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Background: Cannabis interest and use is increasing in the United States, yet research on its use among cancer patients is limited. Methods: Individuals with cancer completed an anonymous cross-sectional questionnaire. Multivariable logistic regressions estimated odds ratios (OR) between patients' demographic and clinical characteristics with cannabis-related interest, current use, and provider recommendation. Results: Participants (n = 943) were, on average, 61.7 years old. Older patients were less likely to use cannabis products (OR = 0.42, confidence interval [95% CI]: 0.26–0.69) and less likely to be interested in cannabis (OR = 0.60, 95% CI: 0.44–0.84) than younger patients. Those with higher education were less likely to be using cannabis (OR = 0.41, 95% CI: 0.25–0.67) and less likely to have received a provider recommendation of cannabis use than the least educated (OR = 0.38, 95% CI: 0.19–0.76). Cancer spread and type were significant correlates of provider recommendation of cannabis use. Conclusions: Additional research is warranted to better understand cancer patients' motivations for cannabis use and interest. [ABSTRACT FROM AUTHOR]

B-vitamins contribute to DNA synthesis, maintenance, and regulation. Few studies have examined associations of supplemental sources of B-vitamins with the incidence of upper gastrointestinal (GI) cancers [including gastric (GCA) and esophageal (ECA) cancers]; the only prior study to comprehensively examine such intakes reported potential elevated risks of ECA. We examined 159,401 postmenopausal women, ages 50–79 years at baseline, including 302 incident GCA and 183 incident ECA cases, over 19 years of follow-up within the Women's Health Initiative observational study and clinic trials. Adjusted Cox regression models estimated hazard ratios (HR) and 95% confidence intervals (CI) for associations of supplemental B-vitamins [riboflavin (B2), pyridoxine (B6), folic acid (B9), or cobalamin (B12)] with GCA and ECA risk, respectively. Although HRs were generally below 1.0, we observed no statistically significant associations between supplemental intakes of any of the evaluated B-vitamins with the risk of GCA or ECA. As the first prospective study to comprehensively assess these associations, our findings do not corroborate prior research indicating potential harm from supplemental B-vitamin intake for upper GI cancer risk. This study adds evidence that supplemental intakes of B-vitamins may be used by postmenopausal women without regard to their relationship with upper GI cancer risk. [ABSTRACT FROM AUTHOR]

Limited data from prospective studies suggest that higher dietary intake of long-chain omega-3 polyunsaturated fatty acids (LCn3PUFA), which hold anti-inflammatory properties, may reduce endometrial cancer risk; particularly among certain subgroups characterized by body mass and tumor pathology. Data from 12 prospective cohort studies participating in the Epidemiology of Endometrial Cancer Consortium were harmonized as nested case-control studies, including 7268 endometrial cancer cases and 26,133 controls. Habitual diet was assessed by food frequency questionnaire, from which fatty acid intakes were estimated. Two-stage individual-participant data mixed effects meta-analysis estimated adjusted odds ratios (OR) and 95% confidence intervals (CI) through logistic regression for associations between study-specific energy-adjusted quartiles of LCn3PUFA and endometrial cancer risk. Women with the highest versus lowest estimated dietary intakes of docosahexaenoic acid, the most abundant LCn3PUFA in diet, had a 9% increased endometrial cancer risk (Quartile 4 vs. Quartile 1: OR 1.09, 95% CI: 1.01–1.19; P trend = 0.04). Similar elevated risks were observed for the summary measure of total LCn3PUFA (OR 1.07, 95% CI: 0.99–1.16; P trend = 0.06). Stratified by body mass index, higher intakes of LCn3PUFA were associated with 12–19% increased endometrial cancer risk among overweight/obese women and no increased risk among normal-weight women. Higher associations appeared restricted to White women. The results did not differ by cancer grade. Higher dietary intakes of LCn3PUFA are unlikely to reduce endometrial cancer incidence; rather, they may be associated with small to moderate increases in risk in some subgroups of women, particularly overweight/obese women. • We conducted an individual-participant data meta-analysis of dietary omega-3 fatty acids and endometrial cancer risk. • Data were obtained from 12 prospective cohort studies. • Small, positive associations between dietary omega-3 fatty acids and endometrial cancer were observed overall. • Stronger, moderate positive associations were observed among participants with body mass indices ≥25 kg/m2. [ABSTRACT FROM AUTHOR]

