . METHODS This study was design ed and analyzed in accord with a stratified case-cohort sampling scheme , with the six strata defined by sex and three age categories . We measured  serum selenium levels in 590 case subjects with esophageal cancer , 402 with gastric cardia cancers , and 87 with gastric non-cardia cancers as well as in 1062 control subjects .  Relative risks ( RRs ) , absolute risks , and population attributable risk for cancers were estimated on the basis of the Cox proportional hazards models . All statistical tests are two-sided . RESULTS We found highly significant inverse associations of serum selenium levels with the incidence of esophageal ( P : for trend < 10(-4 ) ) and gastric cardia ( P : for trend < 10(-6 ) ) cancers . The RR and 95 % confidence interval ( CI ) for comparison of highest to lowest quartile of serum selenium was 0.56 ( 95 % CI = 0.44 - 0.71 ) for esophageal cancer and 0.47 ( 95 % CI = 0.33 - 0.65 ) for gastric cardia cancer . The population proportion of these cancers that is attributable to low selenium levels was 26.4 % ( 95 % CI = 14.45 - 38.36 ) . We found no evidence for a gradient of serum selenium associated with incidence of gastric non-cardia cancer ( P : for trend = .96 ) , with an RR of 1.07 ( 95 % CI = 0.55 - 2.08 ) for the highest to lowest quartile of serum selenium . CONCLUSIONS Our study supports findings from previous prospect i ve studies and r and omized trials that variations in selenium levels affect the incidence of certain cancers . In the United States , where intervention trials of selenium are in the planning stages , consideration should be given to including population s at high risk for squamous esophageal and gastric cardia cancers Background : Defects in DNA damage recognition and repair have been associated with a wide variety of cancers . We conducted a prospect i ve study to determine whether mutagen sensitivity , as determined by an in vitro assay , was associated with the future development of cancer in patients with Barrett 's esophagus , which is associated with increased risk of progression to esophageal adenocarcinoma . Methods : We measured sensitivity to bleomycin in peripheral blood lymphocytes in a cohort of 220 patients with Barrett 's esophagus . We followed these patients for 1,230 person-years ( range , 3 months to 10.1 years ; median , 6.4 years ) , using development of cancer and aneuploidy as end points . A subset of these patients was evaluated for inactivation of tumor-suppressor genes CDKN2A/p16 and TP53 [ by mutation and loss of heterozygosity ( LOH ) ] in their Barrett 's segments at the time of , or before , the bleomycin test , and the patients were stratified by CDKN2A/p16 and TP53 status in an analysis of mutagen sensitivity and progression . Results : Bleomycin-sensitive patients were found to be at significantly greater risk of developing aneuploidy ( adjusted hazard ratio , 3.71 ; 95 % confidence interval , 1.44 - 9.53 ) and nonsignificantly greater risk of cancer ( adjusted hazard ratio , 1.63 ; 95 % confidence interval , 0.71 - 3.75 ) . Among patients with detectable LOH at the TP53 locus ( on chromosome 17p ) , increasing  bleomycin sensitivity was associated with increased risk of developing cancer ( Ptrend < 0.001 ) and aneuploidy ( Ptrend = 0.005 ) . Conclusions : This study supports the hypothesis that sensitivity to mutagens increases the risk of neoplastic progression in persons with Barrett 's esophagus , particularly those with 17p LOH including TP53 . ( Cancer Epidemiol Biomarkers Prev 2006;15(10):1935–40 OBJECTIVE : Several large studies have shown a negative association between Helicobacter pylori ( H. pylori ) infection and esophageal adenocarcinoma .  Diminution of gastric ghrelin secretion by H. pylori could protect against esophageal malignancy by decreasing appetite , food intake , and acid production , thereby decreasing weight and gastroesophageal reflux . METHODS : We evaluated the association of ghrelin with esophageal adenocarcinoma using a population from a previous nested case-control study . Among 128,992 enrolled in a multiphasic health checkup ( MHC ) between 1964 and 1969 , 52 patients developed esophageal adenocarcinoma by the year 2000 . Three r and om controls from the MHC cohort were matched to each case by age , sex , race , and the date and site of their MHC . Serum sample s collected at the MHC had been previously tested for IgG antibodies against H. pylori and the CagA protein . Serum ghrelin concentrations were determined by a commercial EIA on 52 % of the initial subjects ( 31 cases and 79 controls ) . RESULTS : A concentration of ghrelin greater than 3,200 pg/mL at MHC ( fourth quartile ) was associated with a lower risk of esophageal cancer ( H. pylori and body mass index [ BMI ] adjusted 
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Conclusion Serum pepsinogen I concentrations could aid early detection of oesophageal squamous cell carcinoma .