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Abstract Background The circadian clock and endoplasmic reticulum stress signaling play important roles in oncogenesis and development of cancer. Sleep disorders have been linked to an elevated risk of mortality in general populations. Nonetheless, the evidence for the sleep disorders-mortality association among cancer patients is limited. We aimed to prospectively investigate the association of sleep disorders with all-cause, cancer, and cardiovascular disease (CVD) mortality among cancer individuals. Methods We assessed 3187 participants with cancer from the National Health and Nutrition Examination Survey 2005–2016 cohorts with a median follow-up time of 83.0 months. Multivariable Cox proportional hazards models estimated the adjusted hazard ratio (HR) and 95% confidence interval (CI). Results Multivariable Cox proportional hazards models showed that sleep disorders were associated with a higher risk of all-cause mortality (HR 1.23, 95%CI: 1.06,1.42), cancer mortality (HR 1.30, 95%CI: 1.02, 1.66), and cardiovascular disease mortality (HR 1.35, 95%CI: 1.02, 1.80). After the total group was stratified by gender, the high HRs were observed in men (P

Background: Vascular adhesion protein-1 (VAP-1), a dual-function glycoprotein, has been reported to play a crucial role in inflammation and tumor progression. We conducted a community-based cohort study to investigate whether serum VAP-1 could be a potential biomarker for predicting incident cancers and mortality. Method: From 2006 to 2018, we enrolled 889 cancer-free subjects at baseline. Serum VAP-1 levels were measured using a time-resolved immunofluorometric assay. Cancer and vital status of the participants were obtained by linking records with the computerized cancer registry and death certificates in Taiwan. Results: During a median follow-up of 11.94 years, 69 subjects developed incident cancers and 66 subjects died, including 29 subjects who died from malignancy. Subjects in the highest tertile of serum VAP-1 had a significantly higher risk of cancer incidence (p=0.0006), cancer mortality (p=0.0001), and all- cause mortality (p=0.0002) than subjects in the other tertiles. The adjusted hazard ratios per one standard deviation increase in serumVAP-1 concentrations were 1.28 for cancer incidence (95% CI=1.01-1.62), 1.60 for cancer mortality (95% CI=1.14-2.23), and 1.38 for all-cause mortality (95% CI=1.09-1.75). The predictive performance of serum VAP-1 was better than that of gender, smoking, body mass index, hypertension, diabetes, and estimated glomerular filtration rate but lower than that of age for cancer incidence, cancer mortality, and all-cause mortality, as evidenced by higher increments in concordance statistics and area under the receiver operating characteristic curve. Conclusion: Serum VAP-1 levels are associated with a 12-year risk of incident cancer, cancer mortality, and all-cause mortality in a general population. [ABSTRACT FROM AUTHOR]

The impact of cancer in Alberta is expected to grow considerably, largely driven by population growth and aging. The Future of Cancer Impact (FOCI) initiative offers an overview of the present state of cancer care in Alberta and highlights potential opportunities for research and innovation across the continuum. In this paper, we present a series of detailed projections and analyses regarding cancer epidemiological estimates in Alberta, Canada. Data on cancer incidence and mortality in Alberta (1998–2018) and limited-duration cancer prevalence in Alberta (2000–2019) were collected from the Alberta Cancer Registry. We used the Canproj package in the R software to project these epidemiological estimates up to the year 2040. To estimate the direct management costs, we ran a series of microsimulations using the OncoSim All Cancers Model. Our findings indicate that from 2020, the total number of annual new cancer cases and cancer-related deaths are projected to increase by 56% and 49% by 2040, respectively. From 2019, the five-year prevalence of all cancers in Alberta is projected to increase by 86% by 2040. In line with these trends, the overall direct cost of cancer management is estimated to increase by 53% in 2040. These estimates and projections are integral to future strategic planning and investment. [ABSTRACT FROM AUTHOR]

PurposeThis study investigated the association between dietary patterns, total mortality, and cancer mortality in the United States.MethodsWe 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.ResultsA 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.ConclusionHigher 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.

