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Mouse models are vital for assessing risk from environmental carcinogens, including ionizing radiation, yet the interspecies difference in the dose response precludes direct application of experimental evidence to humans. Herein, we take a mathematical approach to delineate the mechanism underlying the human–mouse difference in radiation‐related cancer risk. We used a multistage carcinogenesis model assuming a mutational action of radiation to analyze previous data on cancer mortality in the Japanese atomic bomb survivors and in lifespan mouse experiments. Theoretically, the model predicted that exposure will chronologically shift the age‐related increase in cancer risk forward by a period corresponding to the time in which the spontaneous mutational process generates the same mutational burden as that the exposure generates. This model appropriately fitted both human and mouse data and suggested a linear dose response for the time shift. The effect per dose decreased with increasing age at exposure similarly between humans and mice on a per‐lifespan basis (0.72‐ and 0.71‐fold, respectively, for every tenth lifetime). The time shift per dose was larger by two orders of magnitude in humans (7.8 and 0.046 years per Gy for humans and mice, respectively, when exposed at ~35% of their lifetime). The difference was mostly explained by the two orders of magnitude difference in spontaneous somatic mutation rates between the species plus the species‐independent radiation‐induced mutation rate. Thus, the findings delineate the mechanism underlying the interspecies difference in radiation‐associated cancer mortality and may lead to the use of experimental evidence for risk prediction in humans. [ABSTRACT FROM AUTHOR]

Background: The American Heart Association recently introduced a novel cardiovascular health (CVH) metric, Life's Essential 8 (LE8), for health promotion. However, the relationship between LE8 and cancer mortality risk remains uncertain. Methods: We investigated 17,076 participants from US National Health and Nutrition Examination Survey (US NHANES) and 272,727 participants from UK Biobank, all free of cancer at baseline. The CVH score, based on LE8 metrics, incorporates four health behaviors (diet, physical activity, smoking, and sleep) and four health factors (body mass index, lipid, blood glucose, and blood pressure). Self-reported questionnaires assessed health behaviors. Primary outcomes were mortality rates for total cancer and its subtypes. The association between CVH score (continuous and categorical variable) and outcomes was examined using Cox model with adjustments. Cancer subtypes-related polygenic risk score (PRS) was constructed to evaluate its interactions with CVH on cancer death risk. Results: Over 141,526 person-years in US NHANES, 424 cancer-related deaths occurred, and in UK Biobank, 8,872 cancer deaths were documented during 3,690,893 person-years. High CVH was associated with reduced overall cancer mortality compared to low CVH (HR 0.58, 95% CI 0.37–0.91 in US NHANES; 0.51, 0.46–0.57 in UK Biobank). Each one-standard deviation increase in CVH score was linked to a 19% decrease in cancer mortality (HR: 0.81; 95% CI: 0.73–0.91) in US NHANES and a 19% decrease (HR: 0.81; 95% CI: 0.79–0.83) in UK Biobank. Adhering to ideal CVH was linearly associated with decreased risks of death from lung, bladder, liver, kidney, esophageal, breast, colorectal, pancreatic, and gastric cancers in UK Biobank. Furthermore, integrating genetic data revealed individuals with low PRS and high CVH exhibited the lowest mortality from eight cancers (HRs ranged from 0.36 to 0.57) compared to those with high PRS and low CVH. No significant modification of the association between CVH and mortality risk for eight cancers by genetic predisposition was observed. Subgroup analyses showed a more pronounced protective association for overall cancer mortality among younger participants and those with lower socio-economic status. Conclusions: Maintaining optimal CVH is associated with a substantial reduction in the risk of overall cancer mortality. Adherence to ideal CVH correlates linearly with decreased mortality risk across multiple cancer subtypes. Individuals with both ideal CVH and high genetic predisposition demonstrated significant health benefits. These findings support adopting ideal CVH as an intervention strategy to mitigate cancer mortality risk and promote healthy aging. [ABSTRACT FROM AUTHOR]

