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The relationship between high plasma high-density lipoprotein cholesterol (HDL-C) and cause and mortality are not well established in healthy older people. This study examined the associations between HDL-C levels and mortality in initially healthy older men and women. This analysis included participants from the Aspirin in Reducing Events in the Elderly (ASPREE; n=18,668) trial and a matched cohort from the UK Biobank (UKB; n=62,849 ≥65 years). Cox regression was used to examine hazard ratios between HDL-C categories <1.03 mmol/L, 1.03–1.55 mmol/L (referent category), 1.55–2.07 mmol/L, and >2.07 mmol/L and all-cause, cancer, cardiovascular disease (CVD), and "non-cancer non-CVD" mortality. Genetic contributions were assessed using a polygenic score for HDL-C. Among ASPREE participants (aged 75±5 years), 1836 deaths occurred over a mean follow-up of 6.3±1.8 years. In men, the highest category of HDL-C levels was associated with increased risk of all-cause (HR 1.60, 95% CI 1.26–2.03), cancer (HR 1.37, 95% CI 0.96–2.00), and "non-cancer non-CVD" mortality (HR 2.35, 95% CI 1.41–3.42) but not CVD mortality (HR 1.08, 95% CI 0.60–1.94). The associations were replicated among UKB participants (aged 66.9±1.5 years), including 8739 deaths over a mean follow-up of 12.7±0.8 years. There was a non-linear association between HDL-C levels and all-cause and cause-specific mortality. The association between HDL-C levels and mortality was unrelated to variations in the HDL-C polygenic score. No significant association was found between HDL-C levels and mortality in women. Higher HDL-C levels are associated with increased risk from cancer and "non-cancer non-CVD" mortality in healthy older men but no such relationship was observed in women. [ABSTRACT FROM AUTHOR]

3,5,6-trichloropyridinol (TCPY) is a metabolite of chlorpyrifos and chlorpyrifos-methyl, whose presence in the environment is of potential toxicity to human. So, it is need to monitor and regualte TCPY levels to protect human health. However, it is not known whether TCPY is associated with all-cause and cancer mortality and to which degree its levels contributed to hazard risk. The study enrolled 3951 participants from the National Health and Nutrition Examination Surveys (NHANES). Ultra-high performance liquid chromatography coupled with electrospray ionization tandem mass spectrometry was used to measure urinary TCPY. Cox proportional hazards regression analysis was performed to explore the associations between TCPY and all-cause and cancer mortality. The study found that the average level of TCPY in the cohort was 1.79 μg/L and was higher in those who had passed away. Individuals in the highest quartile had a 1.56-fold independent increase in rate for all-cause mortality compared to those in the lowest quartile (hazard ratio [HR] 1.56, 95% confidence interval 1.09–2.24, p = 0.002). However, while the univariate model showed a hazard ratio of 2.37 (1.19–4.71) for the highest quartile in regards to cancer mortality, this association disappeared after adjusting for demographics, lifestyles, and comorbidities. Exposure to urinary 3,5,6-trichloropyridinol, as a result of insecticide exposure, increased the rate of all-cause mortality but was not independently associated with cancer mortality. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Diabetes is associated with an increased risk of cancer. Prostasin is an epithelial sodium channel stimulator that has been associated with suppression of tumours, glucose metabolism and hyperglycaemia-associated tumour pathology. However, the association between prostasin, diabetes and cancer mortality has not been well investigated in humans. We aim to investigate the associations between plasma prostasin and diabetes, and to explore whether prostasin has an effect on cancer mortality risk in individuals with hyperglycaemia. Methods: Plasma prostasin was measured using samples from the Malmö Diet and Cancer Study Cardiovascular Cohort, and statistical analysis was performed from both sex-specific quartiles and per 1 SD. The cross-sectional association between plasma prostasin and diabetes was first studied in 4658 participants (age 57.5 ± 5.9 years, 39.9% men). After excluding 361 with prevalent diabetes, the associations of prostasin with incident diabetes and cancer mortality risk were assessed using Cox regression analysis. The interactions between prostasin and blood glucose levels as well as other covariates were tested. Results: The adjusted OR for prevalent diabetes in the 4th vs 1st quartile of prostasin concentrations was 1.95 (95% CI 1.39, 2.76) (p for trend <0.0001). During mean follow-up periods of 21.9 ± 7.0 and 23.5 ± 6.1 years, respectively, 702 participants developed diabetes and 651 died from cancer. Prostasin was significantly associated with the incidence of diabetes. The adjusted HR for diabetes in the 4th vs 1st quartile of prostasin concentrations was 1.76 (95% CI 1.41, 2.19) (p for trend <0.0001). Prostasin was also associated with cancer mortality There was a significant interaction between prostasin and fasting blood glucose for cancer mortality risk (p for interaction =0.022), with a stronger association observed in individuals with impaired fasting blood glucose levels at baseline (HR per 1 SD change 1.52; 95% CI 1.07, 2.16; p=0.019). Conclusions/interpretation: Plasma prostasin levels are positively associated with diabetes risk and with cancer mortality risk, especially in individuals with high blood glucose levels, which may shed new light on the relationship between diabetes and cancer. [ABSTRACT FROM AUTHOR]