Cancer is known as one of the leading causes of death in the world. In addition to early mortality, cancer is associated with disability in affected patients. Among environmental risk factors, special attention has been paid to the role of dietary factors. In recent decades, the consumption of sugar-sweetened beverages (SSBs) and natural fruit juices has increased. Several studies have assessed the effects of these beverages on human health and found that a higher intake of SSBs is associated with a greater risk of obesity, diabetes, cardiovascular diseases, hypertension, and non-alcoholic fatty liver disease. However, current evidence for cancer incidence and mortality is not conclusive. In the current review, we concluded that SSBs intake might be positively associated with cancer incidence/mortality through their increasing effects on obesity, inflammatory biomarkers, serum levels of insulin-like growth factor-I (IGF-I), and advanced glycation end-products. Such a positive association was also seen for natural fruit juices. However, types of natural fruit juices were not considered in most previous studies. In addition, some types of cancer including brain, lung, and renal cancers were not assessed in relation to SSBs and natural fruit juices. Therefore, further studies are needed in this regard.

Abstract Background Klotho has both anticancer and hormone‐like functions. But the research on Klotho and cancer is mainly based on animal experiments and small‐scale clinical research, thus we explored the association between serum Klotho and cancer and cancer mortality based on the National Health and Nutrition Survey (NHANES). Methods Participants were employed from the NHANES 2007–2016, excluding pregnant, chronic renal insufficiency, and incomplete data of cancer questionnaire and serum Klotho level. The association of serum Klotho with cancer and mortality was analyzed by weighted Logistic regression, weighted Cox regression and competitive risk model, respectively. Correlations between serum Klotho and testosterone and estradiol levels were analyzed by Spearman correlation and restricted cubic spline respectively. Results We found Klotho had an inverse effect with risk of pan‐cancer (all p 0.05). Then, stratified analysis found that people aged 60–79, female, overweight and non‐Hispanic whites or Mexican Americans were less likely to develop cancer. In addition, there was a strong nonlinear and linear positive correlation of Klotho with estradiol (p‐nonlinear = 0.0178) and testosterone only among male participants (β = −0.513, p = 0.0137), respectively. Conclusions We found an inverse association between serum Klotho and cancer, but without cancer mortality. And this effect may be partially mediated by estradiol and testosterone. Further prospective studies are needed to prove these findings.

Background: Klotho has both anticancer and hormone‐like functions. But the research on Klotho and cancer is mainly based on animal experiments and small‐scale clinical research, thus we explored the association between serum Klotho and cancer and cancer mortality based on the National Health and Nutrition Survey (NHANES). Methods: Participants were employed from the NHANES 2007–2016, excluding pregnant, chronic renal insufficiency, and incomplete data of cancer questionnaire and serum Klotho level. The association of serum Klotho with cancer and mortality was analyzed by weighted Logistic regression, weighted Cox regression and competitive risk model, respectively. Correlations between serum Klotho and testosterone and estradiol levels were analyzed by Spearman correlation and restricted cubic spline respectively. Results: We found Klotho had an inverse effect with risk of pan‐cancer (all p < 0.02), with each unit increase in Klotho (1ug/g creatinine) associated with a 0.9%–2.2% reduction in the risk of cancer, and higher levels showing a stronger negative association (all p‐trend <= 0.0005). Whereas, we did not observe any association between serum Klotho level with all‐cause mortality and cancer‐specific mortality (all p > 0.05). Then, stratified analysis found that people aged 60–79, female, overweight and non‐Hispanic whites or Mexican Americans were less likely to develop cancer. In addition, there was a strong nonlinear and linear positive correlation of Klotho with estradiol (p‐nonlinear = 0.0178) and testosterone only among male participants (β = −0.513, p = 0.0137), respectively. Conclusions: We found an inverse association between serum Klotho and cancer, but without cancer mortality. And this effect may be partially mediated by estradiol and testosterone. Further prospective studies are needed to prove these findings. [ABSTRACT FROM AUTHOR]

