Site-specific Cancer Incidence Research Articles

The association between pre-existing heart failure and cancer incidence: A systematic review and meta-analysis

Introduction and Objectives: Cardiovascular diseases (CVD) and cancer are some of the most recognized causes of mortality and morbidity worldwide. Cancer is the second leading cause of death in heart failure (HF) populations. Recent studies have hypothesized that HF might promote the development and progression of cancer. We aim to analyze and discuss the most recent evidence on the relationship between HF and cancer development.METHODS: From inception to November 2022, we searched PubMed, Web of Science and ClinicalTrials.gov for relevant articles on patients with HF and a subsequent cancer diagnosis that reported outcomes of overall and site-specific cancer incidence, or mortality.RESULTS: Of 2401 articles identified in our original search, 13 articles met our criteria. Studies reporting risk rate estimates were summarized qualitatively. Studies reporting hazard ratios (HRs), or relative risks were combined in a meta-analysis and revealed that HF was associated with an increased overall cancer incidence with a HR=1.30(95%CI:1.04-1.62) compared with individuals without HF. Subgroup analyses by cancer type revealed increased risk for lung cancer (HR=1.87;95%CI:1.28-2.73), gastrointestinal cancer (HR=1.22;95%CI:1.03-1.45), hematologic cancer (HR=1,60;95%CI:1.23-2.08) and female reproductive cancer (HR=1.67;95%CI:1,27-2.21). Mortality from cancer was higher in HF patients compared with non-HF subjects with a HR=2.17 (95%CI:1,23-3.84).Conclusions: Our systematic review and meta-analysis revealed that HF may result in a subsequent increase in cancer incidence as well as in cancer-related mortality. The most common cancer subtypes in HF patients were lung, female reproductive system, and hematologic cancers. Further research is needed to understand this association better and to provide the best cardiological and oncological care.

FMUPorto - Summaries and comments

FMUPorto - Summaries and comments

Dose–response analysis of protracted absorbed organ dose and site-specific cancer incidence in Sweden after the Chernobyl nuclear power plant accident

Background: Adult males in Sweden exhibit an increased risk of cancer associated with an increased absorbed dose to the colon from the Chernobyl accident. Methods: A closed cohort, with information on hunter status, included all individuals living in northern Sweden in 1986. Complete annual information on exposure to 137Cs at the dwelling coordinate was available for a total of 2,104,101 individuals. A nested case-control method with four controls matched for year of cancer diagnosis and year of birth, was used. Individual absorbed organ doses were calculated between 1986 and 2020 including external and internal exposure. Hazard ratios (HR) per mGy with 95% confidence intervals (95% CI) were calculated using conditional logistic regression adjusted for rural/nonrural habitat, education level and pre-Chernobyl cancer incidence 1980 to 1985. A total of 161,325 cancer cases in males and 144,439 in females were included. Results: The adjusted HR per mGy for all cancer sites combined was 1.027 (95% CI = 1.022, 1.031) in males and 1.011 (95% CI = 1.006, 1.017) in females. In a post hoc analysis accounting for both remaining confounding from hunter lifestyle and the pre-Chernobyl cancer incidence by county, the adjusted HR per mGy for all cancer sites combined was 1.014 (95% CI = 1.009, 1.019) in males and 1.000 (95% CI = 0.994, 1.006) in females. The post hoc analysis suggested an increased risk of cancer in the colon, pancreas, and stomach, respectively, in males, and lymphoma in females. Conclusions: Increased cancer risk estimates were found for some specific cancer sites but remaining uncontrolled confounding due to hunter lifestyle could not be ruled out.

