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Purpose: Understanding how stage at cancer diagnosis influences cause of death, an endpoint that is not susceptible to lead-time bias, can inform population-level outcomes of cancer screening. Methods: Using data from 17 US Surveillance, Epidemiology, and End Results registries for 1,154,515 persons aged 50–84 years at cancer diagnosis in 2006–2010, we evaluated proportional causes of death by cancer type and uniformly classified stage, following or extrapolating all patients until death through 2020. Results: Most cancer patients diagnosed at stages I–II did not go on to die from their index cancer, whereas most patients diagnosed at stage IV did. For patients diagnosed with any cancer at stages I–II, an estimated 26% of deaths were due to the index cancer, 63% due to non-cancer causes, and 12% due to a subsequent primary (non-index) cancer. In contrast, for patients diagnosed with any stage IV cancer, 85% of deaths were attributed to the index cancer, with 13% non-cancer and 2% non-index-cancer deaths. Index cancer mortality from stages I–II cancer was proportionally lowest for thyroid, melanoma, uterus, prostate, and breast, and highest for pancreas, liver, esophagus, lung, and stomach. Conclusion: Across all cancer types, the percentage of patients who went on to die from their cancer was over three times greater when the cancer was diagnosed at stage IV than stages I–II. As mortality patterns are not influenced by lead-time bias, these data suggest that earlier detection is likely to improve outcomes across cancer types, including those currently unscreened. [ABSTRACT FROM AUTHOR]

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]

Purpose: We aimed to examine the association between hypertension grades and the risk of total and site-specific cancer mortality among Japanese men and women. Methods: In the Japan Collaborative Cohort Study, 27,332 participants aged 40–79 years were enrolled and followed up with their mortality until 2009. According to the measured blood pressure (BP) at baseline, we classified the participants into four BP categories based on 2018 European guidelines. The Cox proportional hazard models were used to calculate the multivariable hazard ratios (HRs) with 95% confidence intervals (CIs) of total and site-specific cancer mortality according to the hypertension category. Results: During the 18.5 years of median follow-up, 1,927 cancer deaths were documented. Grade 1 (systolic blood pressure [SBP] 140–159 mmHg or diastolic blood pressure [DBP] 90–99 mmHg) and grade 2–3 hypertension (SBP ≥ 160 mmHg or DBP ≥ 100 mmHg) were associated with an increased risk of total cancer mortality; the multivariable HRs were 1.17 (1.04–1.32) for grade 1, and 1.27 (1.09–1.47) for grade 2–3 hypertension compared to optimal and normal BP (SBP < 130 mmHg and DBP < 85 mmHg). Linear and positive associations were observed between SBP and DBP 10 mmHg increment and the risk of total cancer mortality; HRs were 1.06 (1.03–1.08) for SBP and 1.07 (1.02–1.11) for DBP of 10 mmHg increment. The excess risk was primarily found for esophageal, liver, and pancreatic cancer; the respective multivariable HRs of grade 2–3 hypertension vs optimal and normal BP were 2.57 (1.10–6.04) for esophageal, 1.67 (1.01–2.77) for liver, and 1.95 (1.17–3.23) for pancreatic cancer. Conclusion: Hypertension was associated with the increased risk of total cancer mortality, primarily of esophageal, liver, and pancreatic cancer. [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]

