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Background:. This study aims to examine the relationship between race and rural–urban context in head and neck cancer (HNC) survival and determine factors that potentially drive this disparity. Methods:. Using the National Cancer Database from 2004 to 2015, we identified a retrospective cohort of 146,256 patients with HNC.
The 2010 report of the President's Cancer Panel concluded that the burden of cancer from chemical exposures is substantial, while the programs for testing and regulation of carcinogens remain inadequate. New research on the role of early life exposures and the ability of chemicals to act via multiple biological pathways, including immunosuppression, inflammation, and endocrine disruption as well as mutagenesis, further supports the potential for chemicals and chemical mixtures to influence disease. Epidemiologic observations, such as higher leukemia incidence in children living near roadways and industrial sources of air pollution, and new in vitro technologies that decode carcinogenesis at the molecular level, illustrate the diverse eviden.
Background:. Glomerular hyperfiltration is associated with all-cause mortality. Herein, we evaluated the association between glomerular hyperfiltration and the development of cancer, the most common cause of death, in an Asian population. Methods:. We retrospectively reviewed the National Health Insurance Service database of Korea for people who received national health screenings from 2012 to 2013. Glomerular hyperfiltration was defined as the 95th percentile and greater after stratification by sex and age decile. We performed a multivariate Cox regression analysis using glomerular hyperfiltration at the first health screening as the exposure variable and cancer development as the outcome variable to evaluate the impact of glomerular hyperfi.
Background:. Age-related epigenetic dysregulations are associated with several diseases, including cancer. The number of stochastic epigenetic mutations (SEM) has been suggested as a biomarker of life-course accumulation of exposure-related DNA damage; however, the predictive role of SEMs in cancer has seldom been investigated. Methods:. A SEM, at a given CpG site, was defined as an extreme outlier of DNA methylation value distribution across individuals. We investigated the association of the total number of SEMs with the risk of eight cancers in 4,497 case–control pairs nested in three prospective cohorts. Furthermore, we investigated whether SEMs were randomly distributed across the genome or enriched in functional genomic regions. Results.
Background:. Overweight/obesity and dense breasts are strong breast cancer risk factors whose prevalences vary by race/ethnicity. The breast cancer population attributable risk proportions (PARP) explained by these factors across racial/ethnic groups are unknown. Methods:. We analyzed data collected from 3,786,802 mammography examinations (1,071,653 women) in the Breast Cancer Surveillance Consortium, associated with 21,253 invasive breast cancers during a median of 5.2 years follow-up. HRs for body mass index (BMI) and breast density, adjusted for age and registry were estimated using separate Cox regression models by race/ethnicity (White, Black, Hispanic, Asian) and menopausal status. HRs were combined with observed risk-factor proportions.
Background:. Various studies show an inverse relation between Alzheimer disease and cancer, but findings are likely to be biased by surveillance and survival bias. Plasma amyloid-β (Aβ) is defined as a preclinical feature of Alzheimer disease, with lower levels of Aβ42 being associated with a higher risk of Alzheimer disease. To get more insight into the biological link between Alzheimer disease and cancer, we investigated plasma Aβ levels in relation to the risk of cancer. Methods:. Between 2002 and 2005, we measured plasma Aβ40 and Aβ42 levels in 3,949 participants from the population-based Rotterdam Study. These participants were followed until the onset of cancer, all-cause dementia, death, loss to follow-up, or January 1, 2014, whichever.
Background:. It is biologically plausible that genotoxic estrogens, namely estrogen DNA adducts (EDA), have a role in breast cancer development. Support comes from three prior studies that reported elevated concentrations of EDA relative to estrogen metabolites and conjugates (EDA:EMC) in women with breast cancer relative to control women. Methods:. In postmenopausal women in the Women's Health Initiative (WHI), EDA:EMC in 191 controls was compared with findings in 194 prediagnosis urine samples from breast cancer cases. EDA:EMC determinations were by mass spectrometry as previously described, and logistic regression was employed to estimate ORs. Results:. EDA:EMC did not differ in breast cancer cases compared with controls overall [0.93 (95%
The key characteristics (KC) of human carcinogens provide a uniform approach to evaluating mechanistic evidence in cancer hazard identification. Refinements to the approach were requested by organizations and individuals applying the KCs. We assembled an expert committee with knowledge of carcinogenesis and experience in applying the KCs in cancer hazard identification. We leveraged this expertise and examined the literature to more clearly describe each KC, identify current and emerging assays and in vivo biomarkers that can be used to measure them, and make recommendations for future assay development. We found that the KCs are clearly distinct from the Hallmarks of Cancer, that interrelationships among the KCs can be leveraged to strengt.
Background:. Previous studies have examined the characteristics of open and closed system electronic nicotine delivery system (ENDS) users, but population-level information on nicotine exposure among these users has not been available. Methods:. We analyzed nicotine biomarker and survey data from Wave 3 of the Population Assessment of Tobacco and Health (PATH) study collected from October 2015 to October 2016.
The microbiome has been hypothesized to play a role in cancer development. Because of the diversity of published data, an overview of available epidemiologic evidence linking the microbiome with cancer is now needed. We conducted a systematic review using a tailored search strategy in Medline and EMBASE databases to identify and summarize the current epidemiologic literature on the relationship between the microbiome and different cancer outcomes published until December 2019. We identified 124 eligible articles. The large diversity of parameters used to describe microbial composition made it impossible to harmonize the different studies in a way that would allow meta-analysis, therefore only a qualitative description of results could be pe.