Association of the age of onset of metabolic syndrome with the risk of all cancer types

BackgroundThe association between the age at onset of metabolic syndrome and cancer risk remains unknown. This study explored the association between age at metabolic syndrome onset and the risk of overall and site-specific cancer incidence. MethodsThis study included 31,688 participants with new-onset metabolic syndrome and 31,688 participants matched according to sex, age (±1 y), and examination year among the 179,328 participants who underwent Kailuan health examinations from 2006 to 2017 in Tangshan, China. Weighted Cox regression was used to calculate the hazard ratios and 95% confidence intervals of new-onset metabolic syndrome for overall and site-specific cancer incidence across age groups. Population-attributable risk proportions were used to estimate the number of cases that could be prevented by eliminating the risk factors from the population. ResultsDuring an average follow-up period of 10.22 y, we identified 2,710 cases of cancer and 4,218 deaths that occurred before the diagnosis of cancer. With an increase in metabolic syndrome onset age, the hazards of overall cancer incidence were gradually attenuated. The average hazard ratios (95% confidence intervals) of overall cancer were 1.94 (1.25–2.99) for metabolic syndrome onset age <45 year old, 1.41 (1.15–1.71) for age 45–54 years old, 1.38 (1.11–1.73) for age 55–64 years old, and 1.07 (0.89–1.28) for age ≥65 years old, respectively (p for interaction = 0.005). Similar results were obtained for colorectal, liver, and breast cancers in the site-specific analysis. ConclusionsNew-onset metabolic syndrome was associated with a higher risk of overall cancer and incidence of several types of cancer, and the associations were stronger with a younger age of onset. Trial registrationKailuan Study, ChiCTR2000029767 (Registered February 12, 2020, https://www.chictr.org.cn/showprojEN.html?proj=48316).

Educational Attainment and Cancer Incidence in a Large Nationwide Prospective Cohort.

Educational attainment is a social determinant of health and frequently used as an indicator of socioeconomic status. Educational attainment is a predictor of cancer mortality, but associations with site-specific cancer incidence are variable. The aim of this study was to evaluate the association of educational attainment and site-specific cancer incidence adjusting for known risk factors in a large prospective cohort. Men and women enrolled in the American Cancer Society's Cancer Prevention Study-II Nutrition Cohort who were cancer free at baseline were included in this study (n = 148,965). Between 1992 and 2017, 22,810 men and 17,556 women were diagnosed with incident cancer. Cox proportional hazards regression models were used to estimate age- and multivariable-adjusted risk and 95% confidence intervals of total and site-specific cancer incidence in persons with lower versus higher educational attainment. Educational attainment was inversely associated with age-adjusted cancer incidence among men but not women. For specific cancer sites, the multivariable-adjusted risk of cancer in the least versus most educated individuals remained significant for colon, rectum, and lung cancer among men and lung and breast cancer among women. Educational attainment is associated with overall and site-specific cancer risk though adjusting for cancer risk factors attenuates the association for most cancer sites. This study provides further evidence that educational attainment is an important social determinant of cancer but that its effects are driven by associated behavioral risk factors suggesting that targeting interventions toward those with lower educational attainment is an important policy consideration.

Associations between cardiorespiratory fitness in youth and the incidence of site-specific cancer in men: a cohort study with register linkage

ObjectivesTo assess the associations between cardiorespiratory fitness (CRF) in young men and the incidence of site-specific cancer.MethodsA Swedish population-based cohort study with register linkage of men who underwent military conscription...

Trends in cancer incidence by socioeconomic deprivation in Germany in 2007 to 2018: An ecological registry-based study.

Age-standardized cancer incidence has decreased over the last years for many cancer sites in developed countries. Whether these trends led to narrowing or widening socioeconomic inequalities in cancer incidence is unknown. Using cancer registry data covering 48 million inhabitants in Germany, the ecological association between age-standardized total and site specific (colorectal, lung, prostate and breast) cancer incidence in 2007 to 2018 and a deprivation index on district level (aggregated to quintiles) was investigated. Incidence in the most and least deprived districts were compared using Poisson models. Average annual percentage changes (AAPCs) and differences in AAPCs between deprivation quintiles were assessed using Joinpoint regression analyses. Age-standardized incidence decreased strongly between 2007 and 2018 for total cancer and all cancer sites (except female lung cancer), irrespective of the level of deprivation. However, differences in the magnitude of trends across deprivation quintiles resulted in increasing inequalities over time for total cancer, colorectal and lung cancer. For total cancer, the incidence rate ratio between the most and least deprived quintile increased from 1.07 (95% confidence interval: 1.01-1.12) to 1.23 (1.12-1.32) in men and from 1.07 (1.01-1.13) to 1.20 (1.14-1.26) in women. Largest inequalities were observed for lung cancer with 82% (men) and 88% (women) higher incidence in the most vs the least deprived regions in 2018. The observed increase in inequalities in cancer incidence is in alignment with trends in inequalities in risk factor prevalence and partly utilization of screening. Intervention programs targeted at socioeconomically deprived and urban regions are highly needed.