Background and aims: Studies on cancer incidence and mortality among people with opioid use‐related disorders are lacking. We aimed to measure cancer‐specific incidence, mortality and survival among people diagnosed with opioid use‐related disorders in Norway during 2010–18. Design and setting: This was a cohort study conducted in Norway during 2010–18. Participants: Individuals (n = 20 710) diagnosed with opioid use‐related disorders. Measurements: We conducted a cohort study utilizing a data‐linkage of national health and population registers. Information on opioid use‐related disorders was extracted from specialized healthcare, malignancies from the Cancer Registry of Norway and deaths from Cause of Death Registry. Cancer incidence and mortality were compared with the general population by calculating sex‐specific age‐standardized incidence (SIR) and mortality (SMR) ratios. One‐year survival rates were computed. Findings Compared with the general population, people with opioid use‐related disorders were at an increased risk of developing cancer overall [SIR = 1.2, 95% confidence interval (CI) = 1.1–1.3] with a higher than twofold cancer mortality rate (SMR = 2.3, 95% CI = 2.0–2.7). Excess risk was observed for liver (12.6, 95% CI = 9.1–17.0), larynx (4.7, 95% CI = 1.7–10.2), lung (3.5, 95% CI = 2.8–4.3) and pancreas cancer (2.6, 95% CI = 1.6–4.0), whereas reduced risk was found for melanoma (0.5, 95% CI = 0.3–0.9), breast (0.6, 95% CI = 0.4–0.9) and prostate cancers (0.3, 95% CI = 0.1–0.4). Site‐specific SMRs were significantly elevated for liver (12.3, 95% CI = 8.5–17.2), lung (3.9, 95% CI = 3.0–5.0), pancreas (3.0, 95% CI = 1.7–4.8) and colon cancers (1.9, 95% CI = 1.1–3.1). The average 1‐year survival rate after a cancer diagnosis was low in liver, pancreas and colon cancer, ranging from 10 to 15% less than that of the general population. Conclusions: In Norway, cancer incidence and cancer‐related mortality appear to be elevated among individuals with opioid use‐related disorders. [ABSTRACT FROM AUTHOR]

Introduction: Screening trials and meta-analyses emphasize the ratio of cancer death rates in screening and control arms. However, this measure is diluted by the inclusion of deaths from cancers that only became detectable after the end of active screening. Methods: We review traditional analysis of cancer screening trials and show that ratio estimates are inevitably biased to the null, because follow-up (FU) must continue beyond the end of the screening period and thus includes cases only becoming detectable after screening ends. But because such cases are expected to occur in equal numbers in the two arms, calculation of the difference between the number of cancer deaths in the screening and control arms avoids this dilutional bias. This difference can be set against the number of invitations to screening; we illustrate by reanalyzing data from all trials of tomography screening of lung cancer (LC) using this measure. Results: In nine trials of LC screening from 2000 to 2013, a total of 94,441 high-risk patients were invited to be in screening or control groups, with high participation rates (average 95%). In the older trials comparing computed tomography to chest X-ray, 88,285 invitations averted 83 deaths (1068 per death averted (DA)). In the six more recent trials with no screening in the control group, 69,976 invitations averted 121 deaths (577 invitations per DA). Discussion: Screens per DA is an undiluted measure of screening's effect and it is unperturbed by the arbitrary duration of FU. This estimate can be useful for program planning and informed consent. [ABSTRACT FROM AUTHOR]