Purpose: Insulin levels play an important role in cancer development. However, the link between an insulinogenic diet and cancer is still unclear. Therefore, we performed a systematic review with meta-analysis to investigate the association between dietary insulin index (II) and load (IL) with cancer risk and mortality. Methods: A comprehensive search between electronic databases (Web of Science, PubMed/Medline, Scopus, and Google Scholar) was conducted to identify relevant studies up to January 2022. The relative risks (RR) and Odds ratios (OR) were extracted from eligible studies, and meta-analysis was performed to calculate the pooled effect size. Result: 12 papers including 14 studies (10 cohorts and 4 case–control) were included for the meta-analysis. Among them, 10 studies reported effect size for the risk of cancer, and 4 studies reported effect size for cancer mortality. We observed no significant association between II and IL with cancer overall (RRII: 1.03, 95%CI: 0.91–1.17, RRIL: 1.16, 95%CI: 0.94–1.42) and in cohort studies, however, in case–control studies was related with higher odds of cancer (ORII: 2.30, 95%CI: 1.21–4.38, ORIL: 2.57, 95%CI: 1.64–4.02). Higher II and IL scores were associated with the increased risk of total (RRII: 1.29, 95%CI: 1.02–1.63) and (RRIL: 1.39, 95%CI: 1.06–1.83) and colorectal cancer mortality (RRII: 1.29, 95%CI: 1.13–1.48) and (RRIL: 1.37, 95%CI: 1.18–1.60). Conclusion: Higher dietary II and IL were not associated with cancer risk in overall and cohort studies, whereas related with a higher risk of cancer in case–control studies. We observed a significant positive relation of II and IL with cancer mortality, especially CRC mortality. [ABSTRACT FROM AUTHOR]

The objective of this study was to investigate whether leukocyte telomere length (LTL) predicts the risk for cancer mortality among American Indians participating in the Strong Heart Study (1989–1991). Participants (aged 45–74 years) were followed annually until December 2015 to collect information on morbidity/mortality. LTL was measured by qPCR using genomic DNA isolated from peripheral blood. The association between LTL and risk for cancer mortality was examined using a multivariable Cox proportional hazard model, adjusting for age, gender, education, study site, smoking, alcohol use, physical activity, systolic blood pressure, fasting blood glucose, obesity, and low- and high-density lipoprotein. Of 1945 participants (mean age 56.10 ± 8.17 at baseline, 57% women) followed for an average 20.5 years, 220 died of cancer. Results showed that longer LTL at baseline significantly predicts an increased risk of cancer death among females (HR 1.57, 95% CI 1.08–2.30), but not males (HR 0.74, 95% CI 0.49–1.12) (p for interaction 0.009). Specifically, compared with the women with the longest LTL (fourth quartile), those in the third, second, and first quartiles showed 53%, 41%, and 44% reduced risk for cancer death, respectively. The findings highlight the importance of sex-specific analysis in future telomere research. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: The aims of the study were to evaluate the association between type 2 diabetes and the risk of death from any cancer and specific cancers in East and South Asians. Methods: Pooled analyses were conducted of 19 prospective population-based cohorts included in the Asia Cohort Consortium, comprising data from 658,611 East Asians and 112,686 South Asians. HRs were used to compare individuals with diabetes at baseline with those without diabetes for the risk of death from any cancer and from site-specific cancers, including cancers of the oesophagus, stomach, colorectum, colon, rectum, liver, bile duct, pancreas, lung, breast, endometrium, cervix, ovary, prostate, bladder, kidney and thyroid, as well as lymphoma and leukaemia. Results: During a mean follow-up of 12.7 years, 37,343 cancer deaths (36,667 in East Asians and 676 in South Asians) were identified. Baseline diabetes status was statistically significantly associated with an increased risk of death from any cancer (HR 1.26; 95% CI 1.21, 1.31). Significant positive associations with diabetes were observed for cancers of the colorectum (HR 1.41; 95% CI 1.26, 1.57), liver (HR 2.05; 95% CI 1.77, 2.38), bile duct (HR 1.41; 95% CI 1.04, 1.92), gallbladder (HR 1.33; 95% CI 1.10, 1.61), pancreas (HR 1.53; 95% CI 1.32, 1.77), breast (HR 1.72; 95% CI 1.34, 2.19), endometrium (HR 2.73; 95% CI 1.53, 4.85), ovary (HR 1.60; 95% CI 1.06, 2.42), prostate (HR 1.41; 95% CI 1.09, 1.82), kidney (HR 1.84; 95% CI 1.28, 2.64) and thyroid (HR 1.99; 95% CI 1.03, 3.86), as well as lymphoma (HR 1.39; 95% CI 1.04, 1.86). Diabetes was not statistically significantly associated with the risk of death from leukaemia and cancers of the bladder, cervix, oesophagus, stomach and lung. Conclusions/interpretation: Diabetes was associated with a 26% increased risk of death from any cancer in Asians. The pattern of associations with specific cancers suggests the need for better control (prevention, detection, management) of the growing epidemic of diabetes (as well as obesity), in order to reduce cancer mortality. [ABSTRACT FROM AUTHOR]

Aims We assessed the impact of the combination of type 2 diabetes (T2DM) and smoking on total cancer mortality using cohort data of a general Japanese population. Methods Of 1908 residents who received health checkups in two towns in 1994, 794 males were included as study participants. Smoking status was defined as three categories: never smoker, ex-smoker and current smoker. Individuals with T2DM were defined as individuals with fasting plasma glucose C7.0 mmol/l and/or receiving medication for T2DM. Participants were divided into six groups according to T2DM and smoking status: non-DM (NDM) and never smoker, NDM and ex-smoker, NDM and current smoker, DM and never smoker, DM and ex-smoker, and DM and current smoker groups. All participants were followed up for a maximum of 13 years. We calculated the hazard ratio (HR) using Cox's proportional hazard model and subhazard ratio (SHR) using competing risk regression analyses in each group. Results During the follow-up period, there were 169 allcause deaths (62 cancer deaths and 40 CVD deaths). When using Cox regression analysis, HRs were higher in the ex-smoker and current smoker groups than in the never-smoker group, and HRs were also higher in the DM groups than in the NDM groups. When using competing risk analysis, SHRs were almost the same as the HRs of Cox regression analysis (DM and ex-smoker 6.06, DM and current smoker 10.12). Conclusions The combination of T2DM and smoking is a strong risk factor for total cancer mortality in Japanese men. [ABSTRACT FROM AUTHOR]