Patients with cancer have been reported to show elevated plasma concentrations of vitamin B12, thus causing uncertainties regarding safety of vitamin B12. We conducted a systematic literature search and a scoping review of human studies published in PubMed between January 2005 and March 2022, to investigate the association between vitamin B12 (concentrations of B12 biomarkers, intake, and genetic determinants) and cancer. Except for liver cancer, the association between plasma vitamin B12 concentrations and cancer was not consistent across the studies. Vitamin B12 intake from food, or food and supplements, showed even less consistent associations with cancer. There was no evidence for temporality, coherence, or a biologically meaningful dose-response relationship between plasma vitamin B12 concentrations and cancer. Genetically determined high plasma vitamin B12 was likely to be associated with cancer. Available randomized controlled trials have used a high dose of multivitamin supplements and cancer was the unplanned outcome, thus the causality of B12 in cancer cannot be judged based on these trials. Additionally, low plasma vitamin B12 concentrations were common in patients with cancer. Therefore, there is not sufficient evidence to assume that high plasma vitamin B12, high B12 intake, or treatment with pharmacological doses of vitamin B12, is causally related to cancer. Low vitamin B12 status in patients with cancer needs to be diagnosed and treated in order to prevent the hematological and neurological sequela of the deficiency. [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]

Chronic health conditions are commonplace in older populations. The process of aging impacts many of the world's top health concerns. With the average life expectancy continuing to climb, understanding patterns of morbidity in aging populations has become progressively more important. Cancer is an age-related disease, whose risk has been proven to increase with age. Limited information is published about the epidemiology of cancer and the cancer contribution to mortality in the 85+ age group, often referred to as the oldest-old. In this review, we perform a comprehensive assessment of the most recent (2011-2016) literature on cancer prevalence, incidence and mortality in the oldest-old. The data shows cancer prevalence and cancer incidence increases until ages 85-89, after which the rates decrease into 100+ ages. However the number of overall cases has steadily increased over time due to the rise in population. Cancer mortality continues to increase after age 85+. This review presents an overview of plausible associations between comorbidity, genetics and age-related physiological effects in relation to cancer risk and protection. Many of these age-related processes contribute to the lowered risk of cancer in the oldest-old, likewise other certain health conditions may "protect" from cancer in this age group.

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Background The risk of cancer in adulthood can be influenced by exposure to environmental factors (e.g. food shortage and stress) in early life. Objectives This study compared the risk of cancer morbidity and mortality between Chinese adults who were or were not exposed to the Great Chinese Famine (1959–1961) in utero or during early childhood. Methods The Kailuan Study participants (n  = 101,095) were classified into 5 famine exposure groups by birth year collected at study baseline (2006–2007): after 1961 (unexposed), 1959–1961 (in utero exposed), 1956–1958 (infancy and early childhood exposed, aged 0.1–2.9 y), 1953–1955 (childhood exposed, aged 3.0–5.9 y), and before 1953 (exposed, aged 6+ y). They were further classified by the severity of famine exposure. Cancer and cancer mortality cases from 2006 to 2016 were confirmed by reviewing medical records. Cox proportional hazard models were computed, adjusting for sex, socioeconomic status, and other time-varying cancer-related covariates. Results During a median follow-up of 10.0 y, we identified 3560 incident cancer cases and 1749 cancer deaths. Famine exposure at all ages was positively associated with the risk of cancer morbidity and mortality (P  < 0.001 for all, compared with unexposed). Severe exposure to famine in early childhood, but not other ages, had a higher risk of composite cancer events [adjusted HR = 2.04 (95% CI: 1.47, 2.84) for 0.1–2.9 y; and 1.61 (95% CI: 1.15, 2.25) for 3.0–5.9 y], relative to the less severely exposed groups of the same age range. When cancer morbidity and mortality were studied separately, similar patterns were observed. Conclusions In utero and early childhood exposures to famine, especially severe famine, were associated with a higher risk of cancer morbidity and mortality in adulthood. Awareness should be raised regarding the long-term effect of early life nutritional status. Trial registration number: ChiCTR-TNRC-11001489 (http://www.chictr.org.cn/showprojen.aspx?proj=8050). [ABSTRACT FROM AUTHOR]