Perceived mental health (PMH) was reportedly associated with mortality in general populations worldwide. However, little is known about sex differences and pathways potentially linking PMH to mortality. We explored the relationship between PMH and mortality in Italian men and women, and analysed potential explanatory factors. We performed longitudinal analyses on 9045 men and 9467 women (population mean age 53.8 ± 11.2 years) from the Moli-sani Study. Baseline PMH was assessed through a self-administered Short Form 36-item questionnaire. Cox proportional hazard regression was used to estimate hazard ratios (HRs) and 95 % confidence intervals (95%CI) of death across sex-specific quartiles of PMH, controlling for age, chronic health conditions, and perceived physical health. Socioeconomic, behavioural, and physiological factors were examined as potential explanatory factors of the association between PMH and mortality. In women, HRs for the highest (Q4) vs. bottom quartile (Q1) of PMH were 0.75 (95%CI 0.60–0.96) for all-cause mortality and 0.59 (0.40–0.88) for cardiovascular mortality. Part of these associations (25.8 % and 15.7 %, for all-cause and cardiovascular mortality, respectively) was explained by physiological factors. In men, higher PMH was associated with higher survival (HR = 0.82; 0.69–0.98, for Q4 vs. Q1) and reduced hazard of other cause mortality (HR = 0.67; 0.48–0.95). More than half of the association with all-cause mortality was explained by physiological factors. PMH was measured at baseline only. PMH was independently associated with mortality in men and women. Public health policies aimed at reducing the burden of chronic diseases should prioritize perceived mental health assessment along with other interventions. • Perceived mental health (PMH) is associated with all-cause and cardiovascular (CVD) mortality in women. • PMH is associated with all-cause and other cause mortality in men. • Physiological factors explained 25.8% and 15.7% of the association of PMH with all-cause and CVD mortality in women. • In men, the association of PMH with all-cause mortality was largely explained by physiological factors. [ABSTRACT FROM AUTHOR]

Background: Empirical evidence from European countries has shown that economic conditions in early life are associated with mortality risk. This study aims to assess the effects of economic conditions in early life, as well as their interaction with parental education, on the risk of adult mortality in the U.S. Methods: To capture exogenous variation of economic conditions early in life, we use the Gross Domestic Product (GDP) cyclical deviation during a respondent's birth year. Using the linked U.S. General Social Survey and National Death Index data (1979–2008), we employed parametric frailty survival models to examine the effects of economic conditions in early life on all-cause and cause-specific mortality. Results: We found that exposure to recession in the first year of life was associated with increased all-cause mortality only among women (hazard ratio = 1.54, 95% CI 1.03–2.31). This adverse effect was also found in women's mortality from cancers (hazard ratio = 2.24, 95% CI 1.18–4.28). We also found a significant interaction between economic conditions in infancy and paternal education on women's mortality risk—higher paternal education was protective against mortality under good economic conditions in infancy; however, higher paternal education was associated with greater mortality risk under poor economic conditions in infancy. We discuss how aspiration theory may explain these results. Conclusion: Our study concludes that worse macroeconomic conditions early in life heighten the risk of mortality among women, and paternal education moderates this relationship. [ABSTRACT FROM AUTHOR]

Aims Methods Results Conclusions The relationship between α‐Klotho (αK) and mortality is controversial and has not been examined in a large, diverse cohort. We investigated the association between serum αK protein levels with all‐cause and cause‐specific mortality in a cohort representative of the US population.We used National Health and Nutrition Examination Survey (NHANES) data from 2007 to 2016. A nonlinear association between mortality and αK levels as a quadratic variable were examined using Cox proportional hazard models and competing risk models. Multivariable models were adjusted for age, gender, race, hypertension, diabetes, smoking, alcohol use, physical activity, body mass index (BMI), serum cholesterol, estimated glomerular filtration rate, highest educational status attained and family income to poverty threshold ratio.Of the 13 749 participants, 1569 (11%) died, 7092 (52%) were female, and 5918 (43%) were Caucasian. The mean (SD) of age was 58 (11) years, BMI 29.7 (6.7) kg/m2, and αK was 0.85 (0.31) ng/mL. In the adjusted Cox proportional hazards model with quadratic αK, we found a U‐shaped relationship between all‐cause mortality and αK levels (continuous αK hazard ratio [HR] = 0.56, 95% confidence interval [CI]: 0.37, 0.85; P = .007; squared‐αK HR = 1.25, 95% CI: 1.11, 1.41; P < 0.001). A similar U‐shaped relationship was noted between αK and cancer mortality in the adjusted Cox proportional hazards model (continuous αK HR = 0.45, 95% CI: 0.19, 1.06; P = 0.07; squared αK HR = 1.32, 95% CI: 1.07, 1.61; P = 0.009). No relationship was present with cardiovascular or other‐cause mortality.In this large diverse cohort, we report a U‐shaped relationship between αK with all‐cause and cancer mortality. Further research to elucidate the underlying biological mechanism of these relationships is needed. [ABSTRACT FROM AUTHOR]