Evidence-based guidelines for cancer survivorship do not recommend dietary supplementation, yet older cancer survivors report high prevalence of dietary supplement use, specifically multivitamin (MVM), calcium, and vitamin D. Female cancer survivors (≥65 years) who were ≤5 years post-cancer diagnosis completed questionnaires assessing health-related quality of life (HRQoL), diet quality, and supplement intake. Intakes of MVM, calcium, and vitamin D supplementation were 61.4%, 76.9%, and 35.3%, respectively. Women who used MVM supplements had significantly higher dietary quality mean scores for total vegetables (4.5 ± 0.9 to 4.1 ± 1.1), greens and beans (4.1 ± 1.3 to 3.6 ± 1.6), whole fruit (4.7 ± 0.8 to 4.3 ± 1.3), and whole grains (2.9 ± 1.8 to 2.3 ± 1.6) than those who did not use these supplements. After controlling for demographic and clinical variables, the odds of MVM use was 1.07 times greater among those women who had higher total HEI scores. Participants with lower HRQoL were 4% more likely to take an MVM. Understanding the prevalence of supplementation, associations with diet quality, and perceived benefits of supplementation may help healthcare providers in educating survivors and promoting adherence to the evidence-based guidelines. [ABSTRACT FROM AUTHOR]

Uterine leiomyomata (UL) are associated with severe reproductive morbidity and are the primary indication for hysterectomy in the United States. A recent prospective cohort study of Black women reported positive associations between intakes of marine-sourced ω-3 fatty acids and UL risk. We examined whether intakes of dietary fat were associated with UL incidence in a 5-year prospective study of premenopausal Black women living in Detroit who underwent serial ultrasound. At baseline (2010–2012) and 20, 40, and 60 months of follow-up, participants underwent transvaginal ultrasound. Among 1,171 UL-free women at baseline, incident UL were detected in 277 women. Cox regression was used to estimate hazard ratios and 95% confidence intervals for the association of dietary fat and UL incidence. Intakes of total fat and saturated, monounsaturated, polyunsaturated, and trans -fat were not appreciably associated with UL incidence. Intake of the marine ω-3 polyunsaturated fatty acid, docosahexaenoic acid, was associated with 49% higher UL incidence (quartile 4 vs. 1: hazard ratio = 1.49, 95% confidence interval: 1.04, 2.14; P for trend = 0.01). Intakes of total marine ω-3 polyunsaturated fatty acids were similarly associated with elevated UL incidence (hazard ratio = 1.35, 95% confidence interval: 0.94, 1.93; P for trend = 0.03). It remains unclear whether the fatty acids or persistent environmental pollutants drive the association. [ABSTRACT FROM AUTHOR]

Purpose: We examined quitting behaviors among a cohort of dual users (cigarettes and electronic cigarettes [e-cigarettes]) and exclusive cigarette smokers for: (1) cigarette smoking reduction, (2) quit attempts, (3) abstinence from cigarettes, and (4) abstinence from all tobacco products.Methods: Participants enrolled in the Tobacco User Adult Cohort and categorized as "daily" user of cigarettes and "daily" or "some days per week" use of e-cigarettes (ie, dual users; n = 88) or "daily" user of cigarettes only (ie, cigarette smokers; n = 617) served as the analytic sample. Participants were interviewed face to face every 6 months, through 18 months. Data on self-reported current product(s) used, cessation interest, quit attempts and abstinence from cigarettes, and all tobacco products were collected.Results: No difference in reduction of cigarette consumption over time was noted between groups. Rates of reporting an attempt to quit all tobacco products (≥ 24 hours of not using any tobacco in an attempt to quit) also did not differ by group. Compared to cigarette smokers, dual users were more likely to report abstinence from cigarettes at 6 months (OR = 2.54, p = .045) but not at 12 or 18 months. There was no significant difference in abstinence from all tobacco products by group at 6, 12, or 18 months.Conclusions: Although dual use of e-cigarettes has been cited as a potential cessation tool for cigarette smokers, our findings indicated that this association was only observed in the short term. We also found no evidence of any association between dual use and eventual abstinence from all tobacco products.Implications: Our study observed that, in the natural environment, dual users of cigarettes and e-cigarettes were more likely than cigarette smokers to quit cigarettes in the short term but no more likely to quit using cigarettes and all tobacco products over time. [ABSTRACT FROM AUTHOR]

