***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: CONTEXT Diabetes is a serious and costly disease that is becoming increasingly common in many countries . The role of diabetes as a cancer risk factor remains unclear . OBJECTIVE To examine the relationship between fasting serum glucose and diabetes and risk of all cancers and specific cancers in men and women in Korea . DESIGN , SETTING , AND PARTICIPANTS Ten-year prospect i ve cohort study of 1,298,385 Koreans ( 829,770 men and 468,615 women ) aged 30 to 95 years who received health insurance from the National Health Insurance Corp and had a biennial medical evaluation in 1992 - 1995 ( with follow-up for up to 10 years ) . MAIN OUTCOME MEASURES Death from cancer and registry-documented incident cancer or hospital admission for cancer . RESULTS During the 10 years of follow-up , there were 20,566 cancer deaths in men and 5907 cancer deaths in women . Using Cox proportional hazards models and controlling for smoking and alcohol use , the stratum with the highest fasting serum glucose ( > or = 140 mg/dL [ > or = 7.8 mmol/L ] ) had higher death rates from all cancers combined ( hazard ratio [ HR ] , 1.29 ; 95 % confidence interval [ CI ] , 1.22 - 1.37 in men and HR , 1.23 ; 95 % CI , 1.09 - 1.39 in women ) compared with the stratum with the lowest level ( < 90 mg/dL [ < 5.0 mmol/L ] ) . By cancer site , the association was strongest for pancreatic cancer , comparing the highest and lowest strata in men ( HR , 1.91 ; 95 % CI , 1.52 - 2.41 ) and in women ( HR , 2.05 ; 95 % CI , 1.43 - 2.93 ) . Significant associations were also found for cancers of the esophagus , liver , and colon/rectum in men and of the liver and cervix in women , and there were significant trends with glucose level for cancers of the esophagus , colon/rectum , liver , pancreas , and bile duct in men and of the liver and pancreas in women . Of the 26,473 total cancer deaths in men and women , 848 were estimated as attributable to having a fasting serum glucose level of less than 90 mg/dL. For cancer incidence , the general patterns reflected those found for mortality . For persons with a diagnosis of diabetes or a fasting serum glucose level greater than 125 mg/dL ( 6.9 mmol/L ) , risks for cancer incidence and mortality were generally elevated compared with those without diabetes . CONCLUSION In Korea , elevated fasting serum glucose levels and a diagnosis of diabetes are independent risk factors for several major cancers , and the risk tends to increase with an increased level of fasting serum glucose Insulin resistance likely increases the risk of chronic liver disease ( CLD ) and liver cancer , but long-term prospect i ve studies with measured fasting glucose and insulin are lacking . We evaluated the associations of prediagnostic fasting glucose , insulin , and the homeostasis model assessment of insulin resistance ( HOMA-IR ) with liver cancer and CLD mortality in a prospect i ve study of Finnish male smokers with extended follow-up time ( ≤22 years ) and information on known risk factors using data from 138 incident primary liver cancer cases , 216 CLD deaths , and 681 matched controls .  Fasting glucose and insulin  were measured in baseline serum . We used unconditional logistic regression to estimate ORs and 95 % confidence intervals adjusted for age , alcohol , education , smoking , body mass index , and hepatitis B and C viral status . Among those without self-reported diabetes , glucose was positively associated with liver cancer [ quartile 3 vs. quartile 1 ( Q3/Q1 ) : OR = 1.88 ; 1.03–3.49 ; Q4/Q1 : OR = 2.40 ; 1.33–4.35 ; Ptrend = 0.002 ] , and undiagnosed , biochemically defined , diabetes was associated with higher risk of liver cancer ( OR = 2.95 ; 1.46–5.96 ) and CLD mortality ( OR = 1.88 ; 1.00–3.56 ) . Serum insulin and HOMA-IR were also positively associated with liver cancer ( Q4/Q1 : OR = 3.41 ; 1.74–6.66 ; Ptrend < 0.0001 ; OR = 3.72 ; 1.89–7.32 , Ptrend < 0.0001 , respectively ) and CLD ( OR = 2.51 ; 1.44–4.37 ; Ptrend = 0.0002 ; OR = 2.31 ; 1.34–3.97 ; Ptrend = 0.001 , respectively ) , with stronger associations observed for liver cancer diagnosed > 10 years after baseline . In conclusion , elevated fasting glucose and insulin and insulin resistance were independently associated with risk of liver cancer and CLD mortality , suggesting a potentially important etiologic role for insulin and glucose dysregulation even in the absence of diagnosed diabetes . Cancer Prev Res ; 9(11 ) ; 866–74 . © 2016 AACR Background : Given the close correlation between smoking and alcohol intake in most epidemiologic studies , it is difficult to exclude the residual confounding effect of alcohol in the association between smoking and hepatocellular carcinoma ( HCC ) . Method : We evaluated the association