It is unknown whether the well-known association between vitamin D deficiency and mortality could be explained by the immune system modulating effects of vitamin D, which may protect from a systemic inflammatory response (SIR) to adverse health conditions. This study aims to investigate the interrelationships of vitamin D deficiency, biomarkers of SIR, and mortality. We used multivariate logistic regression with adjustment for 51 covariates to assess the associations of vitamin D deficiency with disadvantageous levels of nine biomarkers of SIR in the UK Biobank cohort. Furthermore, we tested with Cox regression and mediation analysis whether biomarkers of SIR and vitamin D deficiency were independently associated with mortality. We included 397,737 participants aged 37–73 years. Vitamin D deficiency was associated with disadvantageous levels of all blood cell count-based biomarkers, but not with C-reactive protein (CRP)-based biomarkers after adjustment for body weight. Vitamin D deficiency and all biomarkers of SIR were significantly associated with all-cause mortality and mortality from cancer, cardiovascular and respiratory disease. The strength of these associations was unaltered if vitamin D deficiency and biomarkers of SIR were put in the same model. This finding was further supported by the mediation analyses. This study showed that vitamin D deficiency is associated with disadvantageous levels of blood cell count-based but not CRP-based biomarkers of SIR. Vitamin D deficiency and systemic inflammation were independently and strongly associated with mortality. The potential of clinical interventions against both vitamin D deficiency and underlying causes of systemic inflammation should be explored. [ABSTRACT FROM AUTHOR]

To study the association between environmental phenols exposure, including benzophenone-3 (BP3) and triclosan, and all-cause mortality and cancer mortality in adults. A total of 8035 participants were included from the National Health and Nutrition Examination Survey (2003–2012). Urinary BP3 and triclosan were measured with liquid chromatography-tandem mass spectrometry. The associations between urinary BP3 and triclosan with cancer and all-cause mortality were explored by multivariable logistic regressions and restricted cubic splines. During an average of 7.25-year follow-up, 696 cases (8.7%) of all-cause mortality and 137 cases (1.71%) of cancer mortality occurred. The average levels of BP3 and triclosan were 12.2 and 10.3 ng/mL, respectively. Compared with the lowest quartile, the multivariable-adjusted hazard ratio of the highest quartile was 0.64 (95% confidence interval: 0.50 to 0.81; P < 0.001) for BP3 and 0.76 (0.61 to 0.94; P = 0.011) for triclosan. However, no significant associations between urinary BP3 and triclosan and cancer mortality were observed. BP3 and triclosan exposure decreased the risk of all-cause mortality while they were not associated with cancer mortality. [ABSTRACT FROM AUTHOR]

Purpose of Review: Differences in socioeconomic status (SES) and social determinants of health (SDH) account for many of the disparities seen among patients diagnosed with breast cancer. This review outlines how low SES/SDH factors impact patients along the continuum of breast cancer care from screening to survivorship. Recent Findings: Factors such as place of residence, race, income, insurance status, and social networks all strongly correlate with the degree to which patients have access to and utilize breast cancer screening, their composite treatment once diagnosed, the financial impact of treatment, and ultimately, their disease and survival outcomes. The increased complexity of community and social networks creates difficulty in understanding the interplay of SES/SDH factors and breast cancer outcomes and has provided challenges in targeted interventions to reduce disparities. Summary: Recent research has underscored that non-biologic SES/SDH factors have important and sizable impacts on breast cancer care. Targeted efforts to address these disparities must respond to a dynamic and complex interplay between biologic and SES/SDH factors. Providing high-quality, guideline-concordant, multidisciplinary care to all patients regardless of social factors remains the most important strategy across all healthcare settings. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) is inherently a complex immune-inflammatory condition, and heightened inflammation and immune dysfunction are closely related to an increased risk of death. However, evidence regarding the relationship between immune-inflammatory levels and all-cause, cardiovascular, and cancer mortality among patients with CKD is scarce. Methods: Patients with non-dialysis dependent CKD undergoing coronary angiography (CAG) were included from five Chinese tertiary hospitals. Systemic immune inflammation index (SII) was calculated by multiplying peripheral platelet count with neutrophil-to-lymphocyte ratio, and patients were categorized into four groups by SII quartiles. Cox regression models and competing risk Fine and Gray models were used to examining the relationships between SII levels and all-cause, cardiovascular, and cancer mortality. Results: A total of the 19,327 patients (68.8 ± 10.03 years, female 32.0%) were included in this study. During a median follow-up of 4.5 years, 5,174 deaths occurred, including 2,861 cardiovascular deaths and 375 cancer deaths. Controlling for confounders, all-cause mortality (Q2, Q3, Q4: hazard ratio(HR) [95 CI%] = 1.15 [1.06–1.26], 1.30 [1.19–1.42], 1.48 [1.35–1.62], respectively; p for trend < 0.001) and cardiovascular mortality (Q2, Q3, Q4: HR [95 CI%] = 1.16 [1.03–1.31], 1.40 [1.24–1.58], 1.64 [1.44–1.85], respectively; p for trend < 0.001) increased with higher SII levels, and SII levels was related to cancer mortality comparing last quartile to first quartile of SII (Q2, Q3, Q4: HR [95 CI%] = 1.12 [0.83–1.52], 1.22 [0.90–1.67], 1.50 [1.09–2.08], respectively; p for trend < 0.001). Conclusion: Elevated immune inflammation level on admission was an independent risk factor for all-cause, cardiovascular, and cancer mortality among CKD patients. Further research is needed to validate the predictive value of SII for mortality risk among CKD patients. [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]