Use of immunosuppression and subsequent cancer incidence: cohort study

ObjectiveEvaluate the association between cancer incidence and immunosuppressive treatment in patients with ocular inflammatory disease (OID).Methods and analysisWe performed a retrospective cohort study of patients from 10 US OID subspecialty...

Differences in site-specific cancer incidence by individual- and area-level income in Canada from 2006 to 2015.

Income, a component of socioeconomic status, influences cancer risk as a social determinant of health. We evaluated the independent associations between individual- and area-level income and site-specific cancer incidence in Canada. We used data from the 2006 and 2011 Canadian Census Health and Environment Cohorts, which are probabilistically linked datasets constituted by 5.9 million and 6.5 million respondents of the 2006 Canadian long-form census and 2011 National Household Survey, respectively. Individuals were linked to the Canadian Cancer Registry through 2015. Individual-level income was derived using after-tax household income adjusted for household size. Annual tax return postal codes were used to assign area-level income quintiles to individuals for each year of follow-up. We calculated age-standardized incidence rates (ASIR) and rate ratios for cancers overall and by site. We conducted multivariable negative binomial regression to adjust these rates for other demographic and socioeconomic variables. Individuals of lower individual- and area-level income had higher ASIRs compared to those in the wealthiest income quintile for head and neck, oropharyngeal, esophageal, stomach, colorectal, anal, liver, pancreas, lung, cervical and kidney and renal pelvis cancers. Conversely, individuals of wealthier individual- and area-level income had higher ASIRs for melanoma, leukemia, Hodgkin's lymphoma, non-Hodgkin's lymphoma, breast, uterine, prostate and testicular cancers. Most differences in site-specific incidence by income quintile remained after adjustment. Although Canada's publicly funded healthcare system provides universal coverage, inequalities in cancer incidence persist across individual- and area-level income gradients. Our estimates suggest that individual- and area-level income affect cancer incidence through independent mechanisms.

Albuminuria and the risk of cancer: the Stockholm CREAtinine Measurements (SCREAM) project.

Studies investigating the association of chronic kidney disease and cancer have focused on estimated glomerular filtration (eGFR) rather than on albuminuria. This study aimed to examine whether albuminuria is associated with cancer incidence, and whether this association is independent of eGFR. We included subjects of the Stockholm Creatinine Measurements (SCREAM) project without a history of cancer-250768 subjects with at least one urine albumin-creatinine ratio (ACR) test (primary cohort) and 433850 subjects with at least one dipstick albuminuria test (secondary cohort). Albuminuria was quantified as KDIGO albuminuria stages. The primary outcome was overall cancer incidence. Secondary outcomes were site-specific cancer incidence rates. Multivariable Cox proportional hazards regression models adjusted for confounders including eGFR to calculate hazard ratios and 95% confidence intervals (HRs, 95% CIs). During a median follow-up of 4.3 (interquartile range 2.0-8.2) years, 21901 subjects of the ACR cohort developed de novo cancer. In multivariable analyses, adjusting among others for eGFR, subjects with an ACR of 30-299mg/g or ≥300mg/g had a 23% (HR 1.23; 95% CI 1.19-1.28) and 40% (HR 1.40; 95% CI 1.31-1.50) higher risk of developing cancer, respectively, when compared with subjects with an ACR <30mg/g. This graded, independent association was also observed for urinary tract, gastrointestinal tract, lung and hematological cancer incidence (all P<.05). Results were similar in the dipstick albuminuria cohort. Albuminuria was associated with the risk of cancer independent of eGFR. This association was primarily driven by a higher risk of urinary tract, gastrointestinal tract, lung and hematological cancers.