Simple Summary: Socioeconomic inequalities in cancer incidence and mortality have been studied extensively, but there has been no investigation of the spatial distribution of incidence and mortality within a country to see if they are consistent with each other and with deprivation. To fill this gap, we examined the spatial distribution of cancer incidence and mortality and their association with each other and with socioeconomic deprivation at the municipal level in Hungary, one of the countries with the most unfavourable cancer burden in the world. For different types of cancer, while mortality always showed positive associations with deprivation, there was only partial overlap between areas of high incidence and mortality across the country, with clusters often independent of deprivation. Even where incidence and mortality overlapped geographically, there were often significant differences in mortality risk. Discrepancies in the spatial distribution of cancer incidence and mortality are indicators of an unmet need for cancer prevention and/or treatment. There is a rich body of literature on the distribution of cancer incidence and mortality in socioeconomically different world regions, but none of the studies has compared the spatial distribution of mortality and incidence to see if they are consistent with each other. All malignant neoplasms combined and cervical, colorectal, breast, pancreatic, lung, and oral cancers separately were studied in the Hungarian population aged 25–64 years for 2007–2018 at the municipality level by sex. In each case, the spatial distribution of incidence and mortality were compared with each other and with the level of deprivation using disease mapping, spatial regression, risk analysis, and spatial scan statistics. A positive association between deprivation and mortality was found for each type of cancer, but there was no significant association for male colorectal cancer (relative risk (RR) 1.00; 95% credible interval (CI) 0.99–1.02), pancreatic cancer (RR: 1.01; 95%CI 0.98–1.04), and female colorectal cancer incidence (RR: 1.01; 95%CI 0.99–1.03), whereas a negative association for breast cancer (RR: 0.98; 95%CI 0.96–0.99) was found. Disease mapping analyses showed only partial overlap between areas of high incidence and mortality, often independent of deprivation. Our results highlight not only the diverse relationship between cancer burden and deprivation, but also the inconsistent relationship between cancer incidence and mortality, pointing to areas with populations that require special public health attention. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, but few studies have evaluated mortality risks among individuals with IBS. We explored the association between IBS and all-cause and cause-specific mortality in the UK Biobank. METHODS: We included 502,369 participants from the UK Biobank with mortality data through 2022. IBS was defined using baseline self-report and linkage to primary care or hospital admission data. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and cause-specific mortality using multivariable Cox proportional hazards regression models within partitioned follow-up time categories (0-5, >5-10, and >10 years). RESULTS: A total of 25,697 participants (5.1%) had a history of IBS at baseline. After a median follow-up of 13.7 years, a total of 44,499 deaths occurred. Having an IBS diagnosis was strongly associated with lower risks of all-cause (HR50.70,95%CI50.62-0.78) and all-cancer (HR50.69,95%CI50.60-0.79) mortality in the first 5 years of follow-up. These associations were attenuated over follow-up, but even after 10 years of follow-up, associations remained inverse (all-cause: HR5 0.89, 95%CI5 0.84-0.96; all-cancer: HR 5 0.87, 95% CI 5 0.78-0.97) after full adjustment. Individuals with IBS had decreased risk of mortality from breast, prostate, and colorectal cancers in some of the follow-up time categories. DISCUSSION: We found that earlier during follow-up, having diagnosed IBS was associated with lower mortality risk, and the association attenuated over time. Additional studies to understand whether specific factors, such as lifestyle and healthcare access, explain the inverse association between IBS and mortality are needed. [ABSTRACT FROM AUTHOR]

