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Abstract Cancer-directed surgeries (CDS) play a crucial role in prostate cancer (PCa) management along with possible survival and therapeutic benefits. However, barriers such as socioeconomic factors may affect patients’ decision of refusing recommended CDS. This study aimed to uncover risk factors and the impact on survival associated with CDS refusal. We retrospectively reviewed the Surveillance, Epidemiology, and End Results database for patients diagnosed with PCa between 2000 and 2019. Multiple sociodemographic and clinical characteristics were extracted to assess predictors for physicians’ surgical recommendations and patients’ surgical refusal, respectively. Propensity score matching was performed to balance the covariates. The impact of surgical refusal on mortality risk was also investigated. A total of 185,540 patients were included. The physician’s recommendation of CDS was significantly influenced by the patient’s age, race, income, home location, diagnosis year, Gleason score, prostate-specific antigen (PSA), and TNM stage. About 5.6% PCa patients refused CDS, most of whom were older, non-White race, lack of partners, living outside of metropolitan areas, with higher PSA or lower clinical TNM stage. Patients who refused CDS had an increased risk of cancer-specific mortality and overall mortality than those who performed CDS. Physicians may weigh a host of sociodemographic and clinical factors prior to making a CDS recommendation. Patients’ refusal of recommended CDS affected survival and was potentially modifiable by certain sociodemographic factors. Physicians should fully consider the hindrances behind patients’ CDS refusal to improve patient-doctor shared decision-making, guide patients toward the best alternative and achieve better outcomes.

Abstract Background This study explored the association of cardiovascular disease (CVD) with cancer mortality risk in individuals with or without a history of cancer, to better understand the interplay between CVD and cancer outcomes. Methods Utilizing data from the National Health and Nutrition Examination Survey (NHANES) spanning 1999 to 2018, a retrospective cohort analysis was conducted. This analysis accounted for the survey’s complex design to ensure national representativeness. The association of CVD with cancer mortality was assessed through multivariable Cox proportional hazards models. Results The present study included 59,653 participants, of whom 54,095 did not have cancer and 5558 had a history of cancer. In individuals without cancer, heart failure (HF) was associated with an increased risk of mortality from cancer (HR, 1.36; 95% CI, 1.09–1.69; P = 0.005). In participants with cancer, HF correlated with a higher risk of mortality from cancer (HR, 1.76; 95% CI, 1.32–2.34; P

Background Objectives Search strategy Selection criteria Data collection and analysis Main results Conclusions The associations between hysterectomy and cardiovascular disease (CVD) and mortality remains unlcear and a meta‐analysis with cohort studies is lacking.This study aimed to conduct a systematic review and meta‐analysis of cohort studies to investigate the relationship between hysterectomy and CVD, coronary heart disease (CHD), stroke, heart failure, and all‐cause, cardiovascular and cancer mortality. We further explored the effect of oophorectomy on the association between hysterectomy and these health outcomes.PubMed, EMBASE and Web of Science were searched up to 24 July 2023.Cohort studies.Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were pooled using a random‐effects model. We used I2 to assess the heterogeneity between studies.Forty‐three studies were included in the meta‐analysis. Hysterectomy was significantly associated with an increased risk of CVD (pooled HR 1.11, 95% CI 1.09–1.13; n = 6; I2 = 0) and stroke (HR 1.09, 95% CI 1.04–1.14; n = 7; I2 = 52%), but with a decreased risk of cancer mortality (HR 0.93, 95% CI 0.86–1.00; n = 4; I2 = 81%). No significant association was observed between hysterectomy and CHD (n = 10; I2 = 83%), all‐cause mortality (n = 8; I2 = 81%) or cardiovascular mortality (n = 7; I2 = 89%). Hysterectomy with and without oophorectomy was significantly associated with CVD and stroke risk, but showed a larger effect size for hysterectomy with oophorectomy. A significantly increased risk of CHD was observed in the subgroup of hysterectomy with oophorectomy, but not for the subgroup of hysterectomy alone.Hysterectomy may increase the risk of CVD, CHD and stroke, but not all‐cause, cardiovascular or cancer mortality. Hysterectomy with oophorectomy may have a higher risk of CVD, CHD and stroke than hysterectomy alone. However, the results on CHD and mortality related to hysterectomy should be interpreted cautiously because of the high level of heterogeneity and unstable subgroup analyses. [ABSTRACT FROM AUTHOR]

Public health measures necessitated by the COVID-19 pandemic have affected cancer pathways by halting screening, delaying diagnostic tests and reducing the numbers starting treatment. Specifically, this moves individuals from observed and treated pathways to unobserved and untreated pathways. We introduce a semi-Markov model that includes both, extending an industry-based multiple state model used for life and critical illness insurance. Our model includes events related to cancer diagnosis and progression based on publicly available population data for women aged 65–89 in England and on relevant medical literature. We quantify age-specific excess deaths, for a period up to 5 years, along with years of life expectancy lost and changes in cancer mortality by cancer stage. Our analysis suggests a 3–6% increase in breast cancer deaths, and a 4–6% increase in registrations of advanced breast cancer, robust under sensitivity analysis. This should be applicable to actuarial work in areas where longevity and advanced age morbidity affect healthcare, retirement and insurance. [ABSTRACT FROM AUTHOR]

Simple Summary: This article discusses a common approach to the early detection of oral cancer, which focuses on identifying and monitoring certain mouth conditions, known as oral potentially malignant disorders (OPMDs). However, despite this strategy, the death rates from cancers of the lip and mouth have not improved in 30 years. Surprisingly, only around 10% of oral cancers actually start as premalignant, and most OPMDs rarely turn into cancer. The article suggests that only a few specific types of these disorders, which have a higher risk of becoming cancerous and/or are prevalent in populations, really need intervention. It also questions the effectiveness of regarding OPMDs as heralding malignancy and calls for a different approach to reduce deaths for oral cancer. Despite the profession placing great emphasis on oral potentially malignant disorders (OPMDs) as a gateway for early recognition and consequently better outcomes for oral cancer, the death rates for lip and oral cavity cancer have remained stagnant for three decades. Evidence shows that only a small fraction of oral cancers are in fact preceded by OPMDs, and that most OPMDs have an annual transformation rate of less than 1%. As OPMDs encompass a very heterogeneous group of oral conditions, it could be argued that only patients with oral mucosal diseases bearing a substantial risk of malignant transformation warrant close surveillance and treatment, these include proliferative leukoplakia, erythroplakia, non-homogeneous leukoplakia, as well as diseases presenting with severe dysplasia at biopsy. In this narrative review, I discuss the intricate epidemiology of the malignancies that we colloquially refer to as oral cancer, explore the limitations of focusing on OPMDs to reduce the incidence and mortality of oral cavity cancer, and argue that a may-be cancer label represents overdiagnosis for most OPMDs. [ABSTRACT FROM AUTHOR]