OBJECTIVES: This report describes the extended follow-up (1941–2015) of a cohort of 38 549 automobile manufacturing workers with potential exposure to metalworking fluids (MWF). The outcomes of interest were mortality from cancers of the esophagus, stomach, intestine, rectum, bladder, liver, pancreas, larynx, lung, skin, prostate, brain, and female breast, as well as leukemia. This report includes 5472 deaths from cancer, more than ten times the numbers of deaths in our last summary report published 20 years ago. METHODS: Standardized mortality ratios were computed for the entire study period. Adjusted hazard ratios (HR) were estimated in Cox proportional hazard models with categorical variables for cumulative exposure to each type of MWF. RESULTS: Exposure–response patterns are consistent with prior mortality reports from this cohort. We found increased risk of skin and female breast cancer with straight fluids. For the first time, we found elevated risk of stomach cancer mortality. Overall, many of the exposure–response results did not suggest an association with MWF. CONCLUSIONS: Mortality is a poor proxy for cancer diagnosis for treatable cancers and not the optimal outcome measure in etiological studies. Although the HR presented here handle bias from the healthy worker hire effect and left truncation, they do not handle bias from healthy worker survivor effect, which likely results in underestimates of the health impacts of MWF. Although this updated summary provides some information on the risk of cancer from MWF, targeted future analyses will help clarify associations.

Patients with cancer have been reported to show elevated plasma concentrations of vitamin B12, thus causing uncertainties regarding safety of vitamin B12. We conducted a systematic literature search and a scoping review of human studies published in PubMed between January 2005 and March 2022, to investigate the association between vitamin B12 (concentrations of B12 biomarkers, intake, and genetic determinants) and cancer. Except for liver cancer, the association between plasma vitamin B12 concentrations and cancer was not consistent across the studies. Vitamin B12 intake from food, or food and supplements, showed even less consistent associations with cancer. There was no evidence for temporality, coherence, or a biologically meaningful dose-response relationship between plasma vitamin B12 concentrations and cancer. Genetically determined high plasma vitamin B12 was likely to be associated with cancer. Available randomized controlled trials have used a high dose of multivitamin supplements and cancer was the unplanned outcome, thus the causality of B12 in cancer cannot be judged based on these trials. Additionally, low plasma vitamin B12 concentrations were common in patients with cancer. Therefore, there is not sufficient evidence to assume that high plasma vitamin B12, high B12 intake, or treatment with pharmacological doses of vitamin B12, is causally related to cancer. Low vitamin B12 status in patients with cancer needs to be diagnosed and treated in order to prevent the hematological and neurological sequela of the deficiency.

Background: This study evaluates the role of social isolation on inflammation and cancer mortality among women.Methods: Data were abstracted from the U.S. National Health and Nutrition Examination Survey from 1988 to 1994. The Social Network Index was used to assess participants' degree of social isolation. C-reactive protein and fibrinogen levels were included as markers of inflammation. We used the National Death Index to identify causes and dates of mortality. Chi-square and multivariable Cox regressions were employed for statistical analyses.Results: Of 3360 women (median age: 54 years), the most isolated, very isolated, somewhat isolated, and not isolated comprised 14.5, 30.2, 37.1, and 18.2% of the sample, respectively. The most isolated participants were more likely to have low income (56.8% vs 12.2%, p < 0.001), have fewer years of education (40.8% vs 12.3%; p < 0.001), have low physical activity (27.3% vs 14.7%; p < 0.003), be obese (32.5% vs 24.4%; p = 0.02), and be current smokers (34.2% vs 10.3%; p < 0.001) compared to the not isolated ones. Mean fibrinogen levels increased with degree of social isolation (p = 0.003), but C-reactive protein showed no association (p = 0.52). Kaplan-Meier estimates indicated higher cancer mortality rates among participants with elevated fibrinogen levels, though not with statistical significance (p = 0.08). Furthermore, there was no association between social isolation and cancer mortality (p = 0.54). On multivariate analysis, obesity (HR = 1.56; 95% CI: 1.11-2.18), higher education (HR = 1.36; 95% CI: 1.01-1.83), and smoking (HR = 4.42, 95% CI: 2.84-6.88) were independent predictors for cancer mortality, while high physical activity predicted for lower mortality from cancer (HR = 0.67, 95% CI: 0.51-0.87). However, social isolation was not a predictor.Conclusion: Social isolation among women was associated with an increased level of fibrinogen, but not associated with cancer mortality. The relationship between inflammation and cancer mortality warrants further investigation. [ABSTRACT FROM AUTHOR]

