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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]

Background: Kidney function is associated with clinical outcomes in patients with cancer. Objectives: This study aimed to assess the association between kidney function decline and cancer‐related mortality among community‐dwelling elderly individuals. Design: This was a retrospective longitudinal cohort study. Participants: The 61,988 participants were from an elderly health examination database in Taipei City from 2005 to 2012. Measurements Multivariable logistic regression was used to assess the association between baseline covariates and rapidly deteriorating estimated glomerular filtration rate (eGFR). In addition, Cox proportional hazards model and the Fine–Gray model were used to quantify the effects of covariates on total cancer mortality and six specific cancer mortalities. Results: During the follow‐up period, 1482 participants died of cancer. Their baseline average eGFR was 73.8 ± 19.9 mL/min/1.73 m2, and 18.3% had rapid renal function decline (≥5 mL/min/1.73 m2 per year). Rapid renal function decline was positively related to age, baseline eGFR, proteinuria, hypertension, waist circumferences, high log triglyceride levels, and diabetes mellitus (DM) history. In Cox proportional hazard models, participants with rapid eGFR decline had an increased risk of cancer mortality [hazard ratio (95% CI): 1.97 (1.73, 2.24); p < 0.001] compared to those without rapid eGFR decline. In the analysis of site‐specific cancer mortality risk, rapid eGFR decline was associated with six site‐specific cancer mortality, namely gastrointestinal tract, hepatobiliary, lung, prostate, urinary tract, and hematological malignancies. Conclusions: Elderly individuals with rapid kidney function decline had higher cancer mortality risks. Serial assessments of dynamic changes in eGFR might provide information relevant for cancer prognosis. [ABSTRACT FROM AUTHOR]

Aim: To estimate the risk of cancer incidence and mortality among patients with alcoholic liver disease in South Korea. Methods: A matched cohort study was conducted, including 1,042,185 men (alcoholic liver disease cases: 208,437; controls: 833,748) and 100,400 women (alcoholic liver disease cases: 20,080; controls: 80,320), matched for sex, age, smoking, alcohol consumption, and body mass index at a 1:4 ratio. The risk of cancer incidence and mortality in the alcoholic liver disease group was assessed using Cox proportional hazards regression models. Results: Both men and women with alcoholic liver disease had an elevated risk of all‐cancer and liver cancer incidence and mortality in comparison with the control group. In men, alcoholic liver disease was associated with a significantly higher risk of development of 10 cancer types, including lip, oral cavity, and pharynx; esophagus; liver; gallbladder and biliary tract; pancreas; larynx; lung; kidney; thyroid gland; and leukemia. Subgroup analysis by hepatitis B and C infection showed increased hazard ratios of all cancer incidences and mortality in the alcoholic liver disease group, regardless of hepatitis B or C infection status. In both sexes, a higher number and more years of hospital or clinic visits for alcoholic liver disease were associated with an increased risk of incidence and mortality from all cancers and liver cancer. A more profound dose–response relationship between alcoholic liver disease and alcohol consumption was observed in women than in men. Conclusions: Our findings emphasize the need for a clinical surveillance program and the early detection of cancer in patients with alcoholic liver disease. [ABSTRACT FROM AUTHOR]

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

Background: There is extensive interest in understanding how neighborhood socioeconomic status (nSES) may affect cancer incidence or survival. However, variability regarding items included and approaches used to form a composite nSES index presents challenges in summarizing overall associations with cancer. Given recent calls for standardized measures of neighborhood sociodemographic effects in cancer disparity research, the objective of this systematic review was to identify and compare existing nSES indices studied across the cancer continuum (incidence, screening, diagnosis, treatment, survival/mortality) and summarize associations by race/ethnicity and cancer site to inform future cancer disparity studies. Methods: Using PRISMA guidelines, peer‐reviewed articles published between 2010 and 2019 containing keywords related to nSES and cancer were identified in PubMed. Results: Twenty‐four nSES indices were identified from 75 studies. In general, findings indicated a significant association between nSES and cancer outcomes (n = 64/75 studies; 85.33%), with 42/64 (65.63%) adjusting for highly‐correlated individual SES factors (e.g., education). However, the direction of association differed by cancer site, race/ethnicity, and nSES index. Conclusions: This review highlights several methodologic and conceptual issues surrounding nSES measurement and potential associations with cancer disparities. Recommendations pertaining to the selection of nSES measures are provided, which may help inform disparity‐related disease processes and improve the identification of vulnerable populations in need of intervention. [ABSTRACT FROM AUTHOR]