Differential risk of 23 site-specific incident cancers and cancer-related mortality among patients with metabolic dysfunction-associated fatty liver disease: a population-based cohort study with 9.7 million Korean subjects.

Although an association between metabolic dysfunction-associated fatty liver disease (MAFLD) and cardiovascular disease or overall mortality has been reported, it is unclear whether there is an association between MAFLD and cancer incidence or mortality. We aimed to investigate the differential risk of all- and site-specific cancer incidence and mortality according to MAFLD subgroups categorized by additional etiologies of liver disease. Using the Korean National Health Insurance Service database, we stratified the participants into three groups: (1) single-etiology MAFLD (S-MAFLD) or MAFLD of pure metabolic origin; (2) mixed-etiology MAFLD (M-MAFLD) or MAFLD with additional etiological factor(s) (i.e., concomitant liver diseases and/or heavy alcohol consumption); and (3) non-MAFLD. Hepatic steatosis and fibrosis were defined using the fatty liver index and the BARD score, respectively. Cox proportional hazards regression was performed to estimate the risk of cancer events. Among the 9,718,182 participants, the prevalence of S-MAFLD and M-MAFLD was 29.2% and 6.7%, respectively. During the median 8.3 years of follow-up, 510,330 (5.3%) individuals were newly diagnosed with cancer, and 122,774 (1.3%) cancer-related deaths occurred among the entire cohort. Compared with the non-MAFLD group, the risk of all-cancer incidence and mortality was slightly higher among patients in the S-MAFLD group (incidence, adjusted hazard ratio [aHR] = 1.03; 95% confidence interval [CI]: 1.02-1.04; mortality, aHR = 1.06; 95% CI: 1.04-1.08) and highest among patients with M-MAFLD group (incidence, aHR = 1.31; 95% CI: 1.29-1.32; mortality, aHR = 1.45; 95% CI: 1.42-1.48, respectively). The M-MAFLD with fibrosis group (BARD score ≥ 2) showed the highest relative risk of all-cancer incidence (aHR = 1.38, 95% CI = 1.36-1.39), followed by the M-MAFLD without fibrosis group (aHR = 1.09, 95% CI = 1.06-1.11). Similar trends were observed for cancer-related mortality. MAFLD classification, by applying additional etiologies other than pure metabolic origin, can be used to identify a subgroup of patients with poor cancer-related outcomes.

#2499 ALBUMINURIA AND THE RISK OF CANCER: THE STOCKHOLM CREATININE MEASUREMENTS (SCREAM) PROJECT

Abstract Background and Aims Studies investigating the association of chronic kidney disease and cancer have focused on estimated glomerular filtration (eGFR) rather than on albuminuria. The few studies focusing on albuminuria provide results that vary considerably, probably due to a lack of consideration of eGFR, their limited sample sizes, and that different albuminuria measurement techniques were used. This study therefore aimed to investigate the eGFR independent risk of cancer incidence associated with albuminuria measured as ACR as well as by dipstick in a large Swedish population. Method We included subjects of the Stockholm Creatinine Measurements (SCREAM) project without a history of cancer, 250,768 subjects with at least 1 urine albumin-creatinine ratio (ACR) test (primary cohort), and 433,850 subjects with at least 1 dipstick albuminuria test (secondary cohort). Albuminuria was quantified as KDIGO albuminuria stages. The primary outcome was overall cancer incidence. Secondary outcomes were site-specific cancer incidence rates. Multivariable Cox proportional hazards regression models were used to calculate hazard ratios (HRs, 95% CIs) crude, and additionally adjusted for confounders including baseline eGFR. Results During a median follow-up of 4.3 (IQR, 2.0-8.2) years, 21,901 subjects of the ACR cohort developed de novo cancer. In multivariable analyses, adjusting among others for eGFR, subjects with an ACR of 30–299 mg/g or ≥300 mg/g had a 23% (HR, 1.23; 95% CI, 1.19-1.28) and 40% (HR, 1.40; 95% CI, 1.31-1.50) higher risk of developing cancer, respectively, when compared to subjects with an ACR ≪30 mg/g. This graded, independent association was also observed for urinary tract, gastrointestinal tract, lung, and hematological cancer incidence (all P≪0.05). No significant associations of albuminuria with the incidence of melanoma, breast, and prostate cancers were found. Results were similar in the dipstick albuminuria cohort, and were robust in several sensitivity analyses. Conclusion Albuminuria was associated with the risk of cancer independent of eGFR. This association was primarily driven by a higher risk of urinary tract, gastrointestinal tract, lung, and hematological cancers.

