Risk Of Cancer Mortality Research Articles

Comparative effectiveness of digital variance and subtraction angiography in lower limb angiography: A Monte Carlo modelling approach

ObjectiveBy modelling patient exposures of interventional procedures, this study compares the reduction of radiation detriment between Digital Variance Angiography (DVA) and Digital Subtraction Angiography (DSA). MethodsThe paper presents a retrospective risk assessment using an in-house developed tool on 107 patient exposures from a clinical trial of DVA used to diagnose peripheral arterial disease (PAD). DICOM exposure parameters were used to initiate the PENELOPE (PENetration and Energy LOss of Positrons and Electrons) Monte Carlo simulation, radiation quality and quantity, and irradiation geometry. The effective dose and the lifetime attributable risk (LAR) for cancer incidence and mortality are calculated based on the International Commission on Radiation Protection’s (ICRP) 103 recommendations and the Committee on the Biological Effects of Ionising Radiations’ latest (BEIR VII) report, respectively. ResultsThe study found that procedures conducted using DVA significantly reduce the radiation exposure of patients, compared to DSA. The collective effective dose for the DVA group was 58% lower than that for the DSA group. Correspondingly, the LAR of different organs showed a substantial decrease for cancer incidence (25–75%) and mortality (51–84%). ConclusionDVA demonstrates a considerable reduction in physical dosimetric quantities and consequently effective dose and cancer risk, suggesting its potential as a safer alternative to DSA in interventional radiology. The use of DVA supports the optimisation of patient radiation protection and aligns with the principles of ALARA (as low as reasonably achievable).

Association of serum creatinine-cystatin C ratio with all-cause, cardiovascular and cancer mortality in US adults: a nationwide cohort study

ObjectiveTo investigate the association of serum creatinine-cystatin C ratio (Cr/CysC) with long-term all-cause mortality and cause-specific (cardiovascular and cancer) mortality among US general adults.MethodsThis nationally representative cohort study included adults in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2004. Participants were linked to National Death Index data from the survey date through December 31, 2019. Weighted Cox proportional hazards regression models were used to calculate hazard ratios and 95% confidence intervals (CIs), and restricted cubic splines and stratified analyses were also performed.ResultsA total of 12,914 participants were included in this study (mean [SD] age, 45.3 [17.3] years; males, 48.9%). During a median follow-up of 17.9 years (maximum follow-up, 20.8 years), 3439 total deaths occurred, including 1098 cardiovascular deaths and 736 cancer deaths. Cumulative incidence curves revealed that increased Cr/CysC ratio had lower risk of all-cause (P < 0.001), cardiovascular (P < 0.001) and cancer (P < 0.001) mortality. Cox regression an Fine-Gray hazards models demonstrated that the multivariable-adjusted hazard ratios comparing the highest vs. lowest quartile of Cr/CysC ratio were 0.40 (95% CI, 0.34–0.47; P < 0.001) for all-cause mortality, 0.68 (95% CI, 0.52–0.88; P < 0.001) for cardiovascular mortality, and 0.51 (95% CI, 0.36–0.71; P < 0.001) for cancer mortality. Nonlinear association was observed for Cr/CysC ratio and all-cause mortality (P = 0.018 for nonlinearity), and linear associations were observed for Cr/CysC ratio and cardiovascular (P = 0.212 for nonlinearity) and cancer (P = 0.550 for nonlinearity) mortality. Besides, a series of sensitivity analyses ensured the robustness of the results.ConclusionsIn this cohort of US adults, Cr/CysC ratio was negatively associated with all-cause, cardiovascular, and cancer mortality. Our study suggests that Cr/CysC ratio may serve as a simple and effective predictor of long-term health outcomes.

Fasting plasma glucose levels are associated with all-cause and cancer mortality: A population-based retrospective cohort study.

Despite a growing body of research indicating a link between fasting glucose levels and mortality, the relationship between fasting glucose and all-cause and cancer mortality remains inconsistent. In this study, we used Cox regression and restricted cubic spline models to analyze the association and dose-response relationship between fasting plasma glucose levels and all-cause and cancer mortality in a retrospective cohort based on data from the 2015 health check-ups of residents in Quzhou City. After a mean follow-up of 5.31 years for 148,755 study participants, 10,345 deaths occurred, with an all-cause mortality density of 131.09/10,000 person-years, of which 2,845 were cancer deaths, with a cancer mortality density of 36.05/10,000 person-years. There was a "J" shaped dose-response relationship between fasting plasma glucose levels and all-cause and cancer mortality. Relative to normal fasting glucose (NFG), the risk of all-cause mortality (HRs and 95% CIs) in the impaired fasting glucose (IFG) and diabetes mellitus (DM) groups was 1.11 (1.06, 1.16) and 1.43 (1.35, 1.52), respectively, and the risk of cancer mortality in the DM group was 1.22 (1.09, 1.37). In this cohort study, we found that fasting plasma glucose levels were significantly associated with the risk of all-cause and cancer mortality.