Background: This study explored the association of cardiovascular disease (CVD) with cancer mortality risk in individuals with or without a history of cancer, to better understand the interplay between CVD and cancer outcomes. Methods: Utilizing data from the National Health and Nutrition Examination Survey (NHANES) spanning 1999 to 2018, a retrospective cohort analysis was conducted. This analysis accounted for the survey's complex design to ensure national representativeness. The association of CVD with cancer mortality was assessed through multivariable Cox proportional hazards models. Results: The present study included 59,653 participants, of whom 54,095 did not have cancer and 5558 had a history of cancer. In individuals without cancer, heart failure (HF) was associated with an increased risk of mortality from cancer (HR, 1.36; 95% CI, 1.09–1.69; P = 0.005). In participants with cancer, HF correlated with a higher risk of mortality from cancer (HR, 1.76; 95% CI, 1.32–2.34; P < 0.001). Diabetes (DM), hypertension (HBP) and coronary heart disease (CHD) were not significantly associated with an increased risk of mortality from cancer. Significant differences were observed in the interaction between cancer and CHD (HR, 0.68; 95% CI, 0.53–0.87; P = 0.002). For cancer and HBP, a similar trend was noted (HR, 0.75; 95% CI, 0.62–0.91; P = 0.003). No significant differences were found in interactions between HF, DM and cancer. Conclusions: HF was associated with an increased risk of mortality from cancer, regardless of cancer history, while HBP, CHD and DM showed no significant association. These findings underscore the importance of understanding the mechanisms behind the increased risk of cancer mortality following HF. [ABSTRACT FROM AUTHOR]

Aim: To determine the associations between the Chinese visceral adiposity index (CVAI) and the risks of all‐cause and cause‐specific mortality. Materials and Methods: A total of 3 916 214 Chinese adults were enrolled in a nationwide population cohort covering all 31 provinces of mainland China. The CVAI was calculated based on age, body mass index, waist circumference, and triglyceride and high‐density lipoprotein cholesterol concentrations. We used a Cox proportional hazards regression model to determine the hazard ratios and 95% confidence intervals (CIs) for risk of mortality associated with different CVAI levels. Results: The median follow‐up duration was 3.8 years. A total of 86 158 deaths (34 867 cardiovascular disease [CVD] deaths, 29 884 cancer deaths, and 21 407 deaths due to other causes) were identified. In general, after adjusting for potential confounding factors, a U‐shaped relationship between CVAI and all‐cause mortality was observed by restricted cubic spline (RCS). Compared with participants in CVAI quartile 1, those in CVAI quartile 4 had a 23.0% (95% CI 20.0%–25.0%) lower risk of cancer death, but a 23.0% (95% CI 19.0–27.0) higher risk of CVD death. In subgroup analysis, a J‐shaped and inverted U‐shaped relationship for all‐cause mortality and cancer mortality was observed in the group aged < 60 years. Conclusions: The CVAI, an accessible indicator reflecting visceral obesity among Chinese adults, has predictive value for all‐cause, CVD, and cancer mortality risks. Moreover, the CVAI carries significance in the field of health economics and secondary prevention. In the future, it could be used for early screening purposes. [ABSTRACT FROM AUTHOR]

Background: Active surveillance (AS), where treatment is deferred until cancer progression is detected by a biopsy, is acknowledged as a way to reduce overtreatment in prostate cancer. However, a consensus on the frequency of taking biopsies while in AS is lacking. In former studies to optimize biopsy schedules, the delay in progression detection was taken as an evaluation indicator and believed to be associated with the long‐term outcome, prostate cancer mortality. Nevertheless, this relation was never investigated in empirical data. Here, we use simulated data from a microsimulation model to fill this knowledge gap. Methods: In this study, the established MIcrosimulation SCreening Analysis model was extended with functionality to simulate the AS procedures. The biopsy sensitivity in the model was calibrated on the Canary Prostate Cancer Active Surveillance Study (PASS) data, and four (tri‐yearly, bi‐yearly, PASS, and yearly) AS programs were simulated. The relation between detection delay and prostate cancer mortality was investigated by Cox models. Results: The biopsy sensitivity of progression detection was found to be 50%. The Cox models show a positive relation between a longer detection delay and a higher risk of prostate cancer death. A 2‐year delay resulted in a prostate cancer death risk of 2.46%–2.69% 5 years after progression detection and a 10‐year risk of 5.75%–5.91%. A 4‐year delay led to an approximately 8% greater 5‐year risk and an approximately 25% greater 10‐year risk. Conclusion: The detection delay is confirmed as a surrogate for prostate cancer mortality. A cut‐off for a "safe" detection delay could not be identified. [ABSTRACT FROM AUTHOR]

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]

Background: Serum albumin levels and cancer mortality are closely related, yet large-sample studies encompassing a broad spectrum of cancer types are lacking. Methods: This study encompassed patients diagnosed with cancer across the continuous 10 cycles of NHANES surveys from 1999 to 2018. The study population was stratified into two groups based on median albumin levels (≤ 4.2g/dL and > 4.2 g/dL) or cancer aggressiveness (well-survived cancers and poorly-survived cancers). Survival rates were estimated using the Kaplan-Meier method. The Cox proportional hazards model was employed to evaluate the association between serum albumin levels and cancer mortality. Restricted cubic spline (RCS) analysis was conducted to assess the nonlinear relationship between serum albumin levels and the risk of cancer mortality. Results: Kaplan-Meier curves demonstrated that patients with albumin levels ≤ 4.2 g/dL exhibited lower survival rates compared to those with levels > 4.2 g/dL, irrespective of cancer aggressiveness. Following adjustment for confounders, decreased albumin levels were associated with an elevated risk of cancer mortality across all groups [all cancers, HR (95%CI) = 2.03(1.73, 2.37); well survived cancers, HR (95%CI) = 1.78(1.38, 2.32); and poorly survived cancers, HR (95%CI) = 1.99(1.64, 2.42)]. RCS analyses revealed a stable nonlinear negative association between albumin levels and cancer mortality in all groups, regardless of confounder adjustment. Conclusion: Low serum albumin levels predict higher cancer mortality. Furthermore, a nonlinear negative association was observed between serum albumin levels and the risk of cancer mortality. [ABSTRACT FROM AUTHOR]

Kidney transplant (KT) recipients are known to be at risk of developing several cancer types; however, cancer mortality in this population is underinvestigated. Our study aimed to assess the risk of cancer death among Italian KT recipients compared to the corresponding general population. A cohort study was conducted among 7373 individuals who underwent KT between 2003 and 2020 in 17 Italian centers. Date and cause of death were retrieved until 31 December 2020. Indirect standardization was used to estimate standardized mortality ratios (SMRs) and corresponding 95% confidence intervals (CIs). Cancer was the most common cause of death among the 7373 KT recipients, constituting 32.4% of all deaths. A 1.8‐fold excess mortality (95% CI: 1.59‐2.09) was observed for all cancers combined. Lymphomas (SMR = 6.17, 95% CI: 3.81‐9.25), kidney cancer (SMR = 5.44, 95% CI: 2.97‐8.88) and skin melanoma (SMR = 3.19, 95% CI: 1.03‐6.98) showed the highest excess death risks. In addition, SMRs were increased about 1.6 to 3.0 times for cancers of lung, breast, bladder and other hematopoietic and lymphoid tissues. As compared to the general population, relative cancer mortality risk remained significantly elevated in all age groups though it decreased with increasing age. A linear temporal increase in SMR over time was documented for all cancers combined (P <.01). Our study documented significantly higher risks of cancer death in KT recipients than in the corresponding general population. Such results support further investigation into the prevention and early detection of cancer in KT recipients. [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]