Lifestyle-related factors influence risk of endometrial and ovarian cancers, but few studies have examined their joint associations with risk of these cancers. Using multivariable Cox regression models, we assessed the association of a healthy lifestyle index (HLI—a composite score (range, 0–20) involving diet, alcohol consumption, physical activity, body mass index, and smoking; higher scores represent healthier behavior) with risk of endometrial and ovarian cancers among 108,136 postmenopausal women who were recruited in the US Women's Health Initiative study between 1993 and 1998. After a median follow-up of 17.9 years, 1,435 endometrial cancer cases and 904 ovarian cancer cases had been ascertained. Women in the highest quintile of the HLI score had a lower risk of overall, type I, well-differentiated, moderately differentiated, poorly differentiated, and localized endometrial cancer than those in the lowest quintile (for quintile 5 vs. quintile 1, hazard ratio (HR) = 0.61 (95% CI: 0.51, 0.72), HR = 0.60 (95% CI: 0.49, 0.72), HR = 0.66 (95% CI: 0.46, 0.96), HR = 0.69 (95% CI: 0.52, 0.90), HR = 0.49 (95% CI: 0.34, 0.72), and HR = 0.61 (95% CI: 0.50, 0.74), respectively). The HLI score had a weak positive association with risk of serous ovarian cancer. Our findings underscore the potential importance of a healthy lifestyle in lowering endometrial cancer risk among postmenopausal women. [ABSTRACT FROM AUTHOR]

Abstract Background The prevalence of arthritis in the United States is substantial and on the rise. Long-chain n-3 polyunsaturated fatty acids, which have anti-inflammatory properties, have been shown to provide therapeutic benefit to arthritis patients; however, to date few have examined these associations with arthritis risk. Objective The study objective was to examine the associations of long-chain n-3 polyunsaturated fatty acids intake with osteoarthritis (OA) and rheumatoid arthritis (RA) risk among postmenopausal women. Design This was a prospective cohort study. Participants The sample for this analysis consisted of 80,551 postmenopausal women, aged 55 to 79 years and with no history of arthritis, recruited into the Women's Health Initiative Observational Study and Clinical Trials cohort between 1993 and 1998. Women completed a 120-item food frequency questionnaire at baseline. Main outcome measures After a median follow-up of 8 years, 22,306 incident OA and 3,348 RA cases were identified. Statistical analyses performed Adjusted Cox regression models were used to estimate hazard ratios and 95% CI for the associations between dietary LCn-3PUFA intake and OA and RA risk. Results Individual and total long-chain n-3 polyunsaturated fatty acids (Quintile 5 vs Quintile 1: hazard ratio 1.04, 95% CI 0.99 to 1.09 for OA; hazard ratio 1.01, 95% CI 0.90 to 1.13 for RA) were not associated with OA and RA risk. Further, no associations were observed between n-6 polyunsaturated fatty acids intake and either arthritis outcome. Conclusions This study is the first to examine associations of long-chain n-3 polyunsaturated fatty acids intake with OA risk and the largest to examine associations with RA risk. Despite their therapeutic potential, the study provides no evidence of benefit of these nutrients in relation to arthritis risk. [ABSTRACT FROM AUTHOR]

Objectives: Identifying characteristics associated with the use of new and emerging tobacco products is a priority. The enumeration and baseline characteristics of a new cohort of adult tobacco users are described. Methods: Residents, ≥18 years of age, in urban Franklin County, or one of 6 rural Appalachian counties, and who were exclusive users of combustible, smokeless (SLT), or electronic nicotine delivery systems (ENDS) tobacco products, or were dual users, were targeted for recruitment. Participants were interviewed in-person at baseline on sociodemographic characteristics, tobacco product use, and cognitive/affective and purchasing factors. Results: We recruited 1210 participants (urban, N = 595; rural, N = 615). Urban participants were less likely to use tobacco daily, began using tobacco later, used tobacco for less time, and had higher cessation interest. ENDS users were significantly less likely to have made a quit attempt than users of other tobacco products. Duration of tobacco use and nicotine dependence also differed by product type. Conclusion: This cohort's enumeration allowed us to compare factors associated with tobacco product preferences and the use of novel products. The inclusion of rural Appalachia--a region with high tobacco use and disease burden--may provide additional insights into the implementation of tobacco control interventions. [ABSTRACT FROM AUTHOR]