Abstract: Background: Cancer continues to rise as a contributor to premature death in the developing world. Despite this, little is known about whether cancer outcomes are related to a country’s income level, and what aspects of national healthcare systems are associated with improved cancer outcomes. Methods: The most recent estimates of cancer incidence and mortality were used to calculate mortality-to-incidence ratio (MIR) for the 85 countries with reliable data. Countries were categorized according to high-income (Gross Domestic Product (GDP)>$15,000) or middle/low-income (GDP<$15,000), and a multivariate linear regression model was used to determine the association between healthcare system indicators and cancer MIR. Indicators study included per capita GDP, overall total healthcare expenditure (THE), THE as a proportion of GDP, total external beam radiotherapy devices (TEBD) per capita, physician density, and the year 2000 WHO healthcare system rankings. Results: Cancer MIR in high-income countries (0.47) was significantly lower than that of middle/low-income countries (0.64), with a p <0.001. In high-income countries, GDP, health expenditure and TEBD showed significant inverse correlations with overall cancer MIR. A $3040 increase in GDP (p =0.004), a $379 increase in THE (p <0.001), or an increase of 0.59 TEBD per 100,000 population (p =0.027) were all associated with a 0.01 decrease in cancer MIR. In middle/low-income countries, only WHO scores correlated with decreased cancer MIR (p =0.022); 12 specific cancer types also showed similar significant correlations (p <0.05) as overall cancer MIR. Conclusions: The analysis of this study suggested that cancer MIR is greater in middle/low-income countries. Furthermore, the WHO healthcare score was associated with improved cancer outcomes in middle/low-income countries while absolute levels of financial resources and infrastructure played a more important role in high-income countries. [Copyright &y& Elsevier]

BACKGROUND: Recent data suggest that aspirin may be effective for reducing cancer mortality. OBJECTIVE: To examine whether including a cancer mortality-reducing effect influences which men would benefit from aspirin for primary prevention. DESIGN: We modified our existing Markov model that examines the effects of aspirin among middle-aged men with no previous history of cardiovascular disease or diabetes. For our base case scenario of 45-year-old men, we examined costs and life-years for men taking aspirin for 10 years compared with men who were not taking aspirin over those 10 years; after 10 years, we equalized treatment and followed the cohort until death. We compared our results depending on whether or not we included a 22 % relative reduction in cancer mortality, based on a recent meta-analysis. We discounted costs and benefits at 3 % and employed a third party payer perspective. MAIN MEASURE: Cost per quality-adjusted life year (QALY) gained. KEY RESULTS: When no effect on cancer mortality was included, aspirin had a cost per QALY gained of $22,492 at 5 % 10-year coronary heart disease (CHD) risk; at 2.5 % risk or below, no treatment was favored. When we included a reduction in cancer mortality, aspirin became cost-effective for men at 2.5 % risk as well (cost per QALY, $43,342). Results were somewhat sensitive to utility of taking aspirin daily; risk of death after myocardial infarction; and effects of aspirin on stroke, myocardial infarction, and sudden death. However, aspirin remained cost-saving or cost-effective (< $50,000 per QALY) in probabilistic analyses (59 % with no cancer effect included; 96 % with cancer effect) for men at 5 % risk. CONCLUSIONS: Including an effect of aspirin on cancer mortality influences the threshold for prescribing aspirin for primary prevention in men. If such an effect is real, many middle-aged men at low cardiovascular risk would become candidates for regular aspirin use. [ABSTRACT FROM AUTHOR]

Background: Studies conducted in Western countries have found a robust association between higher social support and improved cancer outcomes, particularly for breast cancer incidence and prognosis. However, less is known about the influence of social support on cancer among Asian populations where the measures of social support may differ in social relationships. In this prospective cohort study in Japan, we sought to examine the associations between the incidence and mortality of total and site-specific cancer. Methods: We examined prospectively the association between social support and risk of cancer incidence and mortality within a cohort of 44,152 Japanese men and women, aged 40-69 years, free of prior diagnosis of cancer and cardiovascular disease. Social support was measured by emotional support defined as receipt of confidant support and esteem support from family members or friends and by social isolation. A total of 3,444 cases of newly diagnosed cancer and 1,561 cancer deaths occurred between the baseline questionnaire (1993-1994) and the end of follow-up in January 2004. Results: The multivariate hazard ratios (HR) and 95 % confidence intervals for colorectal cancer incidence and mortality in the highest social support versus lowest social support group were 1.48 (1.06-2.05) and 3.07 (1.65-5.69) in men, respectively. Social support was not associated with other site-specific cancer incidence or cancer outcomes in women. Conclusions: Low social support was associated with higher risk of both colorectal cancer incidence and mortality in men. Social support may affect colorectal cancer onset and prognosis via a range of factors, including healthier lifestyles as well as adherence to therapeutic regimens. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Proinsulin is possibly associated with cancer through activation of insulin receptor isoform A. We sought to investigate the associations between proinsulin and 20 year cancer mortality rates. Methods: The study was performed within the Hoorn Study, a population-based study of glucose metabolism in individuals aged 50-75 years in the Dutch population. Fasting proinsulin levels were measured twice by a double-antibody radioimmunoassay. Participants were continuously followed to register mortality; causes of death were derived from medical records. Cox survival analyses were performed to assess the 20 year risk of death from cancer in relation to proinsulin. All analyses were adjusted for age and sex, with additional adjustments for traditional risk factors. The effect modification of glucose metabolism and sex was tested. Results: Proinsulin levels were measured in 438 individuals (41% normal glucose tolerance, 35.7% impaired glucose metabolism, 23.3% type 2 diabetes). Of these participants, 53 died from cancer. After adjustment for age and sex, proinsulin >16.5 pmol/l (the upper tertile) was significantly associated with a twofold risk of cancer mortality (HR 2.01, 95% CI 1.16, 3.46) compared with individuals with lower proinsulin levels. Additional adjustment for glucose metabolism, BMI and smoking did not substantially change the results (HR 1.91, 95% CI 1.04, 3.52). No interaction with glucose metabolism or sex was observed. Conclusions/interpretation: Individuals with fasting proinsulin levels >16.5 pmol/l have a twofold risk of cancer mortality over a 20 year time span. These findings provide population-based evidence for the independent association between high proinsulin levels and cancer mortality rates. [ABSTRACT FROM AUTHOR]