Abstract Aims A higher risk of cancer among patients with heart failure (HF) has been suggested in recent community‐based studies. This study aimed to investigate the impact of HF during hospitalization with acute coronary syndrome (ACS) on the long‐term cancer risk. Methods and results The study included 572 patients admitted with ACS to three Italian hospitals, discharged cancer‐free, and prospectively followed for 24 years or until death. All but three patients completed the follow‐up, which represented 6440 person‐years (mean age: 66 ± 12 years; 70% males). Baseline HF was diagnosed in 192 (34%) patients. A total of 129 (23%) patients developed cancer (103 without HF and 26 with HF), and 107 (19%) patients died due to it (81 without HF and 26 with HF). The incidence rates for cancer onset and cancer death were not different according to HF status. Cox regression analysis revealed no association between HF or left ventricular ejection fraction (LVEF) and cancer risk. In addition, no difference in cancer risk was observed among patients with HF with preserved ejection fraction, HF with mildly reduced ejection fraction, and HF with reduced ejection fraction. In competing risk regression analysis, the risk of cancer onset associated with HF was sub‐hazard ratio (SHR) 0.47 [95% confidence interval (CI): 0.30–0.72; P = 0.001] and SHR 1.02 (95% CI: 1.01–1.04; P = 0.002) with LVEF. Results were the same in the adjusted model. Yet the fully adjusted model showed an attenuated association between cancer death and HF (SHR: 0.63; 95% CI: 0.37–1.05; P = 0.08) and LVEF (SHR: 1.02; 95% CI: 0.99–1.06; P = 0.08). Consistent results were obtained after using propensity score matching analysis that created 192 pairs. A negative interaction between age and HF and a positive interaction between age and LVEF for cancer risk have also been found. Conclusions An inverse association between baseline HF and long‐term cancer risk has been observed among the ABC Study on heart disease patients who were followed for 24 years after ACS.

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

Abstract 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.

ObjectiveThe objective of this study is to assess the correlation between composite dietary antioxidant index (CDAI) with all-cause mortality and cause-specific mortality in adults with hypertension.MethodsThe cohort study comprised adult participants with hypertension from the NHANES database, spanning 9 cycles from 2001 to 2018. Follow-up was conducted until December 31, 2019. Multi-variable Cox regression analysis was utilized to ascertain hazard ratios (HR) and their corresponding 95% confidence intervals, evaluating the relationship between CDAI and the risks of all-cause and cause-specific mortality. To further investigate the association between CDAI and mortality rates in adults with hypertension, Kaplan–Meier survival curves, restricted cubic splines (RCS), subgroup analyses and sensitivity analyses were employed.ResultsThe analysis included 16,713 adults with hypertension (mean age 56.93 ± 0.23 years, 8,327 [49.61%] male). During the mean follow-up time 102.11 ± 1.22 months, with 3,908 (18.08%) all-cause mortality occurred, 1,082 (4.84%) cardiovascular mortality and 833 (3.80%) cancer mortality. Compared to the lowest quartile of CDAI, the weighted multivariate hazard ratios of participants in the highest quartile was 0.77 (95% CI, 0.68–0.87) for all-cause mortality, 0.83 (95% CI, 0.67–1.04) for cardiovascular mortality, and 0.64 (95% CI, 0.50–0.82) for cancer mortality. RCS analysis demonstrated a nonlinear association of CDAI with all-cause and cancer mortality, and a linear association between CDAI and cardiovascular mortality. The results were robust in subgroup analyses and sensitivity analyses.ConclusionHigher CDAI is associated with reduced all-cause mortality, cardiovascular mortality, and cancer mortality in hypertensive adults. Our findings highlight the importance of an antioxidant diet in improving outcomes in adults with hypertension.

BackgroundSeveral studies have shown that serum copper levels are related to coronary heart disease, diabetes, and cancer. However, the association of serum copper levels with all-cause, cause-specific [including cardiovascular disease (CVD) and cancer] mortality remains unclear.ObjectivesThis study aimed to prospectively examine the association of copper exposure with all-cause, CVD, and cancer mortality among US adults.MethodsThe data for this analysis was obtained from the National Health and Nutrition Examination Survey (NHANES) between 2011 and 2014. Mortality from all-causes, CVD, and cancer mortality was linked to US National Death Index mortality data. Cox regression models were used to estimate the association between serum copper levels and all-cause, CVD, and cancer mortality.ResultsA total of 2,863 adults were included in the main study. During the mean follow-up time of 81.2 months, 236 deaths were documented, including 68 deaths from cardiovascular disease and 57 deaths from cancer. The weighted mean overall serum copper levels was 117.2 ug/L. After adjusting for all of the covariates, compared with participants with low (1st tertile, 0.05).ConclusionsThis prospective study found that serum copper concentrations were linearly associated with all-cause and CVD mortality in US adults. High serum copper levels is a risk factor for all-cause and CVD mortality.

Abstract Background Active surveillance (AS), where treatment is deferred until cancer progression is detected by a biopsy, is acknowledged as a way to reduce overtreatment in prostate cancer. However, a consensus on the frequency of taking biopsies while in AS is lacking. In former studies to optimize biopsy schedules, the delay in progression detection was taken as an evaluation indicator and believed to be associated with the long‐term outcome, prostate cancer mortality. Nevertheless, this relation was never investigated in empirical data. Here, we use simulated data from a microsimulation model to fill this knowledge gap. Methods In this study, the established MIcrosimulation SCreening Analysis model was extended with functionality to simulate the AS procedures. The biopsy sensitivity in the model was calibrated on the Canary Prostate Cancer Active Surveillance Study (PASS) data, and four (tri‐yearly, bi‐yearly, PASS, and yearly) AS programs were simulated. The relation between detection delay and prostate cancer mortality was investigated by Cox models. Results The biopsy sensitivity of progression detection was found to be 50%. The Cox models show a positive relation between a longer detection delay and a higher risk of prostate cancer death. A 2‐year delay resulted in a prostate cancer death risk of 2.46%–2.69% 5 years after progression detection and a 10‐year risk of 5.75%–5.91%. A 4‐year delay led to an approximately 8% greater 5‐year risk and an approximately 25% greater 10‐year risk. Conclusion The detection delay is confirmed as a surrogate for prostate cancer mortality. A cut‐off for a “safe” detection delay could not be identified.

Aims: A higher risk of cancer among patients with heart failure (HF) has been suggested in recent community‐based studies. This study aimed to investigate the impact of HF during hospitalization with acute coronary syndrome (ACS) on the long‐term cancer risk. Methods and results: The study included 572 patients admitted with ACS to three Italian hospitals, discharged cancer‐free, and prospectively followed for 24 years or until death. All but three patients completed the follow‐up, which represented 6440 person‐years (mean age: 66 ± 12 years; 70% males). Baseline HF was diagnosed in 192 (34%) patients. A total of 129 (23%) patients developed cancer (103 without HF and 26 with HF), and 107 (19%) patients died due to it (81 without HF and 26 with HF). The incidence rates for cancer onset and cancer death were not different according to HF status. Cox regression analysis revealed no association between HF or left ventricular ejection fraction (LVEF) and cancer risk. In addition, no difference in cancer risk was observed among patients with HF with preserved ejection fraction, HF with mildly reduced ejection fraction, and HF with reduced ejection fraction. In competing risk regression analysis, the risk of cancer onset associated with HF was sub‐hazard ratio (SHR) 0.47 [95% confidence interval (CI): 0.30–0.72; P = 0.001] and SHR 1.02 (95% CI: 1.01–1.04; P = 0.002) with LVEF. Results were the same in the adjusted model. Yet the fully adjusted model showed an attenuated association between cancer death and HF (SHR: 0.63; 95% CI: 0.37–1.05; P = 0.08) and LVEF (SHR: 1.02; 95% CI: 0.99–1.06; P = 0.08). Consistent results were obtained after using propensity score matching analysis that created 192 pairs. A negative interaction between age and HF and a positive interaction between age and LVEF for cancer risk have also been found. Conclusions: An inverse association between baseline HF and long‐term cancer risk has been observed among the ABC Study on heart disease patients who were followed for 24 years after ACS. [ABSTRACT FROM AUTHOR]