Although local treatments for cervical intraepithelial neoplasia (CIN) are highly effective, it has been reported that treated women remain at increased risk of cervical and other cancers. Our aim is to explore the risk of developing or dying from cervical cancer and other human papillomavirus (HPV)- and non-HPV-related malignancies after CIN treatment and infer its magnitude compared with the general population. Design: Systematic review and meta-analysis. Eligibility criteria: Studies with registry-based follow-up reporting cancer incidence or mortality after CIN treatment. Data synthesis: Summary effects were estimated using random-effects models. Incidence rate of cervical cancer among women treated for CIN (per 100 000 woman-years). Relative risk (RR) of cervical cancer, other HPV-related anogenital tract cancer (vagina, vulva, anus), any cancer, and mortality, for women treated for CIN versus the general population. Twenty-seven studies were eligible. The incidence rate for cervical cancer after CIN treatment was 39 per 100 000 woman-years (95% confidence interval 22–69). The RR of cervical cancer was elevated compared with the general population (3.30, 2.57–4.24; P < 0.001). The RR was higher for women more than 50 years old and remained elevated for at least 20 years after treatment. The RR of vaginal (10.84, 5.58–21.10; P < 0.001), vulvar (3.34, 2.39–4.67; P < 0.001), and anal cancer (5.11, 2.73–9.55; P < 0.001) was also higher. Mortality from cervical/vaginal cancer was elevated, but our estimate was more uncertain (RR 5.04, 0.69–36.94; P = 0.073). Women treated for CIN have a considerably higher risk to be later diagnosed with cervical and other HPV-related cancers compared with the general population. The higher risk of cervical cancer lasts for at least 20 years after treatment and is higher for women more than 50 years of age. Prolonged follow-up beyond the last screening round may be warranted for previously treated women. • Women previously treated for CIN are at elevated risk of cervical and other HPV-related neoplasms. • Risk of cervical cancer remains elevated for at least 20 years after treatment. • Prolonged cervical screening beyond current last screening round at 60 or 65 should be considered. • Increased awareness for prevention or early cancer detection of other HPV-related malignancies is needed. [ABSTRACT FROM AUTHOR]

Abstract Background We examined the association between metabolic dysregulation and cancer mortality in a prospective cohort of Black and White adults. Methods A total of 25,038 Black and White adults were included in the analysis. Metabolic dysregulation was defined in two ways: 1) using the joint harmonized criteria for metabolic syndrome (MetS) and 2) based on factor analysis of 15 variables characterizing metabolic dysregulation. We estimated hazards ratios (HRs) and 95% confidence intervals (CIs) for the association of MetS and metabolic dysregulation with cancer mortality during follow-up using Cox proportional hazards models. Results About 46% of Black and 39% of White participants met the criteria for MetS. Overall, participants with MetS (HR: 1.22, 95% CI: 1.03–1.45) were at increased risk of cancer-related death. In race-stratified analysis, Black participants with MetS had significantly increased risk of cancer mortality compared with those without MetS (HR: 1.32, 95% CI: 1.01–1.72), increasing to more than a 2-fold risk of cancer mortality among those with five metabolic syndrome components (HR: 2.35, 95% CI: 1.01–5.51). Conclusions There are marked racial differences in the prevalence of metabolic dysregulation defined as MetS based on the harmonized criteria. The strong positive associations between MetS and cancer mortality suggests that efforts to improve cancer outcomes in general, and racial disparities in cancer outcomes specifically, may benefit from prevention and management of MetS and its components.