Background: Numerous studies have suggested that fasting plasma glucose (FPG) was associated with the risk of mortality. However, relationship on longitudinal changes of FPG with the risk of mortality remained inconsistent. Methods: We examined the association of FPG at baseline and its longitudinal changes with risk of mortality based on a cohort study in Yinzhou, China, during 2010–2018. Cox regression models and competing risk models were separately used to examine the association of FPG levels and long‐term fluctuation with risk of total and cause‐specific mortality. Results: Subjects who had an impaired fasting glucose or diabetes suffered a higher risk of total mortality than subjects who had a normal fasting glucose (HRs and 95% CIs: 1.17 [1.01–1.35], 1.30 [1.10–1.53], respectively). The HR for total mortality was 1.54 (95% CI: 1.29–1.84) and for cancer mortality was 1.41 (95% CI: 1.04–1.92) in the highest quartile of coefficient of variation of FPG. Trajectory analysis indicated that subjects with a significantly changed FPG suffered a higher risk of total mortality. Conclusion: According to this cohort study, we found that long‐term fluctuation of FPG was significantly associated with the risk of total and cancer mortality. Our findings suggest that long‐term fluctuation of FPG could be used as an efficient indicator for predicting the subsequent risk of mortality. [ABSTRACT FROM AUTHOR]

Background: We hypothesized that lower socioeconomic status (SES) was associated with higher all‐cause mortality in patients newly diagnosed with cancer, particularly in the elderly population. Methods: We collected study patients from the stratified random sample of Korean National Health Insurance Elderly Cohort (2002‐2015). The Cox's proportional hazards model was used to investigate the risk factors for mortality. Income level and composite deprivation index (CDI) 2010 were used to define the SES: low, intermediate, and high SES groups. The comorbidities were measured using Charlson Comorbidity Index score. After a wash‐out period (2002), the final study population was 108 626 (2003‐2015). Results: In multivariate analysis, low SES was associated with poor overall survival (OS) (HR = 1.08, 95% CI: 1.05‐1.12, P < 0.001) and cancer‐specific survival (CSS) (HR = 1.11, 95% CI: 1.06‐1.16, P < 0.001) particularly for patients aged 70‐79 years. High SES was favorable prognostic factor of OS in patients aged 60‐69 years (HR = 0.85, 95% CI: 0.81‐0.89, P < 0.001), 70‐79 years (HR = 0.90, 95% CI: 0.87‐0.93, P < 0.001), and ≥80 years (HR = 0.91, 95% CI: 0.87‐0.96, P < 0.001). However, SES was not associated with CSS in advanced age patients (≥80 years). Patients with low SES manifesting colorectal, urinary, liver, gastric, melanoma, and esophageal cancers demonstrated worse OS, compared to patients with intermediate SES. Also, low SES patients with urinary, liver, or colorectal cancers or melanoma demonstrated worse CSS compared to those with intermediate SES. Conclusion: Low SES at the time of cancer diagnosis is associated with increased risk of OS and CSS in elderly patients. Depending on cancer sites, different patterns of OS and CSS were observed according to SES. Further elucidation of the causes underlying these phenomena is needed along with appropriate support for elderly cancer patients with low SES. [ABSTRACT FROM AUTHOR]

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

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

Limited information is available on risk of peritoneal mesothelioma after asbestos exposure, and in general on the risk of cancer after cessation of asbestos exposure. We updated to 2013 the follow-up of a cohort of 1083 female and 894 male textile workers with heavy asbestos exposure (up to 100 fb/ mL), often for short periods. A total of 1019 deaths were observed, corresponding to a standardized mortality ratio ( SMR) of 1.68 (95% confidence interval [ CI]: 1.57-1.78). SMRs were 29.1 (95% CI: 21.5-38.6) for peritoneal cancer, 2.96 (95% CI: 2.50-3.49) for lung cancer, 33.7 (95% CI: 25.7-43.4) for pleural cancer, and 3.03 (95% CI: 1.69-4.99) for ovarian cancer. For pleural and peritoneal cancer, there was no consistent pattern of risk in relation to time since last exposure, whereas for lung cancer there was an indication of a decline in risk after 25 years since last exposure. The findings of this unique cohort provide novel data for peritoneal cancer, indicating that - as for pleural cancer - the excess risk does not decline up to several decades after cessation of exposure. [ABSTRACT FROM AUTHOR]