Background: Socioeconomic status (SES) is associated with a range of health outcomes, including cancer diagnosis and survival. However, the evidence for this association is inconsistent between countries with and without single‐payer health care systems. In this study, the relationships between neighborhood‐level income, cancer stage at diagnosis, and cancer‐specific mortality in Alberta, Canada, were evaluated. Methods: The Alberta Cancer Registry was used to identify all primary cancer diagnoses between 2010 and 2020. Average neighborhood income was determined by linking the Canadian census to postal codes and was categorized into quintiles on the basis of income distribution in Alberta. Multivariable multinomial logistic regression was used to model the association between income quintile and stage at diagnosis, and the Fine–Gray proportional subdistribution hazards model was used to estimate the association between SES and cancer‐specific mortality. Results: Out of the 143,818 patients with cancer included in the study, those in lower income quintiles were significantly more likely to be diagnosed at stage III (odds ratio [OR], 1.07; 95% CI [confidence interval], 1.06–1.09) or IV (OR, 1.12; 95% CI, 1.11–1.14) after adjusting for age and sex. Lower income quintiles also had significantly worse cancer‐specific survival for breast, colorectal, liver, lung, non‐Hodgkin lymphoma, oral cavity, pancreas, and prostate cancers. Conclusions: Disparities were observed in cancer outcomes across neighborhood‐level income groups in Alberta, which demonstrates that health inequities by SES exist in countries with single‐payer health care systems. Further research is needed to better understand the underlying causes and to develop strategies to mitigate these disparities. The association between socioeconomic status and cancer outcomes in countries with single‐payer health care systems is inconsistent. In this analysis, lower socioeconomic status was found to be associated with both stage at diagnosis and cancer‐specific mortality of major cancer types in a Canadian province. [ABSTRACT FROM AUTHOR]

Cervical cancer (CC) is one of the leading causes of cancer-related deaths among females in Ghana. Despite the magnitude of the public health challenge posed by CC in Ghana, survival data as well as reported incidence and mortality rates are primarily based on studies conducted in the capital city of the country. Even though age at diagnosis is known to affect the overall survival of CC patients, the role of this factor in the prognosis of CC patients in Ghana has not been sufficiently explored. The aim of this study was to determine the 5-year survival rate of Ghanaian woman treated for CC at a large tertiary healthcare facility in Ghana. This research was a single-institution-based quantitative retrospective cohort study conducted among patients with histopathologically confirmed CC. Clinical and socio-demographic data were retrieved from patients' medical records. Data analysis was done using the Statistical Package for the Social Sciences software version 23. Kaplan Meier curves were used to present the survival rates and median survival time. The peak age at diagnosis was between 45 and 80 years with the modal age group of patients between 75 and 80 years. The mean age at diagnosis was 63.3 ± 15.7 years ranging from 27 to 104 years. The overall survival rates at 1, 3 and 5 years were 76.5%, 51.5% and 32.4%, respectively. The median survival time was 65.8 months. Age < 50 years was associated with higher survival estimates than age >50 years. The 5-year overall survival rate of CC patients reported in this study (32.4%) is relatively low compared with countries in the developed world but like previous reports at other healthcare facilities in Ghana as well as in other underdeveloped countries. [ABSTRACT FROM AUTHOR]

Simple Summary: Cancer is a significant contributor to morbidity and mortality worldwide. The purpose of this study was to analyze the cancer burden and trends of 29 groups of malignant neoplasms in Mexico by sex and age from 1990 to 2019. In 2019, there were 222.1 thousand incident cases and 105.6 thousand deaths due to cancer in the general population. The number of new cases and deaths from the 29 cancer groups increased between 10% and 436% from 1990 to 2019, with different patterns by sex and age. Breast, cervical, and colorectal cancers were the leading causes of death among women, while prostate, lung, and colorectal cancers were the leading causes of death among men. In Mexico, malignant neoplasms were the third leading cause of death in 2019, causing significant health loss. The existence of gender disparities emphasizes the need for cancer-specific targeted prevention, diagnosis, and treatment. The global burden of cancer is on the rise, with varying national patterns. To gain a better understanding and control of cancer, it is essential to provide national estimates. Therefore, we present a comparative description of cancer incidence and mortality rates in Mexico from 1990 to 2019, by age and sex for 29 different cancer groups. Based on public data from the Global Burden of Disease Study 2019, we evaluated the national burden of cancer by analyzing counts and crude and age-standardized rates per 100,000 people with 95% uncertainty intervals for 2019 and trends using the annual percentage change from 1990 to 2019. In 2019, cancer resulted in 222,060 incident cases and 105,591 deaths. In 2019, the highest incidence of cancer was observed in non-melanoma skin cancer, prostate cancer, and breast cancer. Additionally, 53% of deaths were attributed to six cancer groups (lung, colorectal, stomach, prostate, breast, and pancreatic). From 1990 to 2019, there was an increasing trend in incidence and mortality rates, which varied by 10–436% among cancer groups. Furthermore, there were cancer-specific sex differences in crude and age-standardized rates. The results show an increase in the national cancer burden with sex-specific patterns of change. These findings can guide national efforts to reduce health loss due to cancer. [ABSTRACT FROM AUTHOR]

Background: Previous studies have shown an association between living alone and cancer mortality; however, findings by sex and race/ethnicity have generally been inconsistent, and data by socioeconomic status are sparse. The association between living alone and cancer mortality by sex, race/ethnicity, and socioeconomic status in a nationally representative US cohort was examined. Methods: Pooled 1998–2019 data for adults aged 18–64 years at enrollment from the National Health Interview Survey linked to the National Death Index (N = 473,648) with up to 22 years of follow‐up were used to calculate hazard ratios (HRs) for the association between living alone and cancer mortality. Results: Compared to adults living with others, adults living alone were at a higher risk of cancer death in the age‐adjusted model (HR, 1.32; 95% CI, 1.25–1.39) and after additional adjustments for multiple sociodemographic characteristics and cancer risk factors (HR, 1.10; 95% CI, 1.04–1.16). Age‐adjusted models stratified by sex, poverty level, and educational attainment showed similar associations between living alone and cancer mortality, but the association was stronger among non‐Hispanic White adults (HR, 1.33; 95% CI, 1.25–1.42) than non‐Hispanic Black adults (HR, 1.18; 95% CI, 1.05–1.32; p value for difference <.05) and did not exist in other racial/ethnic groups. These associations were attenuated but persisted in fully adjusted models among men (HR, 1.13; 95% CI, 1.05–1.23), women (HR, 1.09; 95% CI, 1.01–1.18), non‐Hispanic White adults (HR, 1.13; 95% CI, 1.05–1.20), and adults with a college degree (HR, 1.22; 95% CI, 1.07–1.39). Conclusions: In this nationally representative study in the United States, adults living alone were at a higher risk of cancer death in several sociodemographic groups. In a nationally representative study with up to 22 years of mortality follow‐up, US working‐age adults experiencing social isolation, measured as living alone, were at a higher risk of cancer death than adults living with others. This association persisted among non‐Hispanic White adults and adults with higher education even after accounting for differences in a wide range of sociodemographic, behavioral, and health characteristics. [ABSTRACT FROM AUTHOR]