Racial disparities in the frequency and timing of code status orders among women with breast cancer

BackgroundBlack/African American women with breast cancer have a disproportionately higher risk of mortality compared to other race groups, although their overall incidence of disease is lower. Despite this, advance care planning (ACP) and consequent code status documentation remain low in this vulnerable patient population. Code status orders (i.e., Full code, Do Not Attempt Resuscitation [DNAR], Do Not Intubate [DNI]) allow consideration of patient preferences regarding the use of aggressive treatments, such as cardiopulmonary resuscitation and intubation. The aim of this study is to characterize presence of code status orders and determine whether race affects code status documentation after the first encounter for breast cancer.MethodsData were derived from 7524 women with breast cancer from the University of Chicago Medical Center (UCMC) between 2016 and 2021. Cox regression was used to estimate the effects of race and adjusted for age, ethnicity, inpatient stays, metastatic breast cancer, marital status, and body mass index.ResultsThe sample included 60.5% White, 3.6% Asian/Mideast Indian, 28.9% Black/African American, and 7.0% other or unknown race. Results indicate that code status orders after the first breast cancer encounter were uncommon (7.2%). Black/African American race (HR = 2.74; 95% CI: 1.75, 4.28) emerged as a significant factor associated with any code status orders compared to other race groups even when adjusting for covariates.ConclusionsCode status documentation in this sample of women with breast cancer was low overall, yet rates were higher among Black/African American patients compared to other race groups. In fact, race remains a significant predictor of code status documentation even when accounting for indirect measures of cancer severity. This could be denoting the racial disparities (e.g., higher cancer malignancy such as triple negative breast cancer) in breast cancer mortality risk. Future research is needed to identify factors unique to Black/African American women that would increase code status documentation so that goal concordant care can be prioritized among patients with breast cancer.

Nonlinear association of alkaline phosphatase-to-albumin ratio with all-cause and cancer mortality: Evidence from NHANES 2005 to 2016.

The relationship between the alkaline phosphatase-to-albumin ratio (APAR) and mortality remains unclear. This research looked into the association between APAR levels and cause-specific mortality in US adults. A cohort of 7561 participants from National Health and Nutrition Examination Survey (2005-2016) was analyzed, with mortality outcomes collected from National Death Index records. Cox proportional hazards models and restricted cubic spline (RCS) analysis were utilized to determine hazard ratio (HR) and reveal the nonlinear relationship between APAR levels and mortality. Inflection points were calculated using a recursive algorithm. Followed for an average 99.41 months, a total of 1048 deaths occurred, including 200 cancer deaths and 348 cardiovascular disease-related deaths. Following multivariate adjustment, significant associations were observed between APAR levels and increased all-cause (HR 1.50, 95% CI 1.28-1.75, P < .001) and cardiovascular disease (HR 1.39, 95% CI 1.06-1.82, P = .018) mortality. Furthermore, nonlinear correlations between APAR levels and all-cause and cancer mortality were revealed, characterized by an L-shaped pattern, with mortality rates stabilizing at 1.289 and 2.167, respectively. Participants with APAR levels above the inflection point exhibited a 29.2% increase in all-cause mortality risk per unit increase in APAR levels (HR 1.292, 95% CI 1.217-1.372, P < .001), and a 38.3% increase in cancer mortality risk (HR 1.383, 95% CI 1.199-1.596, P < .001). This study demonstrated nonlinear associations between APAR levels and all-cause and cancer mortality. Thresholds of 1.289 and 2.167 might serve as potential targets for APAR to reduce all-cause and cancer mortality, respectively. Our findings suggest that APAR can be a valuable prognostic tool for clinical mortality risk assessments, helping to identify individuals at higher risk. Nevertheless, these findings necessitate validation through large-scale clinical trials for further substantiation.

Evaluating Usability and Feasibility of Implementing a Novel Cancer Mapping Tool.

Purpose: Cancer registries are often asked to present cancer data for small geographic areas to inform and facilitate targeted interventions and prevention programs. However, it is challenging to compute and visualize reliable cancer estimates for areas with small case counts and populations to support cancer control planning. Methods: We used a Bayesian hierarchical model that borrows strength from neighboring areas and over time to produce cancer estimates for small areas. We developed a visual analytics platform to present these estimates in interactive graphics that demonstrate risk in small areas. In a user-centered design process, development of the tool was informed by cancer registry and public health professionals through focus groups and surveys. Results: The Cancer Analytics and Maps for Small Areas tool (CAMSA) provides age-adjusted cancer incidence and mortality rates and risk probabilities for eight cancers at the county and ZIP-code tabulation area (ZCTA) levels. It allows the user to identify cancer hotpots, including among sub-groups defined by sex and race/ethnicity. Potential end users were enthusiastic about the opportunity to implement CAMSA within their practice, emphasizing the tool's potential for increasing collaborative opportunities at local and state levels. Suggestions for improvement included adding map overlays such as additional cancer risk variables and incorporating functionalities like exportable data tables. Conclusions: CAMSA presents cancer rate and risk estimates for small geographic areas where they may have previously been suppressed. Through our user-informed design process, we developed statistical models and data visualizations to support the needs of an array of potential end users.

