***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: Aims /hypothesisThere has been long-st and ing debate about whether diabetes is a causal risk factor for pancreatic cancer or a consequence of tumour development . Prospect i ve epidemiological studies have shown variable relationships between pancreatic cancer risk and blood markers of glucose and insulin metabolism , overall and as a function of lag times between marker measurements ( blood donation ) and date of tumour diagnosis . Methods Pre-diagnostic levels of HbA1c and C-peptide were measured for 466 participants with pancreatic cancer and 466 individually matched controls within the European Prospect i ve Investigation into Cancer and Nutrition . Conditional logistic regression models were used to estimate ORs for pancreatic cancer . Results Pancreatic cancer risk gradually increased with increasing pre-diagnostic HbA1c levels up to an OR of 2.42 ( 95 % CI 1.33 , 4.39 highest [ ≥6.5 % , 48 mmol/mol ] vs lowest [ ≤5.4 % , 36 mmol/mol ] category ) , even for individuals with HbA1c levels within the non-diabetic range . C-peptide levels showed no significant relationship with pancreatic cancer risk , irrespective of fasting status . Analyses showed no clear trends towards increasing hyperglycaemia ( as marked by HbA1c levels ) or reduced pancreatic beta cell responsiveness ( as marked by C-peptide levels ) with decreasing time intervals from blood donation to cancer diagnosis . Conclusions /interpretationOur data on HbA1c show that individuals who develop exocrine pancreatic cancer tend to have moderate increases in HbA1c levels , relatively independently of obesity and insulin resistance — the classic and major risk factors for type 2 diabetes . While there is no strong difference by lag time , more data are needed on this in order to reach a firm conclusion 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 BACKGROUND Viruses ( such as Epstein-Barr virus ) and pathological conditions ( mainly involving immunosuppression ) have been shown to increase the risk of haematolymphopoietic malignancies . Other associations ( diabetes , tonsillectomy , autoimmune diseases ) have been inconsistently reported . METHODS The association between different haematolymphopoietic malignancies ( lymphomas , myelomas and leukaemias ) and the previous medical history has been studied in a population -based case-control investigation conducted in Italy , based on  face to face interviews to 2669 cases and 1718 population controls ( refusal rates 10 % and 19 % , respectively ) . Controls were a r and om sample of the general population . RESULTS Previous findings were confirmed concerning the association between non-Hodgkin 's lymphoma ( NHL ) and lupus erythematosus ( odds ratio , OR=8.4 ; 95 % CI 1.6 , 45 ) , tuberculosis ( OR=1.6 ; 1.05 , 2.5 ) and hepatitis ( 1.8 ; 1.4 , 2.3 ) . An association was found also between NHL and maternal ( OR=2.8 ; 1.1 , 6.9 ) or paternal tuberculosis ( OR=1.7 ; 0.7 , 3.9 ) . Odds ratios of 4.0 ( 1.4 , 11.8 ) and 4.4 ( 1.1 , 6.6 ) were detected for the association between NHL and Hodgkin 's disease , respectively , and previous infectious mononucleosis , but recall bias can not be ruled out . No association was found with diabetes , tonsillectomy and adenoidectomy . An association with malaria at young age and “ low grade ” lymphatic malignancies is suggested . One interesting finding was the observation of four cases of poliomyelitis among NHL patients , one among Hodgkin 's disease and one among myeloid leukaemia patients , compared with none among the controls ( Fisher 's exact test for NHL and Hodgkin 's disease , p= 0.03 , one tail ) . CONCLUSIONS Some of these findings are confirmatory of previous evidence . Other observations , such as the putative role of the polio virus and of malaria are new . A unifying theory on the mechanisms by which previous medical history may increase the risk of haematolymphopoietic malignancies is still lacking Background A large prospect i ve study in patients with type 2 diabetes ( T2D ) , the German D2C cohort , is presently being enumerated to investigate risk factors of incident cancer in diabetic patients . Study setting A disease management program was offered , on a voluntary basis , to all T2D patients who were members of a statutory health insurance fund in Germany . This first feasibility report uses data from 26.742 T2D patients , who were 40 to 79 years old , resided in the Muenster District , and who were enrolled between June 2003 and July 2008 . Cancer cases were identified through the regional Cancer Registry . Methods Invasive cancer cases were identified using probabilistic record linkage procedures and pseudonymised personal identifiers . Censoring date was December 31 , 2008 . We included only first cancers , leaving 12.650 male and 14.092 female T2D with a total of 88.778 person-years ( py ) . We computed st and ardised incidence ratios ( SIR ) for external comparisons and we employed Cox regression models and