Jordan G Kassab, R Hayden Meeks, Werner TW de Riese Department of Urology, Texas Tech University Health Sciences Center, Lubbock, TX, USACorrespondence: Werner TW de Riese, Email werner.deriese@ttuhsc.eduAbstract: Prostate cancer (PCa) currently stands as the most common malignancy and the second most common cause of death in men worldwide. Dr. C. Huggins revolutionized the field of PCa treatment through his work investigating the therapeutic effects of androgen deprivation. These early surgical castration methods were expanded upon by integrating reversible pharmacologic castration via biologic agonists. Following this, intermittent ADT (iADT) became a medical substitute for its continuous counterpart. This data synthesis aims to highlight and assess the pertinent adverse effects of ADT, to compare mortality for PCa treatment plans, and consequently provide direction for clinicians in choosing the suitable systemic ADT approach. We performed a thorough systematic search across the PubMed database to identify prospective randomized clinical trials (RCTs) comparing continuous and intermittent androgen deprivation therapy (cADT and iADT). Our qualitative analysis aimed to evaluate the potential of iADT as an alternative treatment approach, emphasizing recent clinical outcomes. The analysis of randomized control trials in the literature revealed no discernable statistical difference in PCa-specific mortality in comparison of iADT and cADT treatments. Further, in the analysis of mortality due to non-PCa causes, iADT patients fared more favorably compared to cADT. Due to iADT’s characteristics of being more cost-efficient and less likely to cause undesirable side effects, urologic healthcare professionals should be made aware of these findings when counseling patients on the optimal form of ADT and consulting for future treatment guidelines.Keywords: androgen deprivation therapy, prostate cancer, cancer mortality

Abstract Background The American Heart Association recently introduced a novel cardiovascular health (CVH) metric, Life's Essential 8 (LE8), for health promotion. However, the relationship between LE8 and cancer mortality risk remains uncertain. Methods We investigated 17,076 participants from US National Health and Nutrition Examination Survey (US NHANES) and 272,727 participants from UK Biobank, all free of cancer at baseline. The CVH score, based on LE8 metrics, incorporates four health behaviors (diet, physical activity, smoking, and sleep) and four health factors (body mass index, lipid, blood glucose, and blood pressure). Self-reported questionnaires assessed health behaviors. Primary outcomes were mortality rates for total cancer and its subtypes. The association between CVH score (continuous and categorical variable) and outcomes was examined using Cox model with adjustments. Cancer subtypes-related polygenic risk score (PRS) was constructed to evaluate its interactions with CVH on cancer death risk. Results Over 141,526 person-years in US NHANES, 424 cancer-related deaths occurred, and in UK Biobank, 8,872 cancer deaths were documented during 3,690,893 person-years. High CVH was associated with reduced overall cancer mortality compared to low CVH (HR 0.58, 95% CI 0.37–0.91 in US NHANES; 0.51, 0.46–0.57 in UK Biobank). Each one-standard deviation increase in CVH score was linked to a 19% decrease in cancer mortality (HR: 0.81; 95% CI: 0.73–0.91) in US NHANES and a 19% decrease (HR: 0.81; 95% CI: 0.79–0.83) in UK Biobank. Adhering to ideal CVH was linearly associated with decreased risks of death from lung, bladder, liver, kidney, esophageal, breast, colorectal, pancreatic, and gastric cancers in UK Biobank. Furthermore, integrating genetic data revealed individuals with low PRS and high CVH exhibited the lowest mortality from eight cancers (HRs ranged from 0.36 to 0.57) compared to those with high PRS and low CVH. No significant modification of the association between CVH and mortality risk for eight cancers by genetic predisposition was observed. Subgroup analyses showed a more pronounced protective association for overall cancer mortality among younger participants and those with lower socio-economic status. Conclusions Maintaining optimal CVH is associated with a substantial reduction in the risk of overall cancer mortality. Adherence to ideal CVH correlates linearly with decreased mortality risk across multiple cancer subtypes. Individuals with both ideal CVH and high genetic predisposition demonstrated significant health benefits. These findings support adopting ideal CVH as an intervention strategy to mitigate cancer mortality risk and promote healthy aging.