CYP2D6 Phenotype and Breast Cancer Outcomes: A Bias Analysis and Meta-Analysis.

We evaluated the impact of systematic bias due to loss of heterozygosity (LOH) and incomplete phenotyping in studies examining the relationship between CYP2D6 variants and breast cancer recurrence among women treated with tamoxifen. We performed a systematic review of the literature on tamoxifen, CYP2D6 variants, and breast cancer recurrence. A quantitative bias analysis was performed to adjust for LOH and incomplete phenotyping. Bias-adjusted results were then combined in a meta-analysis. Thirty-three studies informed the bias analysis and meta-analysis on CYP2D6 variants and breast cancer recurrence and/or mortality. An unadjusted meta-analysis suggested increased risk of recurrence and/or mortality for poor relative to normal metabolizers [RR = 1.28; 95% simulation interval (SI), 1.04-1.58] with substantial heterogeneity (I2 = 27%; P for heterogeneity = 0.07). Adjusting for LOH and incomplete genotyping resulted in a slight change in the effect estimate and a decrease in heterogeneity (RR = 1.34; 95% SI, 1.10-1.63; I2 = 0%; P for heterogeneity = 0.17). Intermediate metabolizers had a slightly increased risk of recurrence and/or mortality relative to normal metabolizers (RR = 1.15; 95% SI, 1.00-1.34; I2 = 0%; P for heterogeneity = 0.89). Adjusting for biases such as LOH and incomplete genotyping reduced observed heterogeneity between studies. Individuals with poor CYP2D6 phenotypes were at increased risk for breast cancer outcomes compared with those with normal phenotypes. Reduction in CYP2D6 activity was associated with an increased risk of breast cancer recurrence and/or mortality, and results underscore the importance of quantitatively adjusting for biases when aggregating study results.

Total, dietary, and supplemental calcium intake and risk of all-cause, cardiovascular, and cancer mortality among U.S. adults: a prospective cohort study from the National Health and Nutrition Examination Survey.

The study aimed to investigate the association of total, dietary, or supplemental calcium intake with all-cause, cardiovascular, and cancer mortality in American adults. This prospective cohort study used the National Health and Nutrition Examination Survey from 2005 to 2018. Participants were categorized into tertiles based on calcium intake. Risks of all-cause, cancer, or cardiovascular mortality and the dose-response relationship were estimated using weighted Cox proportional hazard regression and restricted cubic splines, with adjustments for demographic characteristics, comorbidities, laboratory parameters, and dietary data. In total, 6172 participants were included (median age: 61 years), and 869 had died (CVD:217, cancer:224) during a median follow-up of 81 months. After adjusting for confounders, higher total calcium(≥ 1660mg/d) [HR, 95%CI: 0.867 (0.865-0.869)], dietary calcium(≥ 1075mg/d) [HR, 95%CI: 0.711 (0.709-0.713)], and supplemental calcium (≥ 600mg/d) [HR, 95%CI: 0.786 (0.784-0.787)] intake groups were associated with lower all-cause mortality risk compared to the lowest intake group. Similar beneficial associations were found for cardiovascular, cancer mortality, and across subgroups of various ages, genders, races and body mass indexes. In the dose-response analysis, a 'J-shaped' nonlinear relationship was observed between calcium intake and the risk of all-cause, cardiovascular, and cancer mortality. Higher levels of total, dietary, or supplemental calcium were associated with lower all-cause, cardiovascular, or cancer mortality. However, a nonlinear association between calcium intake and mortality suggested that excessive calcium intake beyond a certain threshold may increase mortality risk.