We read with significant interest Weiss et al's recent article outlining a cross-sectional, anonymous, online study examining the prevalence of cannabis-based product use among adults who self-reported a breast cancer diagnosis in the past 5 years.1 This study adds to current knowledge on a vastly understudied topic; however, it is not without important limitations that were not fully discussed. In the current article, Weiss et al1 assess participants' preferences with regard to the use of CBD products versus marijuana products, and this is an important step. Medical marijuana and cannabidiol (CBD) represent $8.1 and $4.3 billion industries, respectively, in North America.13,14 Forecasted market growth is 19% for medical marijuana and 35% for CBD by 2027.13-15 There remains a significant need for high-quality research examining the use of cannabis-based products beyond "current" or "ever" use in patients with cancer. [Extracted from the article]

Background: Published studies have demonstrated inconclusive relationships between serum lipid levels and mortality after cancer. Methods: The primary objective was to evaluate the relationship between fasting lipid levels and mortality after cancer. Data were obtained on baseline lipids and outcomes after cancer from 1263 postmenopausal women diagnosed with 13 obesity‐related cancers who were part of the Women's Health Initiative (WHI) lipid biomarkers cohort. Obesity‐related cancers included incident invasive cancers of the breast, colorectum, endometrium, esophagus (adenocarcinoma), kidney, liver, gallbladder, pancreas, ovaries, small intestine, thyroid, stomach, as well as multiple myeloma. Baseline lipid measurements included high‐density lipoprotein (HDL)‐cholesterol, low‐density lipoprotein (LDL)‐cholesterol, and non‐HDL‐cholesterol. Outcomes were all cause, cancer‐specific, and CVD mortality. Multivariable Cox proportional hazards models were used to measure associations between lipid levels and mortality (all cause, cancer, and CVD) after a cancer diagnosis, with lipids analyzed as continuous variables. Results: Among women with obesity‐related cancer, there were 707 deaths, of which 379 (54%) were due to cancer and 113 (16%) were due to CVD. Mean time from blood draw to cancer diagnosis was 5.1 years (range: 0.05–10 years). LDL‐C values above the 95th percentile were associated with higher risk of all‐cause mortality (p < 0.001), and cancer‐specific mortality (p < 0.001), but not mortality due to CVD. Non‐HDL‐C values above the 65th percentile were associated with higher risk of all‐cause mortality (p = 0.01) and mortality due to CVD (p = 0.003), but not cancer‐specific mortality (p = 0.37). HDL‐C values above the 95th percentile were associated with lower all‐cause mortality (p = 0.002), and above the 65th percentile with lower cancer‐specific mortality (p = 0.003), but no significant relationship with mortality due to CVD was observed. Conclusions: The relationship between pre‐diagnosis fasting lipid levels and mortality after cancer diagnosis is complex. These results suggest that improved lipid control through lifestyle and anti‐lipid medications could have a meaningful impact on outcomes after cancer. [ABSTRACT FROM AUTHOR]

Background: Recent data suggest that the use of nonsteroidal anti-inflammatory drugs (NSAIDs) may be associated with reductions in endometrial cancer risk, yet very few have examined whether their use is related to prognosis among endometrial cancer patients.Methods: Study subjects comprised 4374 participants of the NRG Oncology/Gynecology Oncology Group 210 Study with endometrial carcinoma who completed a presurgical questionnaire that assessed history of regular prediagnostic NSAID use and endometrial cancer risk factors. Recurrences, vital status, and causes of death were obtained from medical records and cancer registries. Fine-Gray semiproportional hazards regression estimated adjusted subhazard ratios (HRs) and 95% confidence intervals (CIs) for associations of NSAID use with endometrial carcinoma-specific mortality and recurrence. Models were stratified by endometrial carcinoma type (ie, type I [endometrioid] vs type II [serous, clear cell, or carcinosarcoma]) and histology.Results: Five hundred fifty endometrial carcinoma-specific deaths and 737 recurrences occurred during a median of five years of follow-up. NSAID use was associated with 66% (HR = 1.66, 95% CI = 1.21 to 2.30) increased endometrial carcinoma-specific mortality among women with type I cancers. Associations were statistically significant for former and current users, and strongest among former users who used NSAIDs for 10 years or longer (HR = 2.23, 95% CI = 1.19 to 4.18, two-sided P trend = .01). NSAID use was not associated with recurrence or endometrial carcinoma-specific mortality among women with type II tumors.Conclusions: In this study, use of NSAIDs was associated with increased endometrial carcinoma-specific mortality, especially in patients with type I tumors. Barring a clear biologic mechanism by which NSAIDs would increase the risk of cause-specific mortality, cautious interpretation is warranted. [ABSTRACT FROM AUTHOR]