Introduction: The purpose of this study was to investigate the association of central lean mass distribution with the risk of mortality. Methods: This cohort study included 40,283 UK Biobank participants. Cox proportional hazards regression models were used to estimate the association of central lean mass distribution, i.e., trunk-to-leg lean mass ratio, assessed by dual-energy X-ray absorptiometry, with the risk of mortality. Results: The median age of the participants was 65 years, and 52% were women. During a median follow-up of 4.18 years, 674 participants died, of whom 366 were due to cancer and 126 were due to cardiovascular causes. Compared with the lowest tertile of a trunk-to-leg lean mass ratio, the multivariable-adjusted (age, sex, ethnicity, lifestyle, comorbidities, body mass index, and appendicular muscle mass index) hazards ratios of the highest tertile of trunk-to-leg lean mass ratio were 1.55 (95% CI: 1.23–1.94), 1.69 (95% CI: 1.26–2.26), and 1.14 (95% CI: 0.72–1.80) for all-cause, cancer, and cardiovascular mortality, respectively. Neutrophil-to-lymphocyte ratio mediated 9.3% (95% CI: 3.3%–40.4%) of the association of trunk-to-leg lean mass ratio with all-cause mortality. There was evidence for additive interactions of trunk-to-leg lean mass ratio with older age and poor diet quality for all-cause mortality. Conclusion: Trunk-to-leg lean mass ratio, assessed by dual-energy X-ray absorptiometry, was positively associated with the risks of all-cause and cancer mortality, independent of general obesity and central obesity, in UK middle-aged and older adults. Central lean mass distribution may interact synergistically with aging and poor diet quality to further increase the risk of death.

Abstract Background There is evidence indicating that both lipoprotein(a) [Lp(a)] and fibrinogen (FIB) are associated with mortality, However, the impact of their combination on mortality has not been determined. Thus, the aim of this study was to examine the association between the combination of Lp(a) and FIB with all-cause and cause-specific mortality. Methods This prospective cohort study enrolled 4,730 participants from the third National Health and Nutrition Examination Survey. The exposure variables included Lp(a), FIB and their combination, while the outcome variables consisted of all-cause, cardiovascular disease (CVD) and cancer-related mortality. Multivariate COX regression, subgroup analysis, sensitivity analysis and restricted cubic spline (RCS) were used to investigate the association between Lp(a), FIB and their combination with all-cause, CVD and cancer-related mortality. Results Over a median follow-up period of 235 months, 2,668 individuals died, including 1,051 deaths attributed to CVD and 549 deaths due to cancer. Multivariate Cox regression analyses revealed independent associations between both Lp(a) and FIB with all-cause, CVD, and cancer-related mortality. Compared to participants in the 1st to 50th percentiles of both Lp(a) and FIB, those in the 90th to 100th percentiles exhibited multivariable adjusted HRs of 1.813 (95% CI: 1.419–2.317, P 0.05). Conversely, the relationship between Lp(a) and the risk of CVD-related mortality, as well as the relationship between FIB and the risk of all-cause and CVD-related mortality, were nonlinear (P for nonlinearity

Abstract Aims To test the association of C-reactive protein (CRP) with all-cause and cause-specific mortality in people with gout. Methods This cohort study included 502 participants with gout from the National Health and Nutrition Examination Survey. Multivariate Cox regression analysis, subgroup analysis, and restricted cubic spline (RCS) analyses were utilized to examine the association of CRP levels with all-cause, cardiovascular, and cancer mortality. Results After adjusting for multiple variables, Cox regression analysis showed that compared with individuals in the lowest tertile of CRP levels, those in the middle and highest tertiles experienced increases in all-cause mortality risk of 74.2% and 149.7%, respectively. Similarly, the cancer mortality risk for individuals in the highest tertile of CRP levels increased by 283.9%. In addition, for each standard deviation increase in CRP, the risks of all-cause and cancer mortality increased by 25.9% and 35.4%, respectively (P 60 years), gender (male), presence or absence of hypertension, non-diabetes, cardiovascular disease, non-cardiovascular disease and non-cancer. Furthermore, the association with cancer mortality was significant in subgroups including males, those without hypertension and cancer, and those with or without diabetes. However, the association with cardiovascular mortality was only significant in the non-hypertension subgroup (P

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 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