Several systematic reviews and meta-analyses have summarized the association between sedentary behavior (SB) and cancer. However, the level of evidence and the potential for risk of bias remains unclear. This umbrella review summarized the current data on SB in relation to cancer incidence and mortality, with a particular emphasis on assessing the risk of bias. We searched PubMed, Web of Science and Cochrane Database for systematic reviews and meta-analyses on the association between SB and cancer incidence and mortality. We also searched for recent observational studies not yet included in existing meta-analyses. We re-calculated summary risk estimates for cancer incidence and mortality using random effects models. We included 14 meta-analyses covering 17 different cancer sites from 77 original studies. We found that high SB levels increase the risk for developing ovarian, endometrial, colon, breast, prostate, and rectal cancers, with relative risks of 1.29 (95% confidence interval (CI) = 1.08–1.56), 1.29 (95% CI = 1.16–1.45), 1.25 (95% CI = 1.16–1.33), 1.08 (95% CI = 1.04–1.11), 1.08 (95% CI = 1.00–1.17), and 1.07 (95% CI = 1.01–1.12), respectively. Also, we found an increased risk of cancer mortality of 1.18 (95% CI = 1.09–1.26). Most associations between SB and specific cancer sites were supported by a "suggestive" level of evidence. High levels of SB are associated with increased risk of several types of cancer and increased cancer mortality risk. [ABSTRACT FROM AUTHOR]

Purpose: We aimed to investigate the relationship between overall nutritional status and cancer mortality. Methods: A total of 12 262 US adults from six consecutive surveys of the National Health and Nutrition Examination Survey (NHANES 2003–2014) were analyzed. The overall health nutritional biomarkers index (HNBI) score, capturing characteristics of 17 biomarkers was developed to assess the overall nutritional status. The lower the HNBI score, the healthier nutritional status would be. Hazard ratio (HR) and 95% confidence intervals (95% CIs) were calculated by Cox proportional hazards regression models to evaluate the association between the HNBI score and cancer mortality. Results: The lower overall HNBI score was associated with decreased risk of cancer mortality, compared with participants in the 4th quartile of overall HNBI score, the HR (95% CIs) for participants in the 1st quartiles was 0.54 (0.33–0.89) (P-trend = 0.019). Healthier lifestyle habits and not obesity interacted with HNBI score, compared with participants with higher HNBI score and smoking currently/not exercising regularly/obesity, participants with lower HNBI score and not smoking currently/exercising regularly/not obesity were associated with lower risk of cancer mortality, the HR (95% CIs) were 0.43 (0.26–0.73), 0.57 (0.33–0.97), and 0.62 (0.47–0.97), respectively. These significant associations remained among participants who were followed-up more than 2 years. Conclusion: Our findings suggested that healthier overall nutritional status was associated with lower risk of cancer mortality among US adults. Not smoking, exercise regularly and not obesity interacted with overall nutritional status. Adherence to better overall nutritional status, lifestyle habits and optimal weight would prevent premature death from cancer. [ABSTRACT FROM AUTHOR]