Single-nucleotide polymorphisms (SNPs) in one-carbon metabolism genes and lifestyle factors (alcohol drinking and breast folate) may be determinants of whole-genome methylation in the breast. DNA methylation profiling was performed using the Illumina Infinium HumanMethylation450 BeadChip in 81 normal breast tissues from women undergoing reduction mammoplasty and no history of cancer. ANCOVA, adjusting for age, race and body mass index, was used to identify differentially methylated (DM) CpGs. Gene expression, by the Affymetrix GeneChip Human Transcriptome Array 2.0, was correlated with DM. Biological networks of DM genes were assigned using Ingenuity Pathway Analysis. Fifty-seven CpG sites (CpGs) were DM in association with eight SNPs in FTHFD, MTHFD1, MTHFR, MTR, MTRR and TYMS (P < 5.0 × 10-5); 56% of the DM CpGs were associated with FTHFD SNPs, including DM within FTHFD. Gene expression was negatively correlated with FTHFD methylation (r = -0.25, P = 0.017). Four DM CpGs identified by SNPs in MTRR, MTHFR and FTHFD were significantly associated with alcohol consumption and/or breast folate. The top biological network of DM CpGs was associated with Energy Production, Molecular Transportation, and Nucleic Acid Metabolism. This is the first comprehensive study of the association between SNPs in one-carbon metabolism genes and genome-wide DNA methylation in normal breast tissues. These SNPs, especially FTHFD, as well as alcohol intake and folate exposure, appear to affect DM in breast tissues of healthy women. The finding that SNPs in FTHFD and MTR are associated with their own methylation is novel and highlights a role for these SNPs as methylation quantitative trait loci. [ABSTRACT FROM AUTHOR]

Dietary long-chain (LC) ω-3 polyunsaturated fatty acids (PUFAs), which derive primarily from intakes of fatty fish, are thought to inhibit inflammation and de novo estrogen synthesis. This study prospectively examined the associations of dietary LC ω-3 PUFAs and fish with endometrial cancer risk in 47,602 African-American women living in the United States, aged 21-69 years at baseline in 1995, and followed them until 2013 (n = 282 cases). Multivariable- adjusted Cox regression models estimated hazard ratios and 95% confidence intervals for associations of LC ω-3 PUFA (quintiled) and fish (quartiled) intake with endometrial cancer risk, overall and by body mass index (BMI; weight (kg)/height (m)²). The hazard ratio for quintile 5 of total dietary LC ω-3 PUFAs versus quintile 1 was 0.79 (95% confidence interval (CI): 0.51, 1.24); there was no linear trend. Hazard ratios for the association were smaller among normal-weight women (BMI <25: hazard ratio (HR) = 0.53, 95% CI: 0.18, 1.58) than among overweight/obese women (BMI ≥25: HR = 0.88, 95% CI: 0.54, 1.43), but these differences were not statistically significant. Fish intake was also not associated with risk (quartile 4 vs. quartile 1: HR = 0.86, 95% CI: 0.56, 1.31). Again hazard ratios were smaller among normal-weight women (HR = 0.65) than among overweight/obese women (HR = 0.94). While compatible with no association, the hazard ratios observed among leaner African-American women are similar to those from recent prospective studies conducted in predominantly white populations. [ABSTRACT FROM AUTHOR]

Background Studies of dietary ω-3 fatty acid intake and prostate cancer risk are inconsistent; however, recent large prospective studies have found increased risk of prostate cancer among men with high blood concentrations of long-chain ω-3 polyunsaturated fatty acids ([LCw-3PUFA] 20:5ω3; 22:5ω3; 22:6ω3].This case-cohort study examines associations between plasma phospholipid fatty acids and prostate cancer risk among participants in the Selenium and Vitamin E Cancer Prevention Trial. Methods Case subjects were 834 men diagnosed with prostate cancer, of which 156 had high-grade cancer. The subcohort consisted of 1393 men selected randomly at baseline and from within strata frequency matched to case subjects on age and race. Proportional hazards models estimated hazard ratios (HR) and 95% confidence intervals (Cl) for associations between fatty acids and prostate cancer risk overall and by grade. All statistical tests were two-sided. Results Compared with men in the lowest quartiles of LCω-3PUFA, men in the highest quartile had increased risks for low-grade (HR = 1.44, 95% Cl = 1.08 to 1.93), high-grade (HR = 1.71, 95% Cl = 1.00 to 2.94), and total prostate cancer (HR = 1.43, 95% Cl = 1.09 to 1.88). Associations were similar for individual long-chain ω-3 fatty acids. Higher linoleic acid (ω-6) was associated with reduced risks of low-grade (HR = 0.75, 95% Cl = 0.56 to 0.99) and total prostate cancer (HR = 0.77, 95% Cl = 0.59 to 1.01); however, there was no dose response. Conclusions This study confirms previous reports of increased prostate cancer risk among men with high blood concentrations of LCω-3PUFA. The consistency of these findings suggests that these fatty acids are involved in prostate tumorigenesis. Recommendations to increase LCω-3PUFA intake should consider its potential risks. [ABSTRACT FROM AUTHOR]