Background: Previous observational studies have suggested that coffee intake may be associated with a reduction in cancer risk. Mendelian randomization (MR) studies can help clarify whether the observed associations are likely to be causal. Here we evaluated whether coffee intake is associated with: (i) overall risk of being diagnosed with/dying from any cancer; and (ii) risk of individual cancers.Methods: We identified 46 155 cases (of which 6998 were fatal) and 270 342 controls of White British ancestry from the UK Biobank cohort (UKB), based on ICD10 diagnoses. Individuals with benign tumours were excluded. Coffee intake was self-reported and recorded based on cup/day consumption. We conducted both observational and summary data MR analyses.Results: There was no observational association between coffee intake and overall cancer risk [odds ratio (OR) per one cup/day increase = 0.99, 95% confidence interval (CI) 0.98, 1.00] or cancer death (OR = 1.01, 0.99, 1.03); the estimated OR from MR is 1.01 (0.94, 1.08) for overall cancer risk and 1.11 (0.95, 1.31) for cancer death. The relationship between coffee intake and individual cancer risks were consistent with a null effect, with most cancers showing little or no associations with coffee. Meta-analysis of our MR findings with publicly available summary data on various cancers do not support a strong causal relationship between coffee and risk of breast, ovarian, lung or prostate cancer, upon correction for multiple testing.Conclusions: Taken together, coffee intake is not associated with overall risk of being diagnosed with or dying from cancer in UKB. For individual cancers, our findings were not statistically inconsistent with earlier observational studies, although for these we were unable to rule out a small effect on specific types of cancer. [ABSTRACT FROM AUTHOR]

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.

Breast cancer is a major cause of cancer mortality. Regarding the advantages of polymeric nanoparticles as drug delivery systems with targeting potential, in this study the antitumor mechanism of targeted docetaxel polymeric nanoparticles of Ecoflex® was exploited. Since the overexpression of HER‐2 receptor in breast cancer cases is associated with poor prognosis and more aggressive disease, the proposed nanoparticles were conjugated to HER‐2 specific aptamer molecules. In vitro cytotoxicity was evaluated by MTT assay. Flow‐cytometry analysis was performed to evaluate the cellular uptake of nanoparticles loaded with a fluorescent probe. Anti‐migration effects of samples were studied. Annexin IV‐FITC and propidium iodide were implemented to investigate apoptosis induction and cell cycle analysis. Enhanced cytotoxicity compared with free docetaxel was explained considering improved cellular uptake of the nanoparticles and induced apoptosis in a larger portion of cells. Lower relative migration demonstrated enhanced anti‐migration effect of nanoparticles, and cell cycle was arrested in G2/M phase using both formulations so the anti‐microtubule mechanism of the drug was not altered. Therefore, this system could offer a potential substitute for the currently marketed docetaxel formulations, which may reduce adverse effects of the drug, while further in vivo and clinical investigations are required. [ABSTRACT FROM AUTHOR]

Background/objectives: The Oslo diet and antismoking study showed that counselling for a healthy lifestyle reduced lifelong coronary mortality in high-risk men. We explored whether the same counselling reduced also cancer risk.Methods: The study randomly allocated males at high coronary risk to either a 5-year intervention for lifestyle changes (cholesterol-lowering dietary changes, weight loss and stopping smoking) or a control group (1 : 1) in 1972/73. We explored the incidence and mortality of all cancers and cancer forms related to smoking, BMI or diet up to 43 years after randomization.Results: A total of 595 men in the intervention and 621 in the control group were included. At inclusion median age was 45 years, 588 (48.4%) subjects were overweight (BMI > 25 kg m-2 ) and 925 (76.1%) current smokers. The intervention did not reduce the risk of cancer after 43 years (adjusted hazard ratio (HR) 0.96, 95% confidence interval (CI) 0.80-1.15). In the first 25 years of follow-up, among the 1088 (89.5%) men who were overweight/obese and/or smokers, the intervention reduced the incidence of those cancer forms related to smoking, BMI or diet (including carcinoma of the respiratory, digestive and urinary tracts; adjusted HR 0.69; 95% CI 0.49-0.99). The intervention had no significant effect on incidence beyond 25 years, or on mortality.Conclusions: The 5-year counselling for a healthy lifestyle did not reduce the overall cancer risk in the very long term. However, in the first 25 years, the counselling reduced the risk of relevant cancer types in overweight/obese subjects and smokers. [ABSTRACT FROM AUTHOR]