Purpose: Cancer is the second leading cause of death in the United States and mortality varies by ethnicity. The objective of this study was to examine the association between cancer mortality and dietary intake among a large multiethnic population. Methods: A prospective cohort design was used to examine cancer mortality among 146,389 participants. Multiethnic cohort study participants represent five ethnic groups: African American, Native Hawaiian, Japanese American, Latino, and Caucasian. Hazard ratios for cancer mortality by intake levels of five food groups and discretionary fat were calculated using Cox proportional hazards models stratified by sex and ethnicity. Results: There were a total of 2,028 male and 1,464 female fatal cancer cases at the end of follow-up. Among Japanese American men only, there was a significant protective effect seen in those reporting a high grain intake (HR = 0.49, 95 % CI 0.35-0.69); there was no effect of grain consumption in any other ethnic-sex group. There was no evidence that ethnicity modified associations between fruit, vegetable, meat, dairy, or discretionary fat intake and cancer mortality among men. Associations between food group consumption and risk for cancer mortality among women were similar across ethnic groups. Conclusions: The considerable reduction in cancer risk associated with high grain consumption among a specific ethnic-sex group, Japanese American men, warrants further investigation. Additional research is needed to validate this observation and determine whether this was a chance finding, or possibly due to differential intake of specific grain subtypes, and/or related to a sex-specific cancer type. [ABSTRACT FROM AUTHOR]

The aim of this study on cancer mortality among Turkish immigrants, for the first time, traditional comparisons in migrant health research have been extended simultaneously in two ways. First, comparisons were made to cancer mortality from the immigrants' country of origin and second, cancer mortality among Turkish immigrants across four host countries (Belgium, Denmark, France and the Netherlands) was compared. Population-based cancer mortality data from these countries were included. Age-standardized mortality rates were computed for the local-born and Turkish population of each country. Relative differences in cancer mortality were examined by fitting country-specific Poisson regression models. Globocan data on cancer mortality in Turkey from 2008 were used in order to compare mortality rates of Turkish immigrants with those from their country of origin. Turkish immigrants had lower all-cancer mortality than the local-born populations of their host countries, and mortality levels comparable to all-cancer mortality rates in Turkey. In the Netherlands and France breast cancer mortality was consistently lower in Turkish immigrants women than among local-born women. Lung cancer mortality was slightly lower in Turkish immigrants in the Netherlands and France but varied considerably between migrants in these two host countries. Stomach cancer mortality was significantly higher in Turkish immigrants when compared to local-born French and Dutch. Our findings indicate that exposures both in the country of origin and in the host country can have an effect on the cancer mortality of immigrants. Despite limitations affecting any cross-country comparison of mortality, the innovative multi-comparison approach is a promising way to gain further insights into determinants of trends in cancer mortality of immigrants. [ABSTRACT FROM AUTHOR]

Objectives: Metalworking fluids (MWFs) have been associated with cancer of several sites, but the risks have been primarily examined in men or in studies that adjusted for gender in analyses. To evaluate whether risks were similar in women, we report cancer mortality risk among 4,825 female autoworkers within the united autoworkers-general motors autoworkers cohort. Methods: Standardized mortality rates (SMRs) were calculated based on Michigan death rates (1980-2004). Internal comparisons (1941-2004) were examined using Cox regression for straight, soluble, and synthetic MWFs, and their corresponding oil- and water-based fractions. Results: MWF exposure levels in the female cohort were generally less than two-third the MWF levels in the male cohort. Female autoworkers had an excess of cancer from all sites (SMR, 1.10; 95 % confidence interval (CI), 0.98-1.22) and lung cancer (SMR, 2.08; 95 % CI, 1.71-2.52). Colon cancer risk increased with straight (mineral oil) MWF exposure (exposure > median; hazard ratio = 3.1; 95 % CI, 1.2-8.0). A protective effect was observed for ovarian cancer with the soluble MWFs and water-based MWF metrics. Although bladder, rectal, and laryngeal cancers and malignant melanoma have been associated with straight MWF exposure and pancreatic cancer with synthetic MWF in men, there were too few deaths in this female subcohort to examine exposure-response relations for these sites. Results were null for lung and breast cancer. Conclusions: Our findings support an association between colon cancer and straight MWFs, but we found limited evidence of risk for other tumor sites at the lower exposure levels experienced by the female autoworkers. [ABSTRACT FROM AUTHOR]

Objectives of study: To test recent claims that cancer inequities are bound to increase as population health improves. Methods: We analyzed 1960-2006 age-standardized US county cancer mortality data, total and site-specific (lung, prostate, colorectal, breast, cervix, stomach), stratified by county income quintile for the US total, black, and white populations. Results: Between 1960 and 2006, US socioeconomic inequities in cancer mortality variously shrunk, widened, reversed, and stagnated, depending on time period and cancer site. For all cancers combined and most, but not all, sites, absolute, but not relative, socioeconomic gaps were greater for the black compared to white population. Compared to the yearly age-specific mortality rates among whites in the most affluent counties, the percent of excess cancer deaths among whites in the lower four county income quintiles first rose above 0 in 1990 and in 2006 equaled 5.4% (95% CI 4.8, 6.0); among blacks, it rose from 6.0% (95% CI 4.5, 7.4) in 1960 to 24.7% (95% CI 23.9, 25.5) in 1990 and remained at this level through 2006. Conclusions: The hypothesis that cancer mortality inequities are bound to increase is refuted by long-term data on total and site-specific cancer mortality stratified by socioeconomic position and race/ethnicity. [ABSTRACT FROM AUTHOR]