Lack of significant associations between single nucleotide polymorphisms in LPAL2-LPA genetic region and all cancer incidence and mortality in Japanese population: The Japan public health center-based prospective study

BackgroundHigh lipoprotein (a) level is an established cardiovascular risk, but its association with non-cardiovascular diseases, especially cancer, is controversial. Serum lipoprotein (a) levels vary widely by genetic backgrounds and are largely determined by the genetic variations of apolipoprotein (a) gene, LPA. In this study, we investigate the association between SNPs in LPA region and cancer incidence and mortality in Japanese. MethodsA genetic cohort study was conducted utilizing the data from 9923 participants in the Japan Public Health Center-based Prospective Study (JPHC Study). Twenty-five SNPs in the LPAL2-LPA region were selected from the genome-wide genotyped data. Cox regression analysis adjusted for the covariates and competing risks of death from other causes, were used to estimate the relative risk (hazard ratios (HR) with 95% confidence intervals (CI)) of overall and site-specific cancer incidence and mortality, for each SNP. ResultsNo significant association was found between SNPs in the LPAL2-LPA region and cancer incidence or mortality (overall/site-specific cancer). In men, however, HRs for stomach cancer incidence of 18SNPs were estimated higher than 1.5 (e.g., 2.15 for rs13202636, model free, 95%CI: 1.28–3.62) and those for stomach cancer mortality of 2SNPs (rs9365171, rs1367211) were estimated 2.13 (recessive, 95%CI:1.04–4.37) and 1.61 (additive, 95%CI: 1.00–2.59). Additionally, the minor allele for SNP rs3798220 showed increased death risk from colorectal cancer (CRC) in men (HR: 3.29, 95% CI:1.59 – 6.81) and decreased CRC incidence risk in women (HR: 0.46, 95%CI: 0.22–0.94). Minor allele carrier of any of 4SNPs could have risk of prostate cancer incidence (e.g., rs9365171 dominant, HR: 1.71, 95%CI: 1.06–2.77). ConclusionsNone of the 25 SNPs in the LPAL2-LPA region was found to be significantly associated with cancer incidence or mortality. Considering the possible association between SNPs in LPAL2-LPA region and colorectal, prostate and stomach cancer incidence or mortality, further analysis using different cohorts is warranted.

Cancer disparities in Appalachian Kentucky.

Cancer is the second leading cause of death in the United States, and the disease burden is elevated in Appalachian Kentucky, due in part to health behaviors and inequities in social determinants of health. This study's goal was to evaluate Appalachian Kentucky's cancer burden compared to non-Appalachian Kentucky, and Kentucky compared to the United States (excluding Kentucky). The following data were analyzed: annual all-cause and all-site cancer mortality rates from 1968 to 2018; 5-year all-site and site-specific cancer incidence and mortality rates from 2014 to 2018; aggregated screening and risk factor data from 2016 to 2018 for the United States (excluding Kentucky), Kentucky, non-Appalachian Kentucky, and Appalachian Kentucky; and human papilloma virus vaccination prevalence by sex from 2018 for the United States and Kentucky. Since 1968, the United States has experienced a large decrease in all-cause and cancer mortality, but the reduction in Kentucky has been smaller and slower, driven by even smaller and slower reductions within Appalachian Kentucky. Appalachian Kentucky has higher overall cancer incidence and mortality rates and higher rates for several site-specific cancers compared to non-Appalachian Kentucky. Contributing factors include screening rate disparities and increased rates of obesity and smoking. Appalachian Kentucky has experienced persistent cancer disparities, including elevated all-cause and cancer mortality rates for 50+ years, widening the gap between this region and the rest of the country. In addition to addressing social determinants of health, increased efforts aimed at improving health behaviors and increased access to health care resources could help reduce this disparity.