hazard ratios ( HR ) within the cohort . Results We identified 759 first cancers among male T2D patients ( 18.7 per 1,000 py ) and 605 among females ( 12.7 per 1,000 py ) . The risk of any incident cancer in T2D was raised ( SIR = 1.14 ; 95 % confidence interval [ 1.10 - 1.21 ] ) , in particular for cancer of the liver ( SIR = 1.94 [ 1.15 - 2.94 ] ) and pancreas ( SIR = 1.45 [ 1.07 - 1.92 ] ) . SIRs decreased markedly with time after T2D diagnosis . In Cox models , adjusting for diabetes duration , body mass index and sex , insulin therapy was related to higher cancer risk ( HR = 1.25 [ 1.17 - 1.33 ] ) . No effect was seen for metformin . Discussion Our study demonstrates feasibility of record linkage between DMP and cancer registries . These first cohort results confirm previous reports . It is envisaged to enhance this cohort by inclusion of further regions of the state , expansion of the follow-up times , and collection of a more detailed medication history Aims /hypothesisDespite the vast body of epidemiological literature on the risk of  cancer in people with diabetes , few studies have examined the pattern of cancer risk during different time windows following diabetes onset . The objective of the study was to examine the risks of site-specific cancer in people with incident type 2 diabetes during different time windows following diabetes onset . Methods This was a population -based retrospective cohort study . The study period was 1 April 1994 to 31 March 2006 ; censoring occurred at 31 March 2006 , at death or on departure from British Columbia , Canada . Using linked health data bases , we identified incident cohorts with and without diabetes , who were matched by age , sex and index year . Following a minimum 2-year cancer washout period , first site-specific cancers were identified prospect ively in both cohorts . Results Within 3 months following diabetes onset , participants with diabetes had significantly increased risks of colorectal , lung , liver , cervical , endometrial , ovarian , pancreatic and prostate cancers . After the initial 3-month period , the risks for colorectal ( HR 1.15 , 95 % CI 1.05 , 1.25 ) , liver ( HR 2.53 , 95 % CI 1.93 , 3.31 ) and endometrial ( HR 1.58 , 95 % CI 1.28 , 1.94 ) cancers remained significantly elevated compared with those without diabetes . The diabetes cohort remained at increased risk of pancreatic cancer in later years , but followed a different pattern : HR 3.71 at 3 months–1 year , 2.94 at 1–2 years , 1.78 at 2–3 years and 1.65 at 3–10 years ( p value for all < 0.01 ) . After an initial period of elevated risk , men with type 2 diabetes subsequently had a decreased risk of prostate cancer ( HR 0.82 , 95 % CI 0.76 , 0.88 ) . Conclusions /interpretationPeople with type 2 diabetes are at increased risk of select cancers ; this risk is particularly elevated at the time of diabetes onset , which is likely to be due to increased ascertainment OBJECTIVE To quantify the association of treated diabetes with cancer incidence and cancer mortality as well as cancer case fatality and all-cause mortality in adults who subsequently develop cancer and to calculate attributable fractions due to diabetes on various cancer outcomes . RESEARCH DESIGN AND METHODS Prospect i ve data on 599 diabetic and 17,681 nondiabetic adults from the CLUE II ( Give Us a Clue to Cancer and Heart Disease ) cohort in Washington County , Maryl and , were analyzed . Diabetes was defined by self-reported use of diabetes medications at baseline . Cancer incidence was ascertained using county and state cancer registries .  Mortality data were obtained from death certificates . RESULTS From 1989 to 2006 , 116 diabetic and 2,365 nondiabetic adults developed cancer , corresponding to age-adjusted incidence of 13.25 and 10.58 per 1,000 person-years , respectively . Adjusting for age , sex , education , BMI , smoking , hypertension treatment , and high cholesterol treatment using Cox proportional hazards regression , diabetes was associated with a higher risk of incident cancer ( hazard ratio 1.22 [ 95 % CI 0.98–1.53 ] ) and cancer mortality ( 1.36 [ 1.02–1.81 ] ) . In individuals who developed cancer , adults with diabetes had a higher risk of cancer case fatality ( 1.34 [ 1.002–1.79 ] ) and all-cause mortality ( 1.61 [ 1.29–2.01 ] ) . For colorectal , breast , and prostate cancers , the attributable fractions result ing from diabetes were larger for cancer fatality and mortality than cancer incidence . CONCLUSIONS In this 
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The findings were similar for men and women , and unrelated to study design .
Meta-regression analyses showed limited effect modification of body mass index , and possible effect modification of age , gender , with some influence of study characteristics ( population source , cancer- and diabetes ascertainment ) .
The systematic review and meta- analysis confirm the previous results of increased cancer risk in diabetes and extend this to additional cancer sites .