We investigated the association of undiagnosed diabetes, previously known diabetes and prediabetes (WHO 1999 classification) with all-cause and cause-specific mortality in an older German population. Previous study results for mortality in patients with very low levels of HbA1c, fasting plasma glucose (FPG), and 2-h plasma glucose (2hPG) are still inconclusive. Thus we have extended the analyses to continuous measures of glycemia. A total of 1,466 subjects aged 55-74 years from the population-based KORA survey S4 (conducted from 1999 to 2001) were included in our observational mortality study (152 subjects with previously known diabetes, and 1,314 further subjects who underwent oral glucose tolerance tests). Mortality was followed up for a maximum of 10.0 years (median follow-up 8.8 years). A total of 180 (12.3%) of the 1,466 subjects have died during the follow-up period. The age- and sex-adjusted hazard ratios for all-cause mortality were 2.6 (95%CI, 1.7-3.8) for known diabetes, 2.8 (95%CI, 1.7-4.4) for undiagnosed diabetes, and 1.1 (95%CI, 0.8-1.7) for prediabetes [reference: normal glucose tolerance (NGT)]. After multivariable adjustment, undiagnosed diabetes was associated with 3.0-fold increased cancer mortality, 1.1-fold increased cardiovascular mortality, and 4.7-fold increased non-cancer, non-cardiovascular mortality compared with NGT. For HbA1c, FPG, and 2hPG, J-shaped associations with all-cause mortality were observed. Undiagnosed diabetes is associated with increased all-cause, cancer, and non-cancer non-cardiovascular mortality, but not with cardiovascular mortality in this older population. All-cause mortality in undiagnosed diabetes is similar to that in previously known diabetes but much higher than mortality in prediabetes and NGT. [ABSTRACT FROM AUTHOR]

ims/hypothesis: The purpose of this study was to explore the relationship between hyperglycaemia in type 2 diabetes and risk of cancer incidence or cancer mortality. We were interested to determine if data from major randomised controlled trials would support a hypothesis that improving glycaemic control may reduce the risk of cancer outcomes. Methods: We included major randomised controlled trials conducted with an overall aim of intensified glycaemic control in type 2 diabetes. We abstracted data from published papers and supplemental material and conducted separate meta-analyses of cancer mortality and cancer incidence. Results: Four trials reported cancer mortality for the intensive (222 events in 53,892 person-years) and standard control (155 events in 38,743 person-years) arms (UK Prospective Diabetes Study [UKPDS] 33, UKPDS 34, Action to Control Cardiovascular Risk in Diabetes [ACCORD] and Veterans Affairs Diabetes Trial [VADT]); the summary risk ratio for cancer mortality was 1.00 (95% CI 0.81-1.24; I = 0%). Excluding the UKPDS metformin trial resulted in a pooled risk estimate of 1.03 (95% CI 0.83-1.29; I = 0%). Three trials reported cancer incidence for the study arms (Action in Diabetes and Vascular Disease: Preterax and Diamicron MR Controlled Evaluation [ADVANCE], PROspective pioglitAzone Clinical Trial In macroVascular Events [PROactive], Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycaemia in Diabetes [RECORD]) with 357 events in 47,974 person-years with improved glycaemic control and 380 events in 45,009 person-years in the control arms; the pooled risk ratio for cancer incidence was 0.91 (95% CI 0.79-1.05; I = 0%). Conclusions/interpretation: Data from large randomised controlled trials of intensified glycaemic control suggest that cancer risk is not reduced by improving glycaemic control in type 2 diabetes. These data therefore do not support the hypothesis that hyperglycaemia is causally linked to increased cancer risk. [ABSTRACT FROM AUTHOR]

We explored the relationship between glucose-lowering agents and cancer mortality rates in type 2 diabetes patients, hypothesising a decreased risk of cancer mortality with metformin use and a dose–risk gradient for insulin therapy. This was a population-based cohort study using administrative data from Saskatchewan Health, Canada. We identified new users of metformin or sulfonylureas from 1 January 1991 to 31 December 1996, with follow-up until death, departure from the province or 31 December 1999. Cox regression analyses were used to estimate the HR of death from cancer, accounting for time-varying exposure to metformin, sulfonylurea, and exogenous insulin therapy. We identified 10,309 new users of metformin or sulfonylurea. The average follow-up was 5.4 (1.9) years, during which 407 (4.0%) cancer deaths occurred. Adjusting for age, sex and chronic disease score, the adjusted HR for metformin use was 0.80 (95% CI 0.65–0.98) compared with sulfonylurea monotherapy users. Adjusted HRs for subsequent insulin use were 2.22 (0.99–5.00), 3.33 (2.26–4.89) and 6.40 (4.69–8.73) for <3, 3 to 11 and ≥12 insulin dispensations/year, respectively, compared with patients not on insulin. We observed a similar risk gradient among the sub-cohort of new insulin users. Our results support previous reports of a decreased risk of cancer outcomes associated with metformin use relative to sulfonylurea monotherapy. We also provide new evidence of a gradient of cumulative insulin dispensations and cancer mortality rates. [ABSTRACT FROM AUTHOR]

Risk of cancer is increased in conditions associated with insulin resistance, but this could be secondary to subclinical inflammation. We evaluated whether insulinemia, indices of insulin resistance or a validated insulin resistance-related biomarker cluster, could predict cancer mortality independently of subclinical inflammation. Fasting insulin and glucose concentrations and insulin-related metabolic variables were recorded in 1,016 white males, of whom 718 also had an oral glucose tolerance test (OGTT). Baseline measurements included the following: fasting insulin and the derived insulin resistance index, HOMA-IR; OGTT insulin and the derived insulin resistance index, Matsuda-IS; the factor score for a validated insulin resistance-related biomarker cluster; white blood cell count; erythrocyte sedimentation rate; and serum albumin and globulin concentrations. There were 105 deaths from cancer during the 21.5-year mean follow-up. Insulin concentrations and insulin resistance were not predictive. Insulin resistance-related biomarker clustering predicted cancer mortality (hazard ratio 1.65, 95% CI 1.26–2.17, p < 0.001). Subclinical inflammation markers were also predictive, but the insulin resistance-related biomarker cluster predicted cancer mortality independently of these and was particularly associated with death from colorectal cancer. Despite insulin concentrations or derived indices of insulin resistance failing to predict cancer mortality, insulin resistance-related biomarker clustering was highly predictive and predicted independently of simple measures of subclinical inflammation. [ABSTRACT FROM AUTHOR]