Income-Related Disparities in Mortality Among Young Adults With Type 2 Diabetes

Previous studies have indicated an inverse association between income and mortality. However, differences in health outcomes according to the income level of young adults with type 2 diabetes (T2D) compared with older adults with T2D have not been elucidated. To estimate the overall and cause-specific mortality risks among patients with T2D according to income and age. This retrospective nationwide cohort study in South Korea included adults aged 20 to 79 years who were diagnosed with T2D between January 1, 2008, and December 31, 2013, and followed up until December 31, 2019, and age- and sex-matched controls without diabetes. Data were analyzed between January 1, 2023, and August 27, 2024. Risks of all-cause, cardiovascular, and cancer mortality were estimated according to participants' income, which was categorized into 3 levels (low, middle, and high) based on the health insurance premium. Logistic regression analyses and Cox proportional hazard regression analyses were performed according to age groups (20-39, 40-59, and 60-79 years). A total of 1 240 780 adults (604 975 patients with T2D and 635 805 age- and sex-matched controls without diabetes) were included in the analyses. Their mean (SD) age was 56.9 (11.8) years, and 626 176 (50.5%) were men. Overall, the risk of mortality increased with lower income among patients with T2D, as well as in comparison with controls without diabetes. There was an inverse association between income and mortality risk in younger individuals (adjusted hazard ratios of all-cause mortality in the low income vs high income subgroups with T2D were 2.88 [95% CI, 2.25-3.69] in those aged 20 to 39 years, 1.90 [95% CI, 1.81-2.00] in those aged 40 to 59 years, and 1.26 [95% CI, 1.23-1.29] in those aged 60 to 79 years; P < .001 for comparing risk ratios between age groups). The pattern of income-related disparities in younger individuals was observed in cardiovascular mortality but less in cancer mortality. In this cohort study of 1 240 780 individuals aged 20 to 79 years, the risk of mortality with low income was most prominent among individuals with T2D aged 20 to 39 years. These findings highlight the need for socioeconomic support to reduce income-related health disparities in younger individuals.

Abstract 4123540: Cardiovascular Health and Cancer Incidence and Mortality: NHANES-III and -Continuous study

Background: Cancer and cardiovascular disease (CVD) are the leading causes of death worldwide. Limited evidence is available regarding the relationship between CVD, cardiovascular risk factors (CVRF), and cancer mortality; and how CVRF further modify that relationship. Methods: The first part included 438 and 2100 CVD patients aged 65+ from NHANES-III and Continuous (1999-2016) datasets, respectively. Competing risk models with subdistribution hazards ratio (aHR) were used to identify risk factors for cancer incidence. The second part included 44,591 adult individuals from NHANES-Continuous merged with Medicare and National Death Index mortality data until the end of 2018. We included individuals with no history of cancer at baseline. We used competing risk modeling to test the relationship between CVD at baseline and cancer mortality. We also conducted a comprehensive risk factor analysis. Results: In the first part (Figure), females in NHANES-III had lower cancer risk (aHR 0.39, P=0.001) compared to males. Poor physical activity was associated with increased cancer risk in both datasets (aHR 2.59 in NHANES-III, aHR 1.59 in Continuous). In NHANES-Continuous, age (aHR 1.07, P&lt;0.001) and current smoking (aHR 2.55, P=0.001) showed a significant association with developing cancer. No other factors investigated showed significant associations. In the second analysis (Table), the included sample size represented 1,738,423,317 individuals (52% females, 67% non-Hispanic Whites, and 9% Hispanics). Competing risk modeling showed a significantly higher risk of cancer mortality in individuals with CVD (aHR 1.37, 95% CI 1.07-1.76, P=0.01) after adjusting for age, sex, and race/ethnicity. Notably, cancer mortality increased with aging (aHR 1.08, 95%CI 1.05-1.11, P&lt;0.0001), current smoking status (aHR 6.78, 95%CI 3.43-13.42, P&lt;0.0001), and obesity (aHR 2.32, 95%CI 1.13-4.79, P=0.02). Finally, a significant interaction (P=0.034) was found where those with CVD and obesity showed higher cancer mortality than those with normal BMI (aHR, 95%CI 1.03-2.91, P=0.04). Conclusions: Our study highlights the close relationship between cardiovascular health and cancer, including among CVD patients. Our findings suggest that physical activity and obesity may play a significant role in cancer incidence and mortality among the general population and CVD patients. These findings emphasize the need for more proactive approach in the management of shared risk factors for CVD and cancer.

Associations of saccharin intake with all-cause, cardiovascular and cancer mortality risk in USA adults.

Saccharin is a widely used sugar substitute, but little is known about the long-term health effects of saccharin intake. Our study aimed to examine the association between saccharin intake and mortality in diabetic and pre-diabetic population and overweight population from NHANES 1988-1994. Cox proportional hazard models were used to evaluate the association between saccharin intake and CVD, cancer and all-cause mortality. After multivariable adjustment, increased absolute saccharin intake was associated with the risk of all-cause mortality (hazard ratio (HR): 1·41, 95 % CI: 1·05, 1·90), CVD mortality (HR: 1·93, 95 % CI: 1·15, 3·25) and cancer mortality (HR: 2·26, 95 % CI: 1·10, 4·45) in diabetic and pre-diabetic population. Among overweight population, higher absolute saccharin intake was associated with the risk of cancer mortality (HR: 7·369, 95 % CI: 2·122, 25·592). Replacing absolute saccharin intake with total sugar significantly reduced all-cause mortality by 12·5 % and CVD mortality by 49·7 % in an equivalent substitution analysis in the diabetic and pre-diabetic population. Aspartame substitution reduced all-cause mortality by 29·2 % and cancer mortality by 30·2 %. Notably, the relative daily intake of saccharin also had similar effects as the absolute intake on all-cause, cardiovascular and cancer mortality in all analyses. This was despite the fact that the relative daily intake in our study was below the Food and Drug Administration limit of 15 mg/kg. In conclusion, our study showed a considerable risk of increased saccharin intake on the all-cause, CVD mortality and cancer mortality.