Background The major decrease in exposure to secondhand smoke (SHS) in public places in recent decades could have contributed to the decline in smoking-related cancer mortality observed in the US population. Methods Prospective study among 11,856 non-smoking adults aged ≥40 years who participated in NHANES 1988–1994 or 1999–2004 and were followed for mortality through 2006. We estimated the amount of change in cancer mortality over time attributed to the intermediate pathway of changes in SHS exposure in public places, after adjustment for risk factors and SHS exposure at home. Results The adjusted smoking-related cancer mortality rate ratios (95% CI) for a two-fold increase in serum cotinine and a 1-hour increase in occupational SHS exposure time were 1.10 (1.03, 1.17) and 1.14 (1.06, 1.24) for all-cancer, and 1.13 (1.03, 1.24) and 1.14 (1.02, 1.26) for smoking-related cancer, respectively. The absolute reduction in mortality comparing 1999–2004 to 1988–1994 was 75.8 (−25.5, 177.0) and 77.0 (2.6, 151.4) deaths/100,000 person-years, for all-cancer and smoking-related cancer, respectively. Among these avoided all-cancer deaths, 45.8 (2.8, 89.5) and 18.1 (−1.2, 39.6)/100,000 person-year were attributable to changes in serum cotinine concentrations and occupational SHS exposure time, respectively. The corresponding numbers of smoking-related cancer avoided deaths were 36.4 (0.7, 72.8) and 9.9 (−3.8, 24.9)/100,000 person-year. Conclusions Declines in SHS exposure were associated with reductions in all-cancer and smoking-related cancer mortality, supporting that smoking bans in public places may have reduced cancer mortality among non-smoking adults. [ABSTRACT FROM AUTHOR]

The severe air pollution across China in the past several years has made the Chinese government recognize its significant impacts on public health and society, and take enormous efforts to improve the air quality all over the country, especially during the Twelfth Five-Year Plan (12th FYP). However, the overall effectiveness of these air pollution control policies remains unclear. In this study, we selected the 31 municipalities and provincial capital cities in mainland China as study settings. We collected the annual average population size, mortality rates (total mortality and mortality due to cardiovascular diseases, respiratory diseases, total cancer, lung cancer and breast cancer) and concentrations of air pollutants (PM 10 , PM 2.5 , SO 2 and NO 2 ) in each capital city from 2010 to 2015 from national or local Statistical Yearbooks. The effect sizes of air pollutants on mortality were obtained from previously published meta analyses or cohort studies. We first estimated the annual mortality rates attributed to the changes in air pollutant concentrations for every city in each year. Then, we further estimated the mortality benefits in the scenarios where the air quality had reached the grade II levels of Chinese Ambient Air Quality Standards (CAAQS) and World Health Organization (WHO) guidelines. In most capital cities, we observed dominant decreases in air pollutant concentrations during the 12th FYP, particularly from 2013 to 2015, which has led to significant mortality benefits for the public. A total of 121,658 deaths (0.441‰) have been prevented due to the decrease of PM 2.5 concentrations from 2013 to 2015 in all included cities. The morality benefits were larger in capital cities located in the key regions (the three main regions and ten city groups) than the other cities. In addition, more mortality benefits could be obtained in the future if the air quality reaches the grade II levels of Chinese Ambient Air Quality Standards (CAAQS) or WHO guidelines. We concluded that substantial mortality benefits achieved during the 12th FYP may be attributed to the improvements in China's air quality, which indicated the significant effectiveness of air pollution control policies. [ABSTRACT FROM AUTHOR]