Background: Cancer mortality has been examined among ethnic South Asian migrants in England and Wales, but not by generation of migration.Methods: Using South Asian mortality records, identified by a name-recognition algorithm, and census information, age-standardised rates among South Asians, and South Asian vs non-South Asian rate ratios, were calculated.Results and Conclusions: All-cancer rates in ethnic South Asians were half of those in non-South Asians in first-generation (all-cancer-standardised mortality ratio (SMR) in males 0.51 and in females 0.56) and subsequent-generation South Asians (SMR in males 0.43 and in females 0.36). The higher mortality in first-generation South Asians for liver (both sexes), oral cavity and gallbladder cancer (females), particularly marked among Bangladeshis, was reduced in subsequent generations. [ABSTRACT FROM AUTHOR]

Insulin and glucose may influence cancer mortality via their proliferative and anti-apoptotic properties. Using longitudinal data from the nationally representative Third National Health and Nutrition Examination Survey (NHANES III; 1988-1994), with an average follow-up of 8.5 years to death, we evaluated markers of glucose and insulin metabolism, with cancer mortality, ascertained using death certificates or the National Death Index. Plasma glucose, insulin, C-peptide, and lipid concentrations were measured. Anthropometrics, lifestyle, medical, and demographic information was obtained during in-person interviews. After adjusting for age, race, sex, smoking status, physical activity, and body mass index, for every 50 mg/dl increase in plasma glucose, there was a 22% increased risk of overall cancer mortality. Insulin resistance was associated with a 41% (95% confidence interval (CI) (1.07-1.87; p = 0.01) increased risk of overall cancer mortality. These associations were stronger after excluding lung cancer deaths for insulin-resistant individuals (HR: 1.67; 95% CI: 1.15-2.42; p = 0.01), specifically among those with lower levels of physical activity (HR: 2.06; 95% CI: 1.4-3.0; p = 0.0001). Similar associations were observed for other blood markers of glucose and insulin, albeit not statistically significant. In conclusion, hyperglycemia and insulin resistance may be 'high-risk' conditions for cancer mortality. Managing these conditions may be effective cancer control tools. [ABSTRACT FROM AUTHOR]

This study compares cancer mortality and incidence of ethnic German migrants from the Former Soviet Union (FSU) in Germany. Data were obtained from two migrant cohorts residing in the federal state of North Rhine-Westphalia (NRW) ( n = 34,393) and Saarland ( n = 18,619). Vital status of the NRW cohort was ascertained through local population registries. Causes of death were obtained from the NRW statistical office or from local health offices. Cancer incidence of the Saarland cohort was derived from the Saarland cancer registry using record linkage. From 1990 to 2005, we observed 708 cancer deaths and 586 incident cancer cases. In males, both cancer incidence and cancer mortality were similar to the German population. Female cancer incidence and mortality were lower, the latter significantly. Site-specific standardized mortality and incidence ratios showed great variation in comparison to Germans and were remarkably similar to each other for most sites. Lung cancer was elevated among males, but lower among females. Stomach cancer was higher contrasting with lower ratios for prostate cancer, male colorectal cancer, and female breast cancer. Results confirm that FSU-migrants suffer from cancers, which may be prevented by prevention programs. Furthermore, we cannot conclude a different health-seeking behavior compared to Germans. [ABSTRACT FROM AUTHOR]

Background: African Americans have higher cancer mortality rates than whites. Understanding the relative contribution of cancer incidence, stage at diagnosis and survival after diagnosis to the racial gap in life expectancy has important implications for directing future health disparity interventions toward cancer prevention, screening and treatment.Objective: We estimated the degree to which higher cancer mortality among African Americans is due to higher incidence rates, later stage at diagnosis or worse survival after diagnosis.Design: Stochastic model of cancer incidence and survival after diagnosis.Patients: Surveillance and Epidemiology End Result cancer registry and National Health Interview Survey data.Measurements: Life expectancy if African Americans had the same cancer incidence, stage and survival after diagnosis as white adults.Results: African-American men and women live 1.47 and 0.91 fewer years, respectively, than whites as the result of all cancers combined. Among men, racial differences in cancer incidence, stage at diagnosis and survival after diagnosis account for 1.12 (95% CI: 0.52 to 1.36), 0.17 (95% CI: -0.03 to 0.33) and 0.21 (95% CI: 0.05 to 0.34) years of the racial gap in life expectancy, respectively. Among women, incidence, stage and survival after diagnosis account for 0.41 (95% CI: -0.29 to 0.60), 0.26 (95% CI: -0.06 to 0.40) and 0.31 (95% CI: 0.05 to 0.40) years, respectively. Differences in stage had a smaller impact on the life expectancy gap compared with the impact of incidence. Differences in cancer survival after diagnosis had a significant impact for only two cancers-breast (0.14 years; 95% CI: 0.05 to 0.16) and prostate (0.05 years; 95% CI 0.01 to 0.09).Conclusions: In addition to breast and colorectal cancer screening, national efforts to reduce disparities in life expectancy should also target cancer prevention, perhaps through smoking cessation, and differences in survival after diagnosis among persons with breast and prostate cancer. [ABSTRACT FROM AUTHOR]

We used longitudinal mortality data sets for the 1990s to compare socioeconomic inequalities in total cancer mortality between women and men aged 30-74 in 12 different European populations (Madrid, Basque region, Barcelona, Slovenia, Turin, Switzerland, France, Belgium, Denmark, Norway, Sweden, Finland) and to investigate which cancer sites explain the differences found. We measured socioeconomic status using educational level and computed relative indices of inequality (RII). We observed large variations within Europe for educational differences in total cancer mortality among men and women. Three patterns were observed: Denmark, Norway and Sweden (significant RII around 1.3-1.4 among both men and women); France, Switzerland, Belgium and Finland (significant RII around 1.7-1.8 among men and around 1.2 among women); Spanish populations, Slovenia and Turin (significant RII from 1.29 to 1.88 among men; no differences among women except in the Basque region, where RII is significantly lower than 1). Lung, upper aerodigestive tract and breast cancers explained most of the variations between gender and populations in the magnitude of inequalities in total cancer mortality. Given time trends in cancer mortality, the gap in the magnitude of socioeconomic inequalities in cancer mortality between gender and between European populations will probably decrease in the future. [ABSTRACT FROM AUTHOR]