Menopausal hormone therapy and incidence, mortality, and survival of breast cancer subtypes: a prospective cohort study

BackgroundMenopausal hormone therapy (MHT) is associated with an increased risk of postmenopausal breast cancer, predominantly the luminal A-like subtype. The impact of MHT on deaths from breast cancer subtypes is less understood. This study aimed to explore associations between MHT use and the incidence, mortality, and survival of intrinsic-like breast cancer subtypes.MethodsData from 160,881 participants with self-reported MHT use from the prospective Norwegian Women and Cancer Study were analyzed. Among them, 7,844 incident breast cancer cases, and 721 breast cancer-specific deaths occurred. Cox proportional hazard regression was performed to calculate hazard ratios (HRs) with 95% confidence intervals (CIs) for the association between MHT use and the incidence, mortality, and survival of breast cancer subtypes.ResultsMHT use was associated with increased risk of overall, luminal A-like, and luminal B-like breast cancer, with respective HRs of 1.44 (95% CI 1.36–1.52), 1.41 (95% CI 1.31–1.52), and 1.23 (95% CI 1.09–1.40) among current estrogen-progestin therapy (EPT) users compared with never users. The risk increased by 4%, 4%, and 2% per year of EPT use for overall, luminal A-like, and luminal B-like breast cancers, respectively. MHT use was also associated with increased risk of overall and luminal A-like breast cancer mortality, with HRs 1.61% (95% CI 1.36–1.91) and 2.15% (95% CI 1.51–3.05) increased risk among current EPT users compared with non-users. Among patients with breast cancer, pre-diagnostic MHT use was not associated with worse survival from overall breast cancer but was inversely associated with survival from triple-negative breast cancer (TNBC; HR death 0.41; 95% CI 0.24–0.73 among current users). Results varied significantly according to tumor subtype (pheterogeneity = 0.02).ConclusionsOur study suggests that MHT use increases the risk of incident and fatal overall and luminal A-like, and incident luminal B-like breast cancer but does not decrease overall survival among patients with breast cancer. Further research is needed to elucidate the mechanisms underlying MHT use and breast cancer lethality, and to explore whether MHT use among patients with TNBC is indeed free from harm.

Postprandial Plasma Glucose With a Fasting Time of 4-7.9h Is Positively Associated With Cancer Mortality in US Adults.

This study investigated the association of postprandial plasma glucose (PPG) with cancer mortality using a general cohort of US adults. This cohort study included 14,860 US adults who attended the third National Health and Nutrition Examination Survey from 1988 to 1994, with mortality being followed up until December 31, 2019. The explanatory variable was the level of plasma glucose, including PPG with a fasting time of 0-3.9h (PPG0-3.9h) and 4-7.9h (PPG4-7.9h), plasma glucose with a fasting time ≥8h (PGfasting), and plasma glucose at 2h after oral glucose tolerance test (PG2hOGTT). Plasma glucose-associated cancer mortality risk was assessed using Cox proportional hazard models. A 1-natural-log-unit increase in PPG4-7.9h was associated with a higher multivariate-adjusted risk for cancer mortality [hazard ratio (HR), 3.24; 95% confidence interval (CI), 1.50-7.00]. However, PPG0-3.9h, PGfasting, PG2hOGTT, haemoglobin A1c, and insulin were not significantly associated with cancer mortality. The positive association of PPG4-7.9h with cancer mortality remained in those without a prior diagnosis of cancer. High PPG4-7.9h is associated with a higher cancer mortality risk in US adults. Lowering PPG4-7.9h may reduce cancer mortality.

Cancer and mortality risks among people with multiple sclerosis: A population-based study in Isfahan, Iran.