Cancer and Potential Prevention with Lifestyle among Career Firefighters: A Narrative Review.

Career firefighters are at considerable risk for chronic diseases, including an increased risk of various cancers, compared to the general population. Over the last two decades, several systematic reviews and large cohort studies have demonstrated that firefighters have statistically significant increases in overall and site-specific cancer incidence and site-specific cancer mortality compared to the general population. Exposure assessment and other studies have documented exposures to a variety of carcinogens in fire smoke and within the fire station. Other occupational factors such as shift work, sedentary behavior, and the fire service food culture may also contribute to this working population's increased cancer risk. Furthermore, obesity and other lifestyle behaviors such as tobacco use, excessive alcohol consumption, poor diet, inadequate physical activity, and short sleep duration have also been associated with an increased risk of certain firefighting-associated cancers. Putative prevention strategies are proposed based on suspected occupational and lifestyle risk factors.

Site-Specific Cancer Incidence by Race and Immigration Status in Canada 2006-2015: A Population-Based Data Linkage Study.

The Canadian Cancer Registry (CCR) does not collect demographic data beyond age and sex, making it difficult to monitor health inequalities. Using data linkage, we compared site-specific cancer incidence rates by race. The 2006 and 2011 Canadian Census Health and Environment Cohorts are population-based probabilistically linked datasets of 5.9 million respondents of the 2006 long-form census and 6.5 million respondents of the 2011 National Household Survey. Race was self-reported. Respondent data were linked with the CCR up to 2015. We calculated age-standardized incidence rate ratios (ASIRR), comparing group-specific rates to the overall population rate with bootstrapped 95% confidence intervals (CI). We used negative binomial regressions to adjust for socioeconomic variables and assess interactions with immigration status. The age-standardized overall cancer incidence rate was lower in almost all non-White racial groups than in the overall population, except for White and Indigenous peoples who had higher incidence rates than the overall population (ASIRRs, 1.03-1.04). Immigrants had substantially lower age-standardized overall cancer incidence rates than nonimmigrants (ASIRR, 0.83; 95% CI, 0.82-0.84). Stomach, liver, and thyroid cancers and multiple myelomas were the sites where non-White racial groups had consistently higher site-specific cancer incidence rates than the overall population. Immigration status was an important modifier of cancer risk in the interaction model. Differences in cancer incidence between racial groups are likely influenced by differences in lifestyles, early life exposures, and selection factors for immigration. Data linkage can help monitor health inequalities and assess progress in preventive interventions against cancer. See related commentary by Withrow and Gomez, p. 876.

Ultra-processed food consumption, cancer risk, and cancer mortality: a prospective cohort study of the UK Biobank

BackgroundDietary patterns worldwide are increasingly displaced by many cheap, highly palatable, and ready-to-eat ultra-processed foods (UPFs). Higher UPF consumption has been linked to increased risk for obesity and cardiometabolic diseases, but prospective evidence is limited on cancer outcomes. This study aimed to examine the association between UPF consumption and risk for overall and site-specific cancer incidence and cancer mortality using the UK Biobank cohort. Methods197 426 participants of the UK Biobank from England, Scotland, and Wales with 24-h dietary recall completed between 2009 and 2012 were included. Incident cancer cases were identified through data linkage to national cancer and mortality registries. Food items consumed were categorised according to their degree of food processing using the NOVA classification system. Individual UPF consumption were derived as a percentage of daily food intake. Prospective association was assessed using multivariable Cox proportional hazards models adjusted for baseline sociodemographic and lifestyle characteristics. For female-specific cancers, menopausal status, use of oral contraceptives, hormone replacement therapy, and parity were additionally adjusted. FindingsMean age was 58·0 years (SD 8·0); 54·6% of participants were women. During a median follow-up time of 9·8 years (IQR 9·4–10·6), 15 921 (8·1%) of 197 426 individuals developed cancer and 4009 (2·0%) cancer deaths were encountered. Consumption of UPFs was associated with a higher incidence of overall cancer (hazard ratio per 10% increment in UPF consumption was 1·02 [95% CI 1·01–1·04]; p=0·005) and ovarian cancer in females (1·19 [1·08–1·30]; p<0·001). Positive associations were identified for mortality of overall, breast, and ovarian cancers. InterpretationThis large UK cohort study presents evidence of positive associations between UPF consumption and risks for incidence and mortality of overall and certain site-specific cancers. Limitations include non-representativeness having based on a cohort of middle-aged volunteers, insufficient details for some food items although a conservative approach was undertaken classifying foods to lower processing categories, and potential residual confounding due to the observational nature of the data. Further investigation into the mechanistic pathways is warranted to better identify targets for intervention. FundingCancer Research UK and World Cancer Research Fund.