We analysed data from a cohort of 1966 subjects (889 men and 1,077 women) employed by an Italian asbestos (mainly textile) company in the period 1946-1984, who were followed-up to 2004. A total of 62,025 person-years of observation were recorded. We computed standardised mortality ratios (SMR) for all causes and selected cancer sites using national death rates for each 5-year calendar period and age group. There were 68 deaths from mesothelioma (25 men and 43 women, 39 pleural and 29 peritoneal) vs 1.6 expected (SMR=4,159), and 109 from lung cancer vs 35.1 expected (SMR=310). The SMRs of pleural/peritoneal cancer were 6661 for subjects exposed only before 30 years of age, 8,019 for those first exposed before 30 and still employed at 30-39 years of age and 5,786 for those first exposed before 30 and still employed at 40 or more years of age. The corresponding SMRs for lung cancer were 227, 446 and 562. The SMR of mesothelioma was strongly related to time since first exposure. The SMR of lung cancer, but not of mesothelioma, appeared to be related to subsequent exposures. [ABSTRACT FROM AUTHOR]

Mortality from all cancers combined and major cancers among men and women aged 20 years and over was compared by country of birth with that of the whole of England and Wales as the reference group. Population data from the 2001 Census and mortality data for 2001–2003 were used to estimate standardised mortality ratios. Data on approximately 399 000 cancer deaths were available, with at least 400 cancer deaths in each of the smaller populations. Statistically significant differences from the reference group included: higher mortality from all cancers combined, lung and colorectal cancer among people born in Scotland and Ireland, lower mortality for all cancers combined, lung, breast and prostate cancer among people born in Bangladesh (except for lung cancer in men), India, Pakistan or China/Hong Kong, lower lung cancer mortality among people born in West Africa or the West Indies, higher breast cancer mortality among women born in West Africa and higher prostate cancer mortality among men born in West Africa or the West Indies. These data may be relevant to causal hypotheses and in relation to health care and cancer prevention.British Journal of Cancer (2006) 94, 1079–1085. doi:10.1038/sj.bjc.6603031 www.bjcancer.com Published online 7 March 2006 [ABSTRACT FROM AUTHOR]

Comparisons of survival rates of given diseases with different treatments or in different places often gave misleading results until the introduction of controlled trials. Recent reports of relatively low survival rates following the treatment of cancer in the UK compared to the rates in other countries, not based on controlled trials, may consequently be misleading. Their validity has, therefore, been tested by comparing the levels and trends in mortality--the ultimate criterion by which the success or failure of any system of care can be judged. For this purpose, rates and trends in rates over 20-50 years have been compared in five European countries of similar economic status (France, Italy, the Netherlands, Sweden, and the UK). The UK rates are not generally worse than those in the other countries and are sometimes better. Exceptions were cancer of the lung, large bowel, and breast, the first of which is explained by differences in the prevalence of smoking. [ABSTRACT FROM AUTHOR]

A cohort of 889 men and 1077 women employed for at least 1 month between 1946 and 1984 by a former Italian leading asbestos (mainly textile) company, characterised by extremely heavy exposures often for short durations, was followed up to 1996, for a total of 53,024 person-years of observation. Employment data were obtained from factory personnel records, while vital status and causes of death were ascertained through municipality registers and local health units. We observed 222 cancer deaths compared with 116.4 expected (standardized mortality ratio, SMR=191). The highest ratios were found for pleural (SMR=4105), peritoneal (SMR=1817) and lung (SMR=282) cancers. We observed direct relationships with duration of employment for lung and peritoneal cancer, and with time since first employment for lung cancer and mesothelioma. Pleural cancer risk was independent from duration (SMR=3428 for employment <1 year, 7659 for 1-4 years, 2979 for 5-9 years and 2130 for > or =10 years). Corresponding SMRs for lung cancer were 139, 251, 233 and 531. Nonsignificantly increased ratios were found for ovarian (SMR=261), laryngeal (SMR=238) and oro-pharyngeal (SMR=226) cancers. This study confirms and further quantifies the central role of latency in pleural mesothelioma and of cumulative exposure in lung cancer. [ABSTRACT FROM AUTHOR]

Objective: Surveillance of chronic diseases includes monitoring trends in age-adjusted rates in the general population. Statistics that are calculated to describe and compare trends include the annual percent change and the percent change for a specified time period. However, it is also of interest to determine the contribution specific diseases make to an overall trend in order to better understand the impact of interventions and changes in the prevalence of risk factors. The objective here is to provide a method for partitioning a linear trend in age-adjusted rates into disease-specific components.Methods: The method presented is based on linear regression. The decreasing trend in age-adjusted cancer mortality rates for the total United States during the period 1991-96 is analyzed to illustrate the method.Results: Trends in mortality for cancers of the colon/rectum, breast, lung/bronchus, and prostate are found to be responsible for 75% of the decreasing trend in cancer mortality.Conclusions: It is possible to partition an overall trend in age-adjusted rates under the assumption that it and the trends for all mutually exclusive and exhaustive subgroups of interest are linear. [ABSTRACT FROM AUTHOR]