Multiple sclerosis (MS) and cancer present substantial global health challenges. Understanding cancer patterns among people with MS (PwMS) is crucial due to potential variations across demographics and geographic regions. Isfahan province in Iran, known for its high MS incidence ratio, offers a significant population for comprehensive studies on MS. In this study, we aim to investigate the association between risk of cancer and MS. Data on PwMS were collected utilizing the National Multiple Sclerosis Registry System of Iran (NMSRI), with diagnoses confirmed using McDonald criteria by neurologists specialized in MS. Cancer incidence was investigated using the Iranian National Population-Based Cancer Registry (INPCR) data, collected following international protocols. Descriptive statistics and regression analyses were employed to assess factors associated with cancer and mortality risks among PwMS. Survival analysis was conducted using Kaplan-Meier curves. Out of 10,049 PwMS, 123 were diagnosed with cancer, with an mean age at the time of cancer diagnosis being 40.41 years and a mean MS duration of 6.76 years. The majority had relapsing-remitting MS (81.2%), and Interferon-β was the most common disease-modifying therapy (DMT) (42.4%). Cancer incidence was 125.6 per 100,000 person-years, peaking at ages 60-64 (677.9 per 100,000 person-years). Receiving monoclonal antibody medications and older age were significantly associated with higher cancer risk (OR:1.542 (1.009-2.357), OR:1.033 (1.015-1.051), respectively). Female breast cancer had the highest incidence ratio among PwMS (40.17 per 100,000 person-years), followed by thyroid (18.38 per 100,000 person-years) and digestive system cancers (17.36 per 100,000 person-years). Breast cancer was the predominant cancer in women, while digestive system cancers were most common among men. Being male and having longer MS duration were linked to higher cancer mortality risk (HR: 2.683, 1.087, respectively). Cancer incidence among 10,049 people with multiple sclerosis was significant, especially in older individuals, with breast cancer being the most common. Male gender and longer MS duration were linked to higher cancer mortality risk.

Association of prophylactic low-dose aspirin use with all-cause and cause-specific mortality in cancer patients

The long-term use of aspirin for preventing cardiovascular disease has been recommended for decades. However, there is currently uncertainty regarding the long-term effects of aspirin use on the risk of all-cause, cardiovascular, and cancer mortality in cancer patients. The aim of this work was to analyze the connection between the prophylactic use of low-dose aspirin and the risk of all-cause death, cardiovascular death, and carcinoma death in carcinoma patients in the United States. A cohort study was conducted using National Health and Nutrition Examination Survey (NHANES) data (2011–2012, 2013–2014, 2015–2016, and 2017–2018) and associated mortality data. The 95% confidence intervals (CIs) and hazard ratios (HRs) between non-aspirin use and prophylactic low-dose aspirin use and the risk of death were measured via Cox proportional hazard regression models. A total of 1819 participants were included in the present research, of whom 945 were nonaspirin users and 874 were prophylactic aspirin users. Compared with non-aspirin users, prophylactic low-dose aspirin users had a decreased risk of all-cause death (HR = 0.647, 95% CI = 0.489–0.857). There was no statistically significant difference in the risk of cardiovascular death (HR = 0.623, 95% CI = 0.362–1.074) or cancer death (HR = 0.709, 95% CI = 0.410–1.226). Prophylactic use of low-dose aspirin may lower all-cause mortality in individuals with cancer but does not have a substantial effect on cardiovascular risk or cancer-specific mortality in this patient population.

Educational inequalities in cervical cancer mortality: A systematic review and meta-analysis

Abstract Background Educational inequalities in mortality continue to persist. We aimed to systematically analyse the association between level of education and cervical cancer mortality. Methods We conducted a systematic review and meta-analysis. We systematically searched Pub-Med, Web of Science, Scopus, EMBASE and Global Health (CAB), EconLit and Sociology Source Ultimate databases. A protocol has been registered with PROSPERO (CRD42023411757). We included studies that measured the association between level of education and cervical cancer mortality using individual level data. Included articles were assessed for study quality and risk of bias using the Joanna Briggs Institute critical appraisal checklists. A random-effects meta-analysis was conducted to evaluate the overall and stratified effects of education on mortality. Findings Our literature search resulted in over 47,000 articles. 30 studies mentioned cervical cancer as a cause of death, and of these, 11 were eligible for the meta-analysis. Results showed an overall risk ratio of 2.41 (95% CI 1.81-3.20) for low education (ISCED 0-2) and 1.62 (95% CI 1.18-2.24) for medium education (ISCED 3-4). Those aged 25-64 with low education had more than twice the risk of cervical cancer (RR = 5.73; 95% CI 5.04-6.51) compared to those aged 25 and above (RR = 2.11; 95% CI 1.82-2.45). Besides, the impact of an additional level of education on reducing risk of cervical cancer mortality was higher in Northern Europe, compared to the South. Interpretation Lower educational attainment is associated with an increase in the risk of cervical cancer mortality, with an additional level of education greatly reducing this risk in Northern Europe. Younger cohorts with low education have a higher risk of cervical cancer mortality. This study provides important information for evidence-based policy seeking to reduce health inequities and inequalities in both the health and education sector. Key messages • Lower educational attainment is linked to a higher risk of cervical cancer mortality. • Younger cohorts (aged 25-64) with low education are at a particularly heightened risk compared to those aged 25 and above.