Background: Meta-analyses of randomized controlled trials have shown that vitamin D supplementation reduces cancer mortality by 13%. Vitamin D fortification of foods may increase vitamin D levels in a similar manner as vitamin D supplementation and could achieve similar reductions in cancer mortality. Whereas some European countries already implemented widespread fortification of foods with vitamin D, in other countries only few or no foods are fortified. In this study, we estimated the reduction in cancer mortality presumably already achieved by current fortification policies in 2017 and the potential for further reductions if all countries had effective fortification. Methods: We reviewed scientific literature, publicly available information, and contacted health authorities to obtain information on current vitamin D food fortification policies in 34 European countries. Together with country-specific cancer death statistics from Eurostat, information on life expectancy, and country-specific fortification policies, we used data from studies on supplementation and serum 25(OH)D increases and cancer mortality to estimate numbers of probably already prevented cancer deaths and numbers of potentially further preventable deaths and years of life lost. Results: Current vitamin D fortification is estimated to prevent approximately 11,000 in the European Union and 27,000 cancer deaths in all European countries considered per year. If all countries considered here would implement adequate vitamin D fortification of foods, an estimated additional 129,000 cancer deaths (113,000 in the European Union) could be prevented, corresponding to almost 1.2 million prevented years of life lost (1.0 million in the EU) or approximately 9% of cancer deaths (10% in the EU). Interpretation: Systematic fortification of foods might considerably reduce the burden of cancer deaths in Europe. [ABSTRACT FROM AUTHOR]

This study compared the temporal and geographic trends of cancer in China with a specific focus on the long-term exposure to soil cadmium (Cd) pollution. The geographic information system (GIS; kriging interpolation method) was used to detect the Cd contained in the soil from the Dabaoshan area, Guangdong Province. The standard rate ratio (SRR) was calculated to describe the relationship between Cd exposure and cancer mortality risk using the low-exposure group as a reference. Eight hundred six cancer deaths (533 male and 273 female) in the total population of 972,970 were identified, and the age-standardized rate (world) was 145.64 per 100,000. Significant dose-response relationships were found using the low-exposure group as the reference group. The Cd soil levels were positively associated with the cancer mortality risk in the community population, particularly for all cancers (SRR = 3.27; 95% CI = 2.42–4.55), esophageal cancer (SRR = 5.42; 95% CI = 1.07–30.56), stomach cancer (SRR = 5.99; 95% CI = 2.00–18.66), liver cancer (SRR = 4.45; 95% CI = 2.16–10.34), and lung cancer (SRR = 2.86; 95% CI = 1.62–5.31) for the total population. Additionally, similar results were obtained when using the 2000 China standard population. Cd exposure significantly affected the standardized mortality rates (China) by age group for all cancers, esophageal cancer, stomach cancer, liver cancer, and lung cancer in the total population, particularly in the age groups of 35–54, 55–74, and ≥ 75 years, respectively. Cd soil level is likely positively associated with increased cancer mortality of all cancer types and esophageal, stomach, liver, and lung cancers but not for other specific categories of cancer. [ABSTRACT FROM AUTHOR]