Objectives: Modifiable lifestyle, environmental, and infectious risk factors associated with cancer impact both cancer incidence and mortality at the population level. Most studies estimating this burden focus on cancer incidence. However, because these risk factors are associated with cancers of disparate mortality rates, the burden associated with cancer incidence could differ from cancer mortality. Therefore, estimating the cancer mortality attributable to these risk factors provides additional insight into cancer prevention. Here, we estimated future cancer deaths and the number of avoidable deaths in Canada due to modifiable risk factors., Methods: The projected cancer mortality data came from OncoSim, a web-based microsimulation tool. These data were applied to the methodological framework that we previously used to estimate the population attributable risks and the potential impact fractions of modifiable risk factors on Canadian cancer incidence., Results: We estimated that most cancer deaths will be attributed to tobacco smoking with an average of 27,900 deaths annually from 2024 to 2047. If Canada's current trends in excess body weight continue, cancer deaths attributable to excess body weight would double from 2786 deaths in 2024 to 5604 deaths in 2047, becoming the second leading modifiable cause of cancer death. Applying targets to reduce these risk factors, up to 34,600 cancer deaths could be prevented from 2024 to 2047., Conclusion: Our simulated results complement our previous findings on the cancer incidence burden since decreasing the overall burden of cancer will be accelerated through a combination of decreasing cancer incidence and improving survival outcomes through improved treatments., (© 2021. The Canadian Public Health Association.)

Objectives: In developing countries where cancer registries are unavailable, mortality statistics from death certification may be a practical source of cancer statistics. We aimed at describing the cancer mortality in Egypt and comparing it to that in the US. Methods: We used the mandatory and routinely available mortality records of Menofeia province in the Nile Delta region of Egypt, which is typical of the rest of Egypt. We determined cancer mortality rates, and compared them with the Surveillance, Epidemiology, and End Results (SEER) mortality rates of the US. Results: Bladder and liver cancers were the two most common causes of cancer mortality in Menofeia, Egypt. When adjusted for age the Egyptian rates were much higher than the US rates (9.5/100,000 and 8.4/100,000 for bladder and liver cancer, respectively, compared with 2.3/100,000 and 2.5/100,000 for the same cancers from SEER data). We also observed that age-specific rates for early-onset colorectal cancer under age 40 and premenopausal breast cancer were higher in Egypt than in the US. Conclusion: This study confirms our earlier observations about the higher proportion of early-onset colorectal cancer in Egypt, and opens the door for future studies to investigate familial clustering of cancer in Egypt. [ABSTRACT FROM AUTHOR]

Objectives: To assess the risk of cancer among workers of a Moscow (Russia) shoe factory exposed to chloroprene (2-chloro-1,3-butadiene) (CP).Methods: This is a retrospective cohort mortality study among 5,185 shoe manufacturing workers employed between 1940 and 1976, and followed from 1979 through 1993. Exposure to CP was assessed by linking the job history with industrial hygiene data. We calculated standardized mortality ratios (SMR) using the Moscow population as reference, and conducted an internal comparison analysis based on Poisson regression modeling.Results: For the entire cohort, all-cause mortality was close to expectation and all-cancer mortality was increased. There was an increase in the mortality from liver cancer (SMR = 2.4, 95 percent confidence interval [CI] = 1.1-4.3), kidney cancer (SMR = 1.8, CI = 0.9-3.4), and leukemia (SMR = 1.9, CI = 1.0-3.3). Mortality from liver cancer and leukemia was associated with various indicators of CP exposure. A similar, although less consistent, pattern was found for kidney cancer mortality; while for the remaining neoplasms, no association was suggested with CP exposure.Conclusions: The association between CP exposure and risk of leukemia may be due to concomitant exposure to benzene. The results for liver cancer point towards a carcinogenic effect of CP. [ABSTRACT FROM AUTHOR]

Objectives: To update the cancer mortality patterns among Iowa (United States) farmers for the years 1987-93 and compare these results with those previously reported for 1971-86 as well as relate the PMR patterns to risk-factor survey data.Methods: We extracted usual occupation and cause of death from 88,090 Iowa death certificates for White males aged 20 and older for the years 1987-93. Proportional mortality ratios (PMR), adjusted for age, and 95 percent confidence intervals (CI) were calculated using deaths among nonfarmers to generate expected numbers. We compared lifestyle profiles for farmers and nonfarmers using male controls (n = 1,596) from a population-based case-control study conducted in Iowa from 1986-89.Results: Iowa farmers had deficit PMRs for all-cause cancer mortality (PMR = 0.92, CI = 0.90-0.94) and for lung (PMR = 0.70, CI = 0.66-0.73), liver (PMR = 0.65, CI = 0.50-0.86), and other cancer sites strongly related to smoking and alcohol use. Farmers at all ages had excess deaths for cancers of the prostate (PMR = 1.26, CI = 1.19-1.33), rectum (PMR = 1.29, CI = 1.07-1.56), brain (PMR = 1.10, CI = 0.92-1.32), multiple myeloma (PMR = 1.17, CI = 0.98-1.40), non-Hodgkin's lymphoma (PMR = 1.09, CI = 0.96-1.23), and Hodgkin's disease (PMR = 1.62, CI = 1.04-2.54). Younger farmers (aged 20 to 64 years) had excess deaths for colon cancer (PMR = 1.52, CI =1.26-1.85) and skin melanoma (PMR = 1.60, CI = 1.07-2.38), while older farmers (aged 65+ years) had excess deaths for cancers of the pancreas (PMR = 1.18, CI = 1.04-1.34), lip (PMR = 1.58, CI = 0.59-4.21), and leukemia (PMR = 1.26, CI = 1.09-1.46). Since the 1970s, the PMR for stomach cancer has declined to expected values, while the PMRs for prostate, large intestine, pancreas, and Hodgkin's disease have increased; PMRs for other sites are consistent with earlier data. A survey from 1986-89 showed that farmers, compared with nonfarmers, smoked less, used less alcohol, had less formal education, and consumed more total calories, and calories from protein, fat, and meat while consuming fewer calories from fruits and vegetables.Conclusions: Iowa farmers continue to be at elevated risk of mortality due to certain cancers, and, of particular interest, the risk for prostate and colon cancer appears to be increasing since 1970. [ABSTRACT FROM AUTHOR]