Sleep characteristics in relation to cardiovascular disease incidence and mortality in individuals with diabetes

Abstract Background/Introduction Evidence regarding the potential health effects of sleep characteristics among individuals with type 2 diabetes (T2D) is limited. Purpose We aimed to examine sleep characteristics in relation to subsequent risk of cardiovascular disease (CVD), including coronary heart disease (CHD), and stroke, and all-cause and cause-specific mortality among individuals with T2D. Methods We prospectively followed 21,902 men and women with T2D at baseline or diagnosed during follow-up (Nurses' Health Study: 1986-2018, Health Professionals Follow-Up Study: 1986-2018). Sleep characteristics, including sleep duration, snoring, sleep apnea, and sleep quality, were repeatedly assessed using self-reported questionnaires at baseline and follow-up. Associations of sleep characteristics with CVD risk and mortality were assessed using Cox proportional hazards models with adjustments for demographic, dietary and lifestyle factors, and medical history. Results During 170,355 and 196,458 person-years of follow-up in participants with T2D, there were 2,486 incident CVD events and 3,922 deaths, respectively. Compared with sleeping for 7-8 h/day, the multivariable-adjusted hazard ratios (HRs) of sleeping for ≤5 h/day were 1.21 (1.02, 1.45) for CVD incidence, 1.24 (1.20, 1.51) for CHD incidence, 1.40 (1.24, 1.58) for total mortality, 1.52 (1.20, 1.92) for CVD mortality, and 1.27 (1.01, 1.61) for other non-CVD and non-cancer mortality, while the HRs of ≥10 h/day were 1.42 (1.21, 1.66) for total mortality, and 1.63 (1.20, 2.10) for other non-CVD and non-cancer mortality. Furthermore, compared with participants without habitual snoring, those with habitual snoring had a 21%, 24%, 18%, and 33% higher risk for CVD incidence, CHD incidence, CVD mortality, and total mortality, respectively. Compared with participants without diagnosed sleep apnea, those with sleep apnea had a 27%-58% higher risk for CVD incidence, CVD mortality, and total mortality. In addition, lower habitual sleep quality, including sleep difficulties and restless sleep, was associated with a substantially higher risk of CVD, CHD, or CVD mortality. No associations were observed between sleep characteristics with risk of stroke and cancer mortality in individuals with T2D. Conclusions Short and long sleep durations as well as habitual snoring, sleep apnea, and lower sleep quality were independently associated with higher risks of CVD incidence and mortality, particularly CVD mortality in individuals with T2D.

Association between PCSK9 inhibitor with cause-specific morality amongst cancer survivors

Abstract Background Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor has emerged as a novel pharmacotherapy for dyslipidemia and been shown to be effective in reducing the risks of atherosclerotic cardiovascular diseases. PCSK9 is aberrantly expressed in a broad spectrum of cancers and has been demonstrated to contribute to cancer prognosis. However, no prior study has investigated the associations between PCSK9 inhibitors (PCSK9i) with cardiovascular and cancer mortality amongst cancer survivors. Purpose This study investigated the effects of PCSK9i on cause-specific mortality amongst cancer survivors. Methods This retrospective study used data from the Tianjin Coronary Artery Disease Cohort, which included medical data from 71 secondary or tertiary hospitals in Tianjin, China. Adult patients with coronary artery disease (CAD) diagnosed with incident cancer between 2017 and 2023 were enrolled in this study. Propensity score matching with a 1:3 ratio for PCSK9i users versus non-users was performed. The primary outcomes included all-cause mortality, cardiovascular mortality, and cancer mortality. Multivariable Cox regression was used to test associations between PCSK9i with outcomes, adjusting for age, gender, cardiovascular and non-cardiovascular comorbidities, lipid-lowing agents and other medication use, lipid level, as well as cancer characteristics. Multivariable competing risk analysis was used as sensitivity analysis. Results A total of 62,341 incident cancer patients were identified. After matching, 424 PCSK9i users and 1,272 non-users were included in this study. During a median follow-up of 1,009 days, 315 patients died, among which 98 died due to cardiovascular cause, 146 died due to cancer cause. Compared to non-users, cancer patients treated with PCSK9i presented with significantly lower risk of all-cause mortality (hazard ratio [HR], 0.33; 95% confidence interval [CI] 0.23-0.47; p &amp;lt;0.001), after adjusting for potential confounders. In addition, PCSK9i therapy was associated with a 63% lower risk of cardiovascular mortality (HR, 0.37; 95%CI 0.20-0.69; p=0.002) and a 75% lower risk of cancer-related mortality (HR, 0.25; 95%CI 0.14-0.45; p&amp;lt;0.001), in relation to non-PCSK9i group. Sensitivity analysis using multivariable competing risk model also suggested a significant association between PCSK9i treatment with reduced risk of cardiovascular mortality (HR, 0.41; 95%CI 0.22-0.76; p=0.005) and cancer mortality (HR, 0.26; 95%CI 0.15-0.48; p&amp;lt;0.001) among cancer survivors. Conclusion The use of PCSK9i was associated lower risks of all-cause, cardiovascular-related, and cancer-related mortality amongst cancer survivors. These findings potentially indicate benefits of PCSK9i beyond adverse cardiovascular events related to atherosclerosis.