Aims: To test the association of C-reactive protein (CRP) with all-cause and cause-specific mortality in people with gout. Methods: This cohort study included 502 participants with gout from the National Health and Nutrition Examination Survey. Multivariate Cox regression analysis, subgroup analysis, and restricted cubic spline (RCS) analyses were utilized to examine the association of CRP levels with all-cause, cardiovascular, and cancer mortality. Results: After adjusting for multiple variables, Cox regression analysis showed that compared with individuals in the lowest tertile of CRP levels, those in the middle and highest tertiles experienced increases in all-cause mortality risk of 74.2% and 149.7%, respectively. Similarly, the cancer mortality risk for individuals in the highest tertile of CRP levels increased by 283.9%. In addition, for each standard deviation increase in CRP, the risks of all-cause and cancer mortality increased by 25.9% and 35.4%, respectively (P < 0.05). Subgroup analyses demonstrated that the association between CRP levels and all-cause mortality remained significant across subgroups of age (≤ 60 and > 60 years), gender (male), presence or absence of hypertension, non-diabetes, cardiovascular disease, non-cardiovascular disease and non-cancer. Furthermore, the association with cancer mortality was significant in subgroups including males, those without hypertension and cancer, and those with or without diabetes. However, the association with cardiovascular mortality was only significant in the non-hypertension subgroup (P < 0.05). Nonlinear association of CRP with all-cause mortality and linear association with cancer mortality were also confirmed (P for nonlinearity = 0.008 and 0.135, respectively). Conclusions: CRP levels were associated with increased all-cause and cancer mortality among individuals with gout. [ABSTRACT FROM AUTHOR]

Ovarian cancer, a leading cause of cancer deaths, poses challenges due to insidious development and vague signs and symptoms. Risk factors include age, reproductive history, genetic mutations, and environmental factors. Treatment involves surgery, chemotherapy, and targeted therapy, with nursing interventions focusing on symptom management and supportive care. [ABSTRACT FROM AUTHOR]

Aims: The aim of this study was to investigate associations between having visited the theatre/cinema and an arts exhibition during the past year and all-cause, cardiovascular disease (CVD), cancer and other-cause mortality. Methods: The 2008 public health postal survey in Scania, Sweden, was distributed to a stratified random sample of the adult population (18–80 years old). The participation rate was 54.1%, and 25,420 participants were included in the present study. The baseline 2008 survey data were linked to cause-of-death register data to create a prospective cohort with 8.3-year follow-up. Associations between visit to the theatre/cinema, visit to an arts exhibition and mortality were investigated in survival (Cox) regression models. Results: Just over a quarter (26.5%) had visited both the theatre/cinema and an arts exhibition during the past year, 36.6% only the theatre/cinema, 4.9% only an arts exhibition and 32% neither of the two. Not visiting the theatre/cinema during the past year was associated with higher all-cause and CVD mortality. Not visiting an arts exhibition was associated with higher all-cause and other-cause mortality. The combination of having visited neither the theatre/cinema nor an arts exhibition during the past year was associated with higher all-cause, CVD and other-cause mortality. Conclusions: There is an association between attending arts and culture activities and a reduced risk of CVD and other-cause mortality but not cancer mortality, although model imperfections are possible. [ABSTRACT FROM AUTHOR]

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]

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]

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]

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]

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]

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]

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]

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]

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

Background: 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]

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: 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]

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]

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]

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]

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]

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]

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.

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.

There is a rich body of literature on the distribution of cancer incidence and mortality in socioeconomically different world regions, but none of the studies has compared the spatial distribution of mortality and incidence to see if they are consistent with each other. All malignant neoplasms combined and cervical, colorectal, breast, pancreatic, lung, and oral cancers separately were studied in the Hungarian population aged 25–64 years for 2007–2018 at the municipality level by sex. In each case, the spatial distribution of incidence and mortality were compared with each other and with the level of deprivation using disease mapping, spatial regression, risk analysis, and spatial scan statistics. A positive association between deprivation and mortality was found for each type of cancer, but there was no significant association for male colorectal cancer (relative risk (RR) 1.00; 95% credible interval (CI) 0.99–1.02), pancreatic cancer (RR: 1.01; 95%CI 0.98–1.04), and female colorectal cancer incidence (RR: 1.01; 95%CI 0.99–1.03), whereas a negative association for breast cancer (RR: 0.98; 95%CI 0.96–0.99) was found. Disease mapping analyses showed only partial overlap between areas of high incidence and mortality, often independent of deprivation. Our results highlight not only the diverse relationship between cancer burden and deprivation, but also the inconsistent relationship between cancer incidence and mortality, pointing to areas with populations that require special public health attention.

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.