Association of chronic kidney disease with total and site-specific cancer incidence in participants of the Japan Public Health Center-based Prospective Study.

Although studies have found an association between chronic kidney disease (CKD) and cancer incidence, the results are inconsistent. This study included participants in the Japan Public Health Center-based Prospective Study who had data on serum creatinine measurements. We assessed the association between estimated glomerular filtration rate (eGFR) and the risk of total and site-specific cancer incidence using a systematic survey in Japan. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) with adjustment for participant demographics and lifestyle factors. A total of 21978 participants who met the inclusion criteria were followed up for a mean period of 12.9 years, during which a total of 2997 incident cancer cases were reported. In the multivariable adjusted models, an eGFR of <45mL/min/1.73 m2 was not significantly associated with total cancer incidence (adjusted HR 1.22, 95% CI 0.94-1.60), compared with an eGFR of 60-89mL/min/1.73 m2 (reference). The HR among those with eGFRs of ≥90mL/min/1.73 m2 was 1.10 (95% CI 1.00-1.22). In this large prospective study, a low eGFR was not significantly associated with an increased risk of total cancer incidence in patients with CKD, which may be partly due to an underpowered sample size. This finding may be due to the many shared risk factors between CKD and cancer.

Residence near industrial complex and cancer incidence: A registry-based cohort of 1,022,637 participants with a follow-up of 21 years, Israel

BackgroundIndustrial complex (IC) residence is associated with higher cancer incidence in adults and children. However, the effect on young adults and the residence duration are not well described. Since the beginning of the 20th century, the Haifa bay area (HBA) has a major IC area with petrochemical industry complex and many other industries. The objectives of the current study were to estimate the association between IC residence and cancer incidence and to evaluate the effect of the residence duration. MethodsThis study is a registry-based cohort (N = 1,022,637) with a follow-up of 21 years. Cox regression models were used to evaluate the associations (hazards ratios (HR) and its 95% confidence intervals (CIs)) between HBA residence and incidence of all cancer sites (n = 62,049) and for site-specific cancer types including: lung cancer (n = 5398), bladder cancer (n = 3790), breast cancer (n = 11,310), prostate cancer (n = 6389) skin cancer (n = 4651), pancreatic cancer (n = 2144) and colorectal cancer (n = 8675). We evaluated the effect of the duration of exposure as categories of 7 years for those with 15 years of follow-up. ResultsIC residence was associated with higher risk for all cancer sites (HR:1.09, 95% CI: 1.06–1.12), for site-specific cancer incidence including: lung cancer (HR:1.14, 95% CI: 1.04–1.23), bladder cancer (HR:1.11, 95% CI: 1.01–1.23), breast cancer (HR:1.04, 95% CI: 0.98–1.10), prostate cancer (HR:1.07, 95% CI: 0.99–1.16), skin cancer (HR:1.22, 95% CI: 1.12–1.33) and colorectal cancer (HR:1.10, 95%CI: 1.03–1.17). Similar risk was also observed among young adults (HR: 1.10, 95% CI: 1.00–1.20). In the analyses for the duration of exposure, IC residence was associated with higher risk for all cancer site for the longest residence duration (15–21 years: HR: 1.08, 95% CI: 1.04–1.13). ConclusionsHarmful associations were found between IC residence and incidence of all cancer sites and site-specific cancers types. Our findings add to the limited evidence of associations between IC residence and cancer in young adults.

Long-term effects of air pollutant exposures on site-specific cancer incidence in elders

Long-term effects of air pollutant exposures on site-specific cancer incidence in elders