This article aims to analyze the effects of cancer mortality on life expectancy at birth in 15 European high-income countries between 1950 and 2019. To establish the 1950-2019 time series of deaths from cancer, mortality data were harmonized from the available datasets of the World Health Organization Mortality database, coded according to the International Classification of Diseases of the 7th, 8th, 9th, and 10th editions. The estimation of the cancer mortality effect on the life expectancy at birth was performed using the algorithm of stepwise replacement for the life expectancy decomposition. The increase in cancer mortality contributed to a decline in overall life expectancy growth until the mid-1990s, coinciding with the aging cohorts of heavy smokers and a long-term reduction in mortality from other non-communicable diseases. Subsequently, since the 1990s, the reduction in cancer mortality has contributed to a significant increase in life expectancy at birth, especially in males. Reduction in cancer mortality was the outcome of various factors, such as alcohol and tobacco control policies, advances in cancer prevention and its treatment, general increase in population well-being, and reduction in risk-factors. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) has a rising global prevalence. However, the understanding of its impact on mortality remains inconsistent so we explored the association between IBD and all-cause and cause-specific mortality. This study included 502,369 participants from the UK Biobank, a large, population-based, prospective cohort study with mortality data through 2022. IBD was defined by baseline self-report or from primary care or hospital admission data. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and cause-specific mortality in multivariable Cox proportional hazards regression models. A total of 5799 (1.2%) participants had a history of IBD at baseline. After a median follow-up of 13.7 years, 44,499 deaths occurred. Having IBD was associated with an increased risk of death from all causes (HR = 1.16, 95% CI = 1.07–1.24) and cancer (HR = 1.16, 95% CI = 1.05–1.30), particularly colorectal cancer (CRC) (HR = 1.56, 95% CI = 1.17–2.09). We observed elevated breast cancer mortality rates for individuals with Crohn's disease, and increased CRC mortality rates for individuals with ulcerative colitis. In stratified analyses of IBD and all-cause mortality, mortality risk differed by individuals' duration of IBD, age at IBD diagnosis, body mass index (BMI) (P Heterogeneity = 0.03) and smoking status (P Heterogeneity = 0.01). Positive associations between IBD and all-cause mortality were detected in individuals diagnosed with IBD for 10 years or longer, those diagnosed before the age of 50, all BMI subgroups except obese individuals, and in never or current, but not former smokers. We found that having IBD was associated with increased risks of mortality from all causes, all cancers, and CRC. This underscores the importance of enhanced patient management strategies and targeted prevention efforts in individuals with IBD. [ABSTRACT FROM AUTHOR]

Background Chronic kidney disease (CKD) is believed to be associated with an increased risk for cancer, especially urinary tract cancer. However, previous studies predominantly focused on the association of decreased estimated glomerular filtration rate (eGFR) with cancer. In this study, we investigated the association of albuminuria with cancer incidence, adjusted for eGFR. Methods We included 8490 subjects in the Prevention of Renal and Vascular End-stage Disease (PREVEND) observational study. Urinary albumin excretion (UAE) was measured in two 24-hour urine specimens at baseline. Primary outcomes were the incidence of overall and urinary tract cancer. Secondary outcomes were the incidence of other site-specific cancers, and mortality due to overall, urinary tract, and other site-specific cancers. Results Median baseline UAE was 9.4 (IQR, 6.3–17.8) mg/24 h. During a median follow-up of 17.7 years, 1341 subjects developed cancer (of which 177 were urinary tract cancers). After multivariable adjustment including eGFR, every doubling of UAE was associated with a 6% (hazard ratios (HR), 1.06, 95% confidence intervals (CI), 1.02–1.10), and 14% (HR, 1.14, 95% CI, 1.04–1.24) higher risk of overall and urinary tract cancer incidence, respectively. Except for lung and hematological cancer, no associations were found between UAE and the incidence of other site-specific cancer. Doubling of UAE was also associated with a higher risk of mortality due to overall and lung cancer. Conclusions Higher albuminuria is associated with a higher incidence of overall, urinary tract, lung, and hematological cancer, and with a higher risk of mortality due to overall and lung cancers, independent of baseline eGFR. [ABSTRACT FROM AUTHOR]

To determine the incidence of all-cause and cancer mortality (CM) in association with immunosuppression. Retrospective cohort study at ocular inflammatory disease (OID) subspecialty centers. We harvested exposure and covariate data retrospectively from clinic inception (earliest in 1979) through 2010 inclusive. Then we ascertained overall and cancer-specific mortalities by National Death Index linkage. We constructed separate Cox models to evaluate overall and CM for each class of immunosuppressant and for each individual immunosuppressant compared with person-time unexposed to any immunosuppression. Patients with noninfectious OID, excluding those with human immunodeficiency infection or preexisting cancer. Tumor necrosis factor (TNF) inhibitors (mostly infliximab, adalimumab, and etanercept); antimetabolites (methotrexate, mycophenolate mofetil, azathioprine); calcineurin inhibitors (cyclosporine); and alkylating agents (cyclophosphamide) were given when clinically indicated in this noninterventional cohort study. Overall mortality and CM. Over 187 151 person-years (median follow-up 10.0 years), during which 15 938 patients were at risk for mortality, we observed 1970 deaths, 435 due to cancer. Both patients unexposed to immunosuppressants (standardized mortality ratio [SMR] = 0.95, 95% confidence interval [CI], 0.90–1.01) and those exposed to immunosuppressants but free of systemic inflammatory diseases (SIDs) (SMR = 1.04, 95% CI, 0.95–1.14) had similar mortality risk to the US population. Comparing patients exposed to TNF inhibitors, antimetabolites, calcineurin inhibitors, and alkylating agents with patients not exposed to any of these, we found that overall mortality (adjusted hazard ratio [aHR] = 0.88, 0.89, 0.90, 1.11) and CM (aHR = 1.25, 0.89, 0.86, 1.23) were not significantly increased. These results were stable in sensitivity analyses whether excluding or including patients with SID, across 0-, 3-, or 5-year lags and across quartiles of immunosuppressant dose and duration. Our results, in a cohort where the indication for treatment was proven unassociated with mortality risk, found that commonly used immunosuppressants—especially the antimetabolites methotrexate, mycophenolate mofetil, and azathioprine; the TNF inhibitors adalimumab and infliximab, and cyclosporine—were not associated with increased overall and CM over a median cohort follow-up of 10.0 years. These results suggest the safety of these agents with respect to overall and CM for patients treated with immunosuppression for a wide range of inflammatory diseases. Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article. [ABSTRACT FROM AUTHOR]

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

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]