Objectives: Dietary patterns, characterised by protein, polyunsaturated fatty acids, and vitamin D, reduce the odds of malnutrition in cancer survivors. However, it is unclear whether these dietary patterns also improve prognosis. This study prospectively examined associations between dietary patterns linked to lower odds of malnutrition and the risk of all-cause and cancer mortality in adult cancer survivors from the UK Biobank cohort. Design: Prospective observational study. Setting and participants: Cancer survivors from the UK Biobank (mean ± SD, 7.1 ± 6.3 years since diagnosis) were included (n = 2415; 59.7 ± 7.1 years; 60.7% female). Measurements: Dietary intake was estimated using the Oxford WebQ 24-h dietary assessment. Dietary patterns (‘high oily fish and nuts’, and ‘low oily fish’) were derived using reduced rank regression (response variables: protein (g/kg/day), polyunsaturated fatty acids (g/day) and vitamin D (μg/day)). Cox proportional hazard models estimated hazard ratios (HR) and 95% confidence intervals (CI) for all-cause and cancer mortality. Nonlinear relationships were examined using restricted cubic splines. Models were adjusted for demographic and health characteristics. Sub-group analyses investigated relationships in sub-samples of adults with i) high nutritional risk (lung, gastrointestinal, haematological, or head and neck tumours) and ii) recent cancer diagnosis (cancer diagnosis within two years prior to assessment). Results: Deaths due to all-causes (n = 305) and cancer (n = 249) were identified during a median 10.4 (IQR: 10.2–10.8) years follow-up. There were no statistically significant linear associations between the dietary patterns and all-cause or cancer mortality. However, a U-shaped association between the ‘high oily fish and nuts’ pattern, characterised by higher intake of oily fish and nuts and seeds, and all-cause mortality (p-non-linearity = 0.004) was identified, as well as with all-cause (p-non-linearity = 0.006) and cancer mortality (p-non-linearity = 0.035) in adults with a high nutritional risk cancer diagnosis (lung, gastrointestinal, haematological, or head and neck tumours), indicating that both above and below mean intake was associated with increased risk. The ‘low oily fish’ pattern, characterised by lower oily fish but higher potato intake, also had a non-linear association with all-cause mortality (p-non-linearity = 0.046) where lower but not higher than mean intake increased mortality risk. No dietary patterns were significantly associated with mortality in adults with a recent cancer diagnosis. Conclusion: ‘High oily fish and nuts’ or ‘low oily fish’ dietary patterns that were protective against malnutrition were associated with risk of all-cause and cancer mortality in adults with cancer. Future research should assess the efficacy of these dietary patterns in the acute treatment period when malnutrition is most prevalent.

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.

Purpose: We aimed to compare cancer mortality among foreign- and Colombian populations in Colombia during the period of 2006–2020. Methods: This retrospective study utilized vital statistics from the Colombian National Department of Statistics (DANE). The dataset included variables such as age group, sex, country of permanent residency, insurance, education level, marital status, ethnicity, and cause of death. The population data to calculate rates was obtained from the Colombian census and the United Nations. Crude and adjusted rates as well as proportional mortality rates were calculated. Results: A total of 561,932 cancer deaths occurred in Colombia from 2006 to 2020. The foreign population (country of permanent residency different to Colombia) had a lower crude cancer mortality rate (31.1 per 100,000 inhabitants) than the Colombian population (81.9 per 100,000 inhabitants). However, the age-adjusted cancer mortality rate among the foreign population was 253.6 per 100,000, compared to 86.1 per 100,000 among the Colombian population. The proportional cancer mortality was 10.4 % among foreign population compared to 17.4 % among Colombian population. Conclusions: The proportional cancer mortality shows that the proportion of cancer-related deaths is greater among the Colombian population compared to the immigrant population. However, immigrants in Colombia have a higher age-adjusted cancer mortality rate than Colombians, indicating that immigrants have worse cancer outcomes than the Colombians even though the immigrant population is younger. This is likely due to the frequent barriers that immigrants encounter in accessing health care in Colombia. Future research needs to focus on access to care for the immigrant population by investigating cancer-related risk factors among immigrants and addressing their barriers to cancer prevention and treatment.