Background:. Nut intake has been associated with reduced cancer-related mortality, but there is very limited evidence on total cancer risk. We investigated the associations of nut and peanut butter intake with the risk of total cancer and smoking- and alcohol-related cancer subgroups. Methods:. In the prospective Netherlands Cohort Study, 120,852 men and women aged 55 to 69 years provided information on lifestyle and dietary habits at baseline in 1986. After 20.3 years of follow-up, 19,255 total cancer cases and 3,499 subcohort members were included in multivariable-adjusted Cox regression analyses, using a case–cohort approach. Results:. No significant associations were found between total nut, tree nut, peanut, and peanut butter intake and t.
Background:. Much of the heritable risk of renal cell carcinoma (RCC) associated with common genetic variation is unexplained. New analytic approaches have been developed to increase the discovery of risk variants in genome-wide association studies (GWAS), including multi-locus testing through pathway analysis. Methods:. We conducted a pathway analysis using GWAS summary data from six previous scans (10,784 cases and 20,406 controls) and evaluated 3,678 pathways and gene sets drawn from the Molecular Signatures Database. To replicate findings, we analyzed GWAS summary data from the UK Biobank (903 cases and 451,361 controls) and the Genetic Epidemiology Research on Adult Health and Aging cohort (317 cases and 50,511 controls). Results:. We ide.
Background:. Accumulating evidence has shown that serum calcium and vitamin D may be associated with or influence various cancer risks. However, no prospective studies have evaluated the independent and joint associations between prediagnostic levels of serum calcium and vitamin D and future risk of incident primary liver cancer. Methods:. We used a nested case–control design to evaluate subjects over 22 years of follow-up. Serum calcium, 25-hydroxy vitamin D [25(OH)D], and three markers of hepatitis B virus and hepatitis C virus were measured in baseline serum from 226 incident primary liver cancer cases and 1,061 matched controls. We calculated ORs and 95% confidence intervals (CI) using logistic regression to estimate the associations betw.
Background:. This study aimed to evaluate the relationship of serum thyrotropin (TSH) and thyroid hormone concentration with liver cancer mortality. Methods:. A cohort of 517,996 Korean adults, who did not have liver cancer at baseline and attended a health screening including free thyroxine (FT4) and TSH, were followed for up to 16 years.
Background:. Prevalence of Helicobacter pylori ( H. pylori ) infection, the main risk factor for gastric cancer, has been decreasing in the United States; however, there remains a substantial racial disparity. Moreover, the time-trends for prevalence of CagA-positive H. pylori infection, the most virulent form, are unknown in the U.S. population. We sought to assess prevalence of CagA-positive H. pylori infection over time by race in the United States. Methods:. We utilized multiplex serology to quantify antibody responses to H. pylori antigens in 4,476 participants across five cohorts that sampled adults from 1985 to 2009. Using log-binomial regression models, we calculated prevalence ratios and 95% confidence intervals for the association b.
Background:. To investigate whether chronic opioid therapy is associated with a higher risk of cancer among noncancer patients with chronic pain. Methods:. A population-based historical cohort study of the South Korean adult population was conducted using data from the National Health Insurance Service.
Non-Hodgkin lymphoma comprises a heterogeneous group of hematologic malignancies, with about 60 subtypes that arise via various pathogenetic mechanisms. Although establishing etiology for specific NHL subtypes has been historically difficult given their relative rarity, environmental exposures have been repeatedly implicated as risk factors across many subtypes. Large-scale epidemiologic investigations have pinpointed chemical exposures in particular, but causality has not been established, and the exact biologic mechanisms underpinning these associations are unclear. Here we review chemical exposures that have been associated with development of NHL subtypes and discuss their biologic plausibility based on current research.
Background:. Tattoos may cause a variety of adverse reactions in the body, including immune reactions and infections. However, it is unknown whether tattoos may increase the risk of lymphatic cancers such as non-Hodgkin lymphoma (NHL) and multiple myeloma. Methods:. Participants from two population-based case–control studies were included in logistic regression models to examine the association between tattoos and risk of NHL and multiple myeloma. Results:. A total of 1,518 participants from the NHL study (737 cases) and 742 participants from the multiple myeloma study (373 cases) were included in the analyses. No statistically significant associations were found between tattoos and risk of NHL or multiple myeloma after adjusting for age, sex,
Background:. Air pollution is a carcinogen and causes pulmonary and cardiac complications. We examined the association of fine particulate matter pollution (PM 2.5 ) and mortality from cancer and all causes among pediatric, adolescent, and young adult (AYA) patients with cancer in Utah, a state with considerable variation in PM 2.5 . Methods:. We followed 2,444 pediatric (diagnosed ages 0–14) and 13,459 AYA (diagnosed ages 15–39) patients diagnosed in 1986–2015 from diagnosis to 5 and 10 years postdiagnosis, death, or emigration. We measured average monthly PM 2.5 by ZIP code during follow-up. Separate pediatric and AYA multivariable Cox models estimated the association of PM 2.5 and mortality. Among AYAs, we examined effect modification of P.

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