Background: Type 2 diabetes mellitus (T2DM) was a major global health threat. As a chronic low-grade inflammatory disease, the prognosis of diabetes was associated with inflammation. The advanced lung cancer inflammation index (ALI) served as a comprehensive index to assess inflammation. This study aimed to estimate the association between ALI and all-cause, cardiovascular disease (CVD), and cancer mortality in T2DM patients. Methods: We extracted cohort data from the National Health and Nutrition Examination Survey (NHANES) spanning 1999-2018 for analysis. The weighted Kaplan-Meier analysis and multivariate-adjusted Cox analysis were utilized to evaluate the relationship between ALI and all-cause, CVD, and cancer mortality in T2DM patients. Restricted cubic spline (RCS) analysis was employed to assess their non-linear relationship. Stratified analysis and interaction analysis were conducted to enhance the robustness of the results. Results: The study incorporated a total of 3,888 patients. An increase in ALI was associated with a reduced risk of all-cause and CVD mortality in T2DM patients, but not related to cancer mortality. There were J-shaped and L-shaped non-linear relationships between ALI and all-cause, CVD mortality in T2DM patients, respectively. The inflection points were 90.20 and 93.06, respectively. For values below the inflection point, every 10U increase in ALI, both all-cause and CVD mortality risk decreased by 9%. Beyond the inflection point, all-cause mortality rose by 3%, while CVD mortality remained unaffected. Gender-stratified RCS analysis indicated a linear negative relationship between CVD mortality and ALI in female T2DM patients, whereas the trend in males aligned with the overall population. Conclusion: Our research initially identified a significant correlation between increased ALI levels with decreased all-cause and CVD mortality in T2DM patients. There were J-shaped and L-shaped non-linear relationships between ALI and all-cause, CVD mortality in T2DM patients, respectively. For female patients, there was a linear negative relation between CVD mortality and ALI, whereas the trend in males aligned with the overall population. These findings suggested that maintaining ALI (for example, control body weight and keep albumin in the normal range) within a certain range in the clinical settings was crucial for improving all-cause and CVD mortality in T2DM patients. [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]

Background Cardiovascular and cancer mortality are the two leading causes of death in the developed world including the USA. However, mortality trends for these diseases are highly dynamic, and the geographic landscape is in transition. We analyze patterns of mortality improvement at county level during recent decades focusing on mortality decline and geographic diversity. Methods We grouped age-adjusted mortality rates of cardiovascular and cancer diseases from CDC WONDER for 2959 US counties into 3-year time periods to improve reliability. We calculated percent mortality decrease between 1981–83 and 2016–19 for both causes to quantify mortality improvements for counties. Results Using standard deviation as an index of disparities, place-based cancer mortalities were 68% larger than cardiovascular disparities. Significantly, 566 US counties had same or higher rates of cancer mortality in 2019 as in 1981. The geographic distribution of mortality improvement in either cause tends to favor largely populated areas along coasts. Less-populated, rural places in the interior and southeastern regions were experiencing less improvement. Conclusions At the county level, large place-based disparities exist for both causes of death with the magnitude of disparities being substantially larger for the reduction in cancer deaths. Put differently, place matters, more for cancer than cardiovascular mortality. [ABSTRACT FROM AUTHOR]

Summary: Background: The place of death profoundly affects end-of-life care quality, particularly in cancer. Assisting individuals at home enhances support, privacy, and control, reducing healthcare costs. This study seeks to elucidate factors associated and trends in place of death by cancer in Brazil. Methods: Using data obtained from the National Mortality Information System, this study extracted tumour topography, sociodemographic characteristics, and the place of death (outcome classified into hospital or home death) by cancer in Brazil from 2002 to 2021. Findings: The analysis included 3,677,415 cases, with 82.3% of deaths occurring in hospitals and 17.7% at home. Most participants were male (53.1%), had gastrointestinal tumours (32.2%), and resided in the Southeastern region (48.7%). Home deaths were more frequent in the Northeastern (30.2%) and Northern (24.8%) regions compared to the Southern (17.1%) and Southeastern (12.2%) regions. A strong inverse correlation was found between home deaths and the Human Development Index of the region. Over the years, there was a reduction in home deaths, followed by a recent increase. Individuals with no formal education, indigenous individuals, and patients from the North, Northeast, and Central-West regions had higher rates of home deaths, while patients with haematological malignancies had lower rates compared to those with gastrointestinal tumours. Interpretation: The minority of deaths by cancer in Brazil occur at home, with distinct trends over time. Home death was associated with regional, racial and educational level differences. Funding: No funding.

Summary: Background: Despite advances in primary and secondary prevention of cardiovascular disease, excess mortality persists within the diabetes population. This study explores the components of this excess mortality and their interaction with sex. Methods: Using Danish registries (2002–2019), we identified residents aged 18–99 years, their diabetes status, and recorded causes of death. Applying Lexis-based methods, we computed age-standardized mortality rates (asMRs), mortality relative risks (asMRRs), and log-linear trends for cause-specific mortality. Findings: From 2002 to 2019, 958,278 individuals died in Denmark (T2D: 148,620; T1D: 7830) during 84.4 M person-years. During the study period, overall asMRs declined, driven by reducing cardiovascular mortality, notably in men with T2D. Conversely, cancer mortality remained high, making cancer the leading cause of death in individuals with T2D. Individuals with T2D faced an elevated mortality risk from nearly all cancer types, ranging from 9% to 257% compared to their non-diabetic counterparts. Notably, obesity-related cancers exhibited the highest relative risks: liver cancer (Men: asMRR 3.58 (3.28; 3.91); Women: asMRR 2.49 (2.14; 2.89)), pancreatic cancer (Men: asMRR 3.50 (3.25; 3.77); Women: asMRR 3.57 (3.31; 3.85)), and kidney cancer (Men: asMRR 2.10 (1.84; 2.40); Women: asMRR 2.31 (1.92; 2.79)). In men with type 2 diabetes, excess mortality remained stable, except for dementia. In women, diabetes-related excess mortality increased by 6–17% per decade across all causes of death, except cardiovascular disease. Interpretation: In the last decade, cancer has emerged as the leading cause of death among individuals with T2D in Denmark, emphasizing the need for diabetes management strategies incorporating cancer prevention. A sex-specific approach is crucial to address persistently higher relative mortality in women with diabetes. Funding: Supported by Steno Diabetes Center Aarhus, which is partially funded by an unrestricted donation from the Novo Nordisk Foundation, and by The Danish Diabetes Academy.

IntroductionThere is evidence suggesting that Bisphenol A (BPA) is associated with increased all-cause mortality in adults. However, the specific nature of the relationship between BPA exposure and cancer mortality remains relatively unexplored.MethodsThe National Health and Nutrition Examination Survey (NHANES) dataset was used to recruit participants. Urinary BPA was assessed using liquid chromatography-mass spectrum (LC–MS). Through the use of multivariable Cox proportional hazard regressions and constrained cubic splines, the relationships between urine BPA and death from all causes and cancer were investigated.ResultsThis study has a total of 8,035 participants, and 137 died from cancers after a 7.5-year follow-up. The median level of BPA was 2.0 g/mL. Urinary BPA levels were not independently associated with all-cause mortality. For cancer mortality, the second quartile’s multivariable-adjusted hazard ratio was 0.51 (95% confidence interval: 0.30 to 0.86; p = 0.011) compared to the lowest quartile. The restricted cubic splines showed that the association was nonlinear (p for nonlinearity = 0.028) and the inflection point was 1.99 ng/mL.ConclusionUrinary BPA exposure was U-shaped associated with the risk of cancer mortality, and a lower level of BPA less than 1.99 ng/mL was associated with a higher risk of cancer mortality.