Remnant cholesterol and cardiovascular and all-cause mortality in Korean adults

Abstract Background Although previous studies have reported that remnant cholesterol (RC) is associated with cardiovascular disease, studies on RC and various mortality related outcomes including cardiovascular mortality in the general population are scarce and most of them are limited to Western populations. Purpose This study aims to evaluate the effect of RC on mortality related outcomes in a relatively young and middle-aged Korean population. Methods This cohort study included 268,219 subjects (mean age, 38 years and 50.6% men) who were enrolled in the Kangbuk Samsung Health Study between 2003 and 2016. Fasting RC was calculated as total cholesterol minus high-density lipoprotein cholesterol minus low-density lipoprotein cholesterol (LDLC). Results The median RC was 0.47 mmol/L (18 mg/dL) and the prevalence of ≥ 1 mmol/L RC was 11.4%. During the median FU of 6.7 years, high RC (RC ≥ 0.47 mmol/L) significantly increased the risk of multivariable-adjusted cardiovascular mortality compared with low RC (HR[95% CI], 1.43[1.07, 1/93]). Compared with the lowest quintile (RC &amp;lt;0.31 mmol/L), the HRs for cardiovascular mortality were 1.95[0.78, 4.84], 2.47[1.03, 5.91], 2.39[1.00, 5.72], and 2.84[1.19, 6.78] in the second, third, fourth, and highest quintiles, respectively. The HRs for all-cause mortality in the 3rd, 4th, and highest quintiles remained significant (1.24[0.97, 1.59], 1.38[1.08, 1.76], 1.34[1.05, 1/71], and 1.32[1.03, 1.69] in the 2nd, 3rd, 4th, and highest quintiles, respectively). However, there was no significant risk for cancer mortality between RC quintiles. Notably, subgroup analysis showed that individuals with high RC and high hsCRP and high RC and high lipoprotein(a) had a more than twofold and threefold increased risk of cardiovascular mortality, respectively, compared with low RC and low hsCRP and low RC and low lipoprotein(a). Conclusions High RC was significantly associated with increased risk of cardiovascular and all-cause mortality, but not with cancer mortality. In particular, high hsCRP and high lipoprotein(a) weighted the risk association between high RC and cardiovascular mortality.

Long-term exposure to ambient air pollution and risk of lung cancer – A comparative analysis of incidence and mortality in four administrative cohorts in the ELAPSE study

BackgroundStudies have linked air pollution to lung cancer incidence and mortality, but few have compared these associations, which may differ due to cancer survival variations. We aimed to evaluate the association between long-term air pollution exposure and lung cancer incidence and compare findings with previous lung cancer mortality analyses within the same cohorts. MethodsWe analyzed four population-based administrative cohorts in Denmark (2000–2015), England (2011–2017), Norway (2001–2016) and Rome (2001–2015). We assessed residential exposure to annual average fine particulate matter (PM2.5), nitrogen dioxide (NO₂), black carbon (BC), and warm-season ozone (O3) using Europe-wide land use regression models. We used Cox proportional hazard models to evaluate cohort-specific hazard ratios (HRs) and 95% confidence intervals (CIs) for lung cancer incidence identified using hospital admission records (English and Roman cohorts) or cancer registries (Danish and Norwegian cohorts). We evaluated the associations at low exposure levels using subset analyses and natural cubic splines. Cohort-specific HRs were pooled using random-effects meta-analyses, separately for incidence and mortality. ResultsOver 93,733,929 person-years of follow-up, 111,949 incident lung cancer cases occurred. Incident lung cancer was positively associated with PM2.5, NO2 and BC, and negatively associated with O3. The negative O3 association became positive after adjustment for NO2. Associations were almost identical or slightly stronger for lung cancer incidence than mortality in the same cohorts, with respective meta-analytic HRs (95% CIs) of 1.14 (1.06, 1.22) and 1.12 (1.02, 1.22) per 5 μg/m3 increase in PM2.5, and 1.10 (1.04, 1.16) and 1.09 (1.02, 1.16) per 10 μg/m3 increase in NO2. Positive associations persisted for both incidence and mortality at low pollution levels with similar magnitude. ConclusionsWe found similarly elevated risks of lung cancer incidence and mortality in association with residential exposure to PM2.5, NO2 and BC in meta-analyses of four European administrative cohorts, which persisted at low pollution levels.