Background: We examined the association between metabolic dysregulation and cancer mortality in a prospective cohort of Black and White adults.Methods: A total of 25,038 Black and White adults were included in the analysis. Metabolic dysregulation was defined in two ways: 1) using the joint harmonized criteria for metabolic syndrome (MetS) and 2) based on factor analysis of 15 variables characterizing metabolic dysregulation. We estimated hazards ratios (HRs) and 95% confidence intervals (CIs) for the association of MetS and metabolic dysregulation with cancer mortality during follow-up using Cox proportional hazards models.Results: About 46% of Black and 39% of White participants met the criteria for MetS. Overall, participants with MetS (HR: 1.22, 95% CI: 1.03-1.45) were at increased risk of cancer-related death. In race-stratified analysis, Black participants with MetS had significantly increased risk of cancer mortality compared with those without MetS (HR: 1.32, 95% CI: 1.01-1.72), increasing to more than a 2-fold risk of cancer mortality among those with five metabolic syndrome components (HR: 2.35, 95% CI: 1.01-5.51).Conclusions: There are marked racial differences in the prevalence of metabolic dysregulation defined as MetS based on the harmonized criteria. The strong positive associations between MetS and cancer mortality suggests that efforts to improve cancer outcomes in general, and racial disparities in cancer outcomes specifically, may benefit from prevention and management of MetS and its components. [ABSTRACT FROM AUTHOR]

Large clinical cancer registries (CCRs) in Germany shall be strengthened by the German Social Code Book V (SGB V) and implemented until the end of 2017. There are currently several large cancer registries that support clinical data for outcome analysis and knowledge acquisition. The various examples of the Munich Cancer Registry outlined in this paper present many-sided possibilities using and analyzing registry data. The main objective of population-based cancer registration within a defined area and the performance of outcomes research is to provide feedback regarding the results to the broad public, the reporting doctors, and the scientific community. These tasks determine principles of operation and data usage by CCRs. Each clinical department delivers its own findings and applied therapy. The compilation of these data in CCRs provides information on patient progress through the regional network of medical care and delivers meaningful information on the course of oncological diseases. Successful implementation of CCRs allows for presenting the statistical outcomes of health-care delivery, improving the quality of care within the region, accelerating the process of implementing innovative therapies, and generating new hypotheses as a stimulus for research activities. [ABSTRACT FROM AUTHOR]

Introduction. Since the 20th century tobacco smoking has had an enormous impact on morbidity and mortality in the adult population, and it remains the greatest single preventable health risk factor worldwide. Cancer is the second leading cause of death in Poland, with lung cancer as the primary cause of cancer-related death in Polish men and women. Given these statistics, this manuscript aims to estimate tobacco-attributable cancer mortality in Poland. Material and methods. Data on cancer mortality come from the WHO Mortality Statistics database. Data on smoking prevalence in Poland come from standardized surveys based on nationally representative samples. Data on relative risks come from the Cancer Prevention Study II. Tobacco-attributable fractions were calculated using standard methodology for calculating population-based attributable fractions. Results. In 2014, there were over 24 thousand tobacco-attributed cancer deaths in men. Lung cancer tops the list of ranked cancer types, with a tobacco-attributable fraction of 93%. Next is laryngeal (TAF = 90%), oropharyngeal (TAF = 86%) and esophageal (TAF = 80%) cancer. Overall, two-thirds of the considered cancer deaths were attributed to tobacco smoke (TAF = 75%). In 2014, there were over 7.5 thousand of cancer deaths related to smoking in women. Here, both laryngeal and lung cancer (both TAF = 76%) top the ranked list. Next are esophageal (TAF = 61%) and oropharyngeal (TAF = 51%) cancers, and when combined almost half of all considered cancer deaths were attributed to tobacco smoke (TAF = 44%). Conclusions. Tobacco smoking and tobacco-attributable cancer mortality remain one of the greatest health burdens in Poles. Each year over 30 thousand Polish men and women die of cancer caused by smoking. All these deaths could be avoided. [ABSTRACT FROM AUTHOR]