IntroductionEarlier research has indicated that being exposed to polychlorinated dibenzo-p-dioxins (PCDDs) in the workplace can heighten the likelihood of cancer-related deaths. Nevertheless, there is limited information available regarding the connection between PCDD exposure and the risk of cancer mortality in the general population (i.e., individuals not exposed to these substances through their occupation).MethodsThe National Health and Nutrition Examination Survey (NHANES) detected PCDDs in the general population, and the death data were recently updated as of December 31, 2019. We conducted Cox regression analysis and controlled for covariates including age, gender, ethnicity, educational attainment, physical activity, alcohol intake, NHANES survey period, BMI category, cotinine concentration, and household earnings.ResultsAfter accounting for confounding factors, the findings indicated that for each incremental rise of 1 log unit in 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin, there was a 76% rise in the likelihood of death from any cause, with a p value of 0.003. An increase of 1 log unit in the concentration of 1,2,3,4,6,7,8-heptachlorodibenzofuran could potentially lead to a 90% higher risk of cancer mortality, as indicated by a p value of 0.034 and a 95% confidence interval of 0.05–2.43. As the concentrations of 1,2,3,4,6,7,8-heptachlorodibenzofuran increased, the dose–response curve indicated a proportional rise in the risk of cancer mortality, accompanied by a linear p value of 0.044. The sensitivity analysis demonstrated that our findings were resilient.DiscussionIn the general population, an elevated risk of cancer mortality was observed in PCDDs due to the presence of 1,2,3,4,6,7,8-heptachlorodibenzofuran. Mechanistic research is required to further confirm it.

Limited information is available on potential predictive value of environmental chemicals for mortality. Our study aimed to investigate the associations between 43 of 8 classes representative environmental chemicals in serum/urine and mortality, and further develop the interpretable machine learning models associated with environmental chemicals to predict mortality. A total of 1602 participants were included from the National Health and Nutrition Examination Survey (NHANES). During 154,646 person-months of follow-up, 127 deaths occurred. We found that machine learning showed promise in predicting mortality. CoxPH was selected as the optimal model for predicting all-cause mortality with time-dependent AUROC of 0.953 (95%CI: 0.951–0.955). Coxnet was the best model for predicting cardiovascular disease (CVD) and cancer mortality with time-dependent AUROCs of 0.935 (95%CI: 0.933–0.936) and 0.850 (95%CI: 0.844–0.857). Based on clinical variables, adding environmental chemicals could enhance the predictive ability of cancer mortality (P

The aim was to investigate associations between marital status and mortality with a prospective cohort study design. A public health survey including adults aged 18–80 was conducted with a postal questionnaire in southern Sweden in 2008 (54.1% participation). The survey formed a baseline that was linked to 8.3-year follow-up all-cause, cardiovascular (CVD), cancer and other cause mortality. The present investigation entails 14,750 participants aged 45–80. Associations between marital status and mortality were investigated with multiple Cox-regression analyses. A 72.8% prevalence of respondents were married/cohabitating, 9.1% never married, 12.2% divorced and 5.9% widows/widowers. Marital status was associated with age, sex, socioeconomic status (SES) by occupation, country of birth, chronic disease, Body Mass Index (BMI), health-related behaviors and generalized trust covariates. Never married/single, divorced, and widowed men had significantly higher hazard rate ratios (HRRs) of all-cause mortality than the reference category married/cohabitating men throughout the multiple analyses. For men, CVD and other cause mortality showed similar significant results, but not cancer. No significant associations were displayed for women in the multiple analyses. Associations between marital status and mortality are stronger among men than women. Associations between marital status and cancer mortality are not statistically significant with low effect measures throughout the multiple analyses among both men and women.

Abstract: Cancer mortality has been shown to be associated with social- and human capital. Several channels have been suggested, such as early detection, better compliance to treatment and better health prior to diagnosis. In this paper we study how health status and social capital jointly affect cancer mortality and cancer severity at the time of diagnosis. The analyses are based on study sample of individuals with cancer diagnosis. Our merged dataset contain information on cancer diagnosis and death from the Cancer Registry of Norway and health status, social capital and other individual level data from several national health surveys measured before the time of diagnosis. Health status and social capital are treated as unobserved latent variables, and we apply generalized structural equation modelling framework to estimate conditional statistical associations of social capital and individual health on cancer severity and mortality. We find that health has negative, and statistically significant effect, on cancer mortality, while we cannot conclude on the association between health and cancer severity (metastasis yes/no). We cannot conclude that cancer mortality and the probability of cancer metastasis is associated nor disassociated with social capital. Our results add nuance to prior studies, which frequently report a significant association between social capital and cancer mortality.

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.

Cancer remains the second leading cause of death globally. Chronic inflammatory environments promote the growth of tumors, and the intake of certain food items can increase systemic inflammation. This study examined the relationship between the inflammatory potential of diet, measured by the Dietary Inflammatory Index (DII), and recurrence, all-cause, and cancer-specific mortality among cancer survivors. Web of Science, Medline, CINHAL, and PsycINFO databases were searched in April 2022. Two independent reviewers screened all searches. Of the 1,443 studies, 13 studies involving 14,920 cancer survivors passed all the screening stages. Three studies reported cancer recurrence, 12 reported all-cause mortality, and six reported cancer-specific mortality. Seven studies calculated DII from pre-diagnosis diets, five from post-diagnosis diets, and one from both pre-and post-diagnosis diets. A random-effects model meta-analysis showed that high DII was not associated with an increased risk of recurrence (HR = 1.09, 95 % CI = 0.77, 1.54, n = 4) and all-cause (HR = 1.08, 95 % CI = 0.99, 1.19, n = 14) and cancer-specific mortality (H = 1.07, 95 % CI = 0.92, 1.25, n = 6). Analysis by the timing of dietary assessment showed that only post-diagnosis DII was associated with an increased risk of all-cause mortality (HR = 1.34, 95 % CI = 1.05, 1.72, n = 6) by 34 %; however, cancer type did not modify these associations. The quality of the study assessed using the Newcastle Ottawa Scale indicated all but one studies were good. The risk of all-cause mortality among cancer survivors could be reduced by consuming more anti-inflammatory diets after cancer diagnosis.

Abstract Objective There are studies on the nutritional status of type 2 diabetes (T2D), but there are no large cohort studies on the prognosis of Controlling Nutritional Status (CONUT) score for T2D. The aim of this study was to examine the association between CONUT score and all-cause mortality as well as cancer mortality in adults with T2D. Methods For this study, we analyzed a total of 3763 adult patients with T2D who were part of the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. Mortality outcomes were determined by linking to the National Death Index records as of December 31, 2019. Cox proportional risk models were used to estimate risk ratios (HRs) and 95% confidence intervals (CIs) for all-cause and cancer deaths. Results During the mean follow-up of 8.17 years, there were 823 deaths from all causes and 155 deaths from cancer. After adjusting for multiple variables, the risk of all-cause mortality was higher in patients with a Mild (CONUT score ≥ 2), compared with patients with a Normal (CONUT score of 0–1). All-cause mortality risk was 39% higher, and cancer mortality risk was 45% higher. Consistent results were observed when stratified by age, sex, race, BMI, smoking status, and glycated hemoglobin levels. Conclusions In a nationally representative sample of American adults with T2D, we found an association between CONUT score and all-cause mortality and cancer mortality.