In the present study, radiation doses and cancer risks resulting from abdominopelvic radiotherapy planning computed tomography (RP-CT) and abdominopelvic diagnostic CT (DG-CT) examinations are compared. Two groups of patients who underwent abdominopelvic CT scans with RP-CT (n = 50) and DG-CT (n = 50) voluntarily participated in this study. The two groups of patients had approximately similar demographic features including mass, height, body mass index, sex, and age. Radiation dose parameters included CTDIvol, dose–length product, scan length, effective tube current, and pitch factor, all taken from the CT scanner console. The ImPACT software was used to calculate the patient-specific radiation doses. The risks of cancer incidence and mortality were estimated based on the BEIR VII report of the US National Research Council. In the RP-CT group, the mean ± standard deviation of cancer incidence risk for all cancers, leukemia, and all solid cancers was 621.58 ± 214.76, 101.59 ± 27.15, and 516.60 ± 189.01 cancers per 100,000 individuals, respectively, for male patients. For female patients, the corresponding risks were 742.71 ± 292.35, 74.26 ± 20.26, and 667.03 ± 275.67 cancers per 100,000 individuals, respectively. In contrast, for DG-CT cancer incidence risks were 470.22 ± 170.07, 78.23 ± 18.22, and 390.25 ± 152.82 cancers per 100,000 individuals for male patients, while they were 638.65 ± 232.93, 62.14 ± 13.74, and 575.73 ± 221.21 cancers per 100,000 individuals for female patients. Cancer incidence and mortality risks were greater for RP-CT than for DG-CT scans. It is concluded that the various protocols of abdominopelvic CT scans, especially the RP-CT scans, should be optimized with respect to the radiation doses associated with these scans. [ABSTRACT FROM AUTHOR]

Purpose: This study investigated the association between dietary patterns, total mortality, and cancer mortality in the United States. Methods: We identified the four major dietary patterns at baseline from 13,466 participants of the NHANES III cohort using principal component analysis (PCA). Dietary patterns were categorized into 'prudent' (fruits and vegetables), 'western' (red meat, sweets, pastries, oils), 'traditional' (red meat, legumes, potatoes, bread), and 'fish and alcohol'. We estimated hazard ratios for total mortality, and cancer mortality using Cox regression models. Results: A total of 4,963 deaths were documented after a mean follow-up of 19.59 years. Higher adherence to the 'prudent' pattern was associated with the lowest risk of total mortality (5th vs. 1st quintile HR 0.90, 95% CI 0.82–0.98), with evidence that all-cause mortality decreased as consumption of the pattern increased. No evidence was found that the 'prudent' pattern reduced cancer mortality. The 'western' and the 'traditional' patterns were associated with up to 22% and 16% increased risk for total mortality (5th vs. 1st quintile HR 1.22, 95% CI 1.11–1.34; and 5th vs. 1st quintile HR 1.16, 95% CI 1.06–1.27, respectively), and up to 33% and 15% increased risk for cancer mortality (5th vs. 1st quintile HR 1.33, 95% CI 1.10–1.62; and 5th vs. 1st quintile HR 1.15, 95% CI 1.06–1.24, respectively). The associations between adherence to the 'fish and alcohol' pattern and total mortality, and cancer mortality were not statistically significant. Conclusion: Higher adherence to the 'prudent' diet decreased the risk of all-cause mortality but did not affect cancer mortality. Greater adherence to the 'western' and 'traditional' diet increased the risk of total mortality and mortality due to cancer. [ABSTRACT FROM AUTHOR]

Purpose: To inform prevention efforts, we sought to determine which cancer types contribute the most to cancer mortality disparities by individual-level education using national death certificate data for 2017. Methods: Information on all US deaths occurring in 2017 among 25–84-year-olds was ascertained from national death certificate data, which include cause of death and educational attainment. Education was classified as high school or less (≤ 12 years), some college or diploma (13–15 years), and Bachelor's degree or higher (≥ 16 years). Cancer mortality rate differences (RD) were calculated by subtracting age-adjusted mortality rates (AMR) among those with ≥ 16 years of education from AMR among those with ≤ 12 years. Results: The cancer mortality rate difference between those with a Bachelor's degree or more vs. high school or less education was 72 deaths per 100,000 person-years. Lung cancer deaths account for over half (53%) of the RD for cancer mortality by education in the US. Conclusion: Efforts to reduce smoking, particularly among persons with less education, would contribute substantially to reducing educational disparities in lung cancer and overall cancer mortality. [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.)