between smoking and risk of HCC  in the Singapore Chinese Health Study , a prospect i ve cohort with a low prevalence of alcohol intake . Information on cigarette smoking and  alcohol consumption was obtained through in-person interviews conducted at enrolment . Results : After a mean of 11.5 years of follow-up , there were 394 incident cases of HCC . Participants who consumed more than two alcoholic drinks per day showed an increased risk for HCC ( hazard ratio (HR)=2.24 ; 95 % confidence interval (CI)=1.46–3.41 ) . After adjusting for alcohol consumption and other potential confounders , current vs never smokers had a statistically significant , increased risk of HCC ( HR=1.63 ; 95 % CI=1.27–2.10 ) that was dose-dependent ( number of cigarettes per day , P for trend<0.001 ) . The observed tobacco – HCC association also was duration -dependent ( years of smoking in ever smokers , P for trend=0.002 ) . When we excluded daily drinkers from the analysis , all risk estimates remained essentially the same and statistically significant . Conclusion : Our findings strongly implicate tobacco smoke as a causal factor of HCC development Insulin-like growth factor-1 ( IGF1 ) is a potent mitogen . IGF-binding protein-3 ( IGFBP3 ) binds and inhibits IGF1 . High circulating IGF1 levels and low IGFBP3 levels are associated with increased risk of several cancers . We examined relationships between serum levels of these factors and hepatoma risk in a case-control study nested in a prospect i ve cohort study ( the Japan Collaborative Cohort Study ( JACC Study ) ) . A baseline survey was conducted from 1988 to 1990 , and 39,242 subjects donated blood sample s. Participants diagnosed with hepatoma by 1997 were considered cases for nested case-control studies . Ninety-one cases and 263 sex- and age-matched controls were analyzed . A conditional logistic model was used to estimate odds ratios ( ORs ) for the incidence of hepatoma associated with serum IGF1 and IGFBP3 levels . Neither IGF1 nor the molar ratio of IGF1/IGFBP3 was correlated with hepatoma risk . After adjustment for hepatitis viral infection , body mass index , smoking , and alcohol intake , a higher molar difference of ( IGFBP3 − IGF1 ) was associated with a decreased hepatoma risk more than IGFBP3 alone ( p for trend < 0.001 and = 0.003 , respectively ) . People in the highest quartile had a lower risk ( OR = 0.098 ; 95 % confidence interval = 0.026–0.368 ) . In subgroup analyses of males and females , the molar difference was associated with a decreased hepatoma risk ( p for trend < 0.05 ) . In non-elderly individuals , the difference was inversely correlated with the incidence of hepatoma ( p for trend < 0.01 ) . The molar difference of ( IGFBP3 − IGF1 ) may be inversely associated with the incidence of hepatoma This study aim ed to investigate the association of fasting insulin and glucose levels with  hepatocellular carcinoma ( HCC ) risk in a case-cohort study within a cohort ( 1989 - 2006 ) of 2903 male government employees chronically infected with hepatitis B virus ( HBV ) in Taiwan .  Insulin , glucose and HBV-related factors  were assayed in baseline plasma among 124 HCC cases and a r and om subcohort of 1084 of the total cohort . After adjustment for demographics and HBV-related factors , including viral load and genotype , the HCC risk was higher for the highest [ > 6.10 μU/ml , hazard ratio ( HR ) = 2.36 , 95 % confidence interval ( CI ) : 1.43 - 3.90 ] and lowest ( < 2.75 μU/ml , HR = 1.57 , 95 % CI : 0.96 - 2.58 ) categories of insulin , compared with insulin of 2.75 - 4.10 μU/ml . The dose-response relationship between insulin and HCC varied by follow-up time , with stronger association for the HCC cases that occurred ≥8 years after baseline ( P for trend < 0.0001 ) . The effect of higher insulin on HCC risk remained after adjustment for other metabolic factors , and was fairly consistent across strata of age , body mass index , and HBV genotypic variants . However , it was more profound among those with viral load < 4.39 log(10 ) copies/ml at recruitment ( > 6.10 μU/ml , HR = 6.15 , 95 % CI : 2.48 - 15.22 ) . Higher insulin  was also associated with an increased risk for cirrhosis diagnosed by ultrasonography and elevated alanine aminotransferase . No association with either cirrhosis or HCC was noted for glucose or diabetes after adjusting for insulin . In conclusion , elevated insulin levels  are an independent risk factor for HCC among HBV carriers , especially for those with lower viral load 
    Output:
    
There is evidence that elevated blood glucose increases risk of liver cancer across the range of prediabetes and diabetes .
Considering the rapidly increasing prevalence of prediabetes and diabetes , controlling blood glucose may lower the risk of liver cancer