Abstract Background Cancer risk varies geographically, and migrants are influenced by different risk factors before, during and after migration. Increased migration from non-Western countries to the Nordic countries calls for a better understanding of the migrants’ cancer risk and the change in risk patterns over time. The aim of this study was to compare the incidence and mortality of breast, colorectal and lung cancer between non-Western immigrant and the native female population in Denmark, Finland, Iceland, and Norway. Material and methods Data from national registries were processed and pre-analysed in each country. Multivariate Poisson regression models were used to model the relative differences in incidence and mortality as rate ratios (RR). The country-specific estimates and summary statistics were pooled together using a random effects model. Results Non-Western immigrant women had significantly lower breast (RR 0.71, 0.65–0.78), colorectal (RR 0.72, 0.57–0.92) and lung (RR 0.55, 0.42–0.72) cancer incidence rates than native women, and the risk of these cancers among immigrant women increased with duration of residence. Differences were parallel in breast, colorectal and lung cancer mortality (RR 0.64, 0.55–0.74; RR 0.66, 0.48–0.92; RR 0.51, 0.34–0.79). Among immigrant women, higher education increased the risk for breast cancer and decreased it for lung cancer. Conclusion The results significantly complement and add to the previous findings of cancer burden and cancer burden transition among migrants and provide evidence of a prolonged cancer risk advantage among non-Western immigrant women. However, the findings show an increasing risk of lifestyle-related cancers with increasing duration of residence in the host country. Further studies are needed to discover underlying reasons for this phenomenon.

Abstract Purpose Cancer is a leading cause of death in the Caribbean, and the Republic of Trinidad and Tobago is no exception. Evidence suggests that cancer incidence and mortality may vary based on demographic factors across the different cancer types. This study aimed to investigate the incidence and mortality trends associated with cancer cases in Trinidad and Tobago for the period 2008–2018, across different age groups, gender, and ethnicity. Methods Data on 15,029 incident cancer cases were reported to the Dr. Elizabeth Quamina Cancer Registry between 2008 and 2018. The retrospective data were analyzed by sex, ancestry, and age, and were reported using Trinidad and Tobago population statistics for the period 2008–2018. Results The incidence of prostate and breast cancers was high among males and females, respectively. Among males, the highest cancer mortality was associated with prostate, lung, colon, blood, and pancreatic cancers, respectively. Among females, the highest cancer mortality was associated with breast, ovary, colon, blood, and pancreatic cancers. The frequency of occurrence of the top five cancer sites was the highest among Afro-Trinidadians followed by Indo-Trinidadians. Most females diagnosed with breast cancer were at a localized stage, while most males diagnosed with breast cancer were at a distant or regional stage. Most individuals diagnosed with blood cancer were at a distant stage. For lung and colon cancer, the stage of diagnosis for most males and females was either distant or unknown. Majority of males are diagnosed with prostate cancer at an unknown stage. Conclusions The findings indicate highest cancer incidence and mortality occur among Afro-Trinidadians. The stage at diagnosis varies across cancer types and gender.

Despite the profession placing great emphasis on oral potentially malignant disorders (OPMDs) as a gateway for early recognition and consequently better outcomes for oral cancer, the death rates for lip and oral cavity cancer have remained stagnant for three decades. Evidence shows that only a small fraction of oral cancers are in fact preceded by OPMDs, and that most OPMDs have an annual transformation rate of less than 1%. As OPMDs encompass a very heterogeneous group of oral conditions, it could be argued that only patients with oral mucosal diseases bearing a substantial risk of malignant transformation warrant close surveillance and treatment, these include proliferative leukoplakia, erythroplakia, non-homogeneous leukoplakia, as well as diseases presenting with severe dysplasia at biopsy. In this narrative review, I discuss the intricate epidemiology of the malignancies that we colloquially refer to as oral cancer, explore the limitations of focusing on OPMDs to reduce the incidence and mortality of oral cavity cancer, and argue that a may-be cancer label represents overdiagnosis for most OPMDs.

We develop a functional proportional hazards mixture cure model with scalar and functional covariates measured at the baseline. The mixture cure model, useful in studying populations with a cure fraction of a particular event of interest is extended to functional data. We employ the expectation–maximization algorithm and develop a semiparametric penalized spline-based approach to estimate the dynamic functional coefficients of the incidence and the latency part. The proposed method is computationally efficient and simultaneously incorporates smoothness in the estimated functional coefficients via roughness penalty. Simulation studies illustrate a satisfactory performance of the proposed method in accurately estimating the model parameters and the baseline survival function. Finally, the clinical potential of the model is demonstrated in two real data examples that incorporate rich high-dimensional biomedical signals as functional covariates measured at the baseline and constitute novel domains to apply cure survival models in contemporary medical situations. In particular, we analyze (i) minute-by-minute physical activity data from the National Health And Nutrition Examination Survey 2003–2006 to study the association between diurnal patterns of physical activity at baseline and all cancer mortality through 2019 while adjusting for other biological factors; (ii) the impact of daily functional measures of disease severity collected in the intensive care unit on post intensive care unit recovery and mortality event. Our findings provide novel epidemiological insights into the association between daily patterns of physical activity and cancer mortality. Software implementation and illustration of the proposed estimation method are provided in R. [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]

Simple Summary: The COVID-19 pandemic may have impacted cancer mortality rates by disrupting patient health behaviors and access to cancer care, as well as being directly affected by infection with SARS-CoV-2. There is limited population-based research that investigates the impact of the COVID-19 pandemic on cancer mortality in the United States. The aim of our retrospective study was to quantify the change in cancer mortality from before the COVID-19 pandemic to during the COVID-19 pandemic in Pennsylvania. We found that mortality rates did not continue their previous downward trajectory and twenty-six counties had an increase in the rate in 2020. The 2015–2019 rates were positively associated with the 2020 rates, and the impact of sociodemographic and geographic factors on the 2020 rates varied by county. Our findings suggest a negative effect of the pandemic on cancer mortality in Pennsylvania and had a varied effect on its counties. Future research could confirm our findings, and if confirmed, may inform cancer research, care, and outreach. Background. We sought to quantify the impact of the COVID-19 pandemic on cancer mortality and identify associated factors in Pennsylvania. Methods. The retrospective study analyzed cross-sectional cancer mortality data from CDC WONDER for 2015 through 2020 for Pennsylvania and its 67 counties. The spatial distributions of 2019, 2020, and percentage change in age-adjusted mortality rates by county were analyzed via choropleth maps and spatial autocorrelation. A Wilcoxon Signed Rank Test was used to analyze whether the rates differed between 2019 and 2020. Quasi-Poisson and geographically weighted regression at the county level were used to assess the association between the 2019 rates, sex (percent female), race (percent non-White), ethnicity (percent Hispanic/Latino), rural–urban continuum codes, and socioeconomic status with the 2020 rates. Results. At the state level, the rate in 2020 did not reflect the declining annual trend (−2.7 per 100,000) in the rate since 2015. Twenty-six counties had an increase in the rate in 2020. Of the factors examined, the 2019 rates were positively associated with the 2020 rates, and the impact of sociodemographic and geographic factors on the 2020 rates varied by county. Conclusions. In Pennsylvania, the 2020 cancer mortality rates did not decline as much as reported before the COVID-19 pandemic. The top five cancer types by rate were the same type for 2019 and 2020. Future cancer control efforts may need to address the impact of the COVID-19 pandemic on trends and geospatial distribution in cancer mortality. [ABSTRACT FROM AUTHOR]