Background Most cancers occur more frequently in men. Numerous explanations for this excess risk have been proposed, yet no study has quantified the degree to which height explains the sex difference even though greater height has been associated with increased risk for many cancers. Methods During the period from 2000 to 2002, 65308 volunteers aged 50 to 76 years were recruited to the Vitamins And Lifestyle (VITAL) study. Cancers of shared anatomic sites (n = 3466) were prospectively identified through 2009 through the Surveillance, Epidemiology, and End Results cancer registry. Age- and race-adjusted hazard ratios (HRs) for the associations between sex and incident cancers were estimated using Cox proportional hazards models, with and without adjustment for height and height squared as measures of body size. Results Men had a 55% increased risk of cancer at shared sites (HR = 1.55; 95% confidence interval [Cl] = 1.45 to 1.66). When height was accounted for, 33.8% (95% Cl = 10.2% to 57.3%) of the excess risk for men was explained by the height differences between sexes. The proportion mediated by height was 90.9%, 57.3%, and 49.6% for kidney, melanoma, and hematologic malignancies, respectively, with little evidence that height mediates the sex difference for gastrointestinal tract, lung, and bladder cancers. For comparison, more than 35 lifestyle and medical risk factors only explained 23.1% of the sex difference in cancer risk at shared sites. Conclusions Height is an important explanatory factor for the excess risk for men for many shared-site cancers. This suggests that some of the excess risk is due to factors associated with height (eg, number of susceptible cells in a specific organ or growth-influencing exposures in childhood). [ABSTRACT FROM AUTHOR]

Abstract: Objective: Chronic inflammation may be an important factor in the initiation and promotion of endometrial cancer. Use of non-steroidal anti-inflammatory drugs (NSAIDs), however, has been inconsistently associated with endometrial cancer risk. Methods: 22,268 female residents of western Washington State, ages 50–76, completed a baseline questionnaire in 2000–2002 and reported on their use of individual NSAIDs over the past 10years. Use was categorized as none, low (<4days/week or <4years), and high (≥4days/week and ≥4years). Over 9years of follow-up, 262 incident invasive endometrial cancers were identified. Multivariable proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI). Results: Relative to non-use, high use of aspirin was inversely associated with endometrial cancer risk (HR 0.64, 95% CI: 0.41–1.01; P trend=0.03). Findings were stronger for regular-strength than low-dose aspirin. High use of non-aspirin NSAIDs (HR 1.15, 95% CI: 0.68–1.95), including ibuprofen (HR 1.29, 95% CI: 0.73–2.28), and naproxen (HR 1.08, 95% CI: 0.39–2.95) was not associated with risk. In subgroup analyses, findings for aspirin were strongest for cancers of endometrioid histology and were restricted to non-smokers. Conclusions: This study provides additional evidence that use of aspirin, but not non-aspirin NSAIDs, may reduce the risk of endometrial cancer, especially in estrogen-mediated cases; however additional prospective studies with high-quality measurement of NSAID use are needed. Aspirin should continue to be examined as a potential agent for cancer chemoprevention. [Copyright &y& Elsevier]

Abstract: Few studies have examined the association between non-steroidal anti-inflammatory drug (NSAID) use and risk of small cell lung cancer (SCLC); among them, findings are mixed. Recently, we found that use of NSAIDs was differentially associated with lung cancer risk by histology. Here, we examine, more comprehensively, the association between individual NSAIDs and SCLC risk. 75,546 residents of western Washington State, ages 50–76, completed a baseline questionnaire in 2000–2002 and reported on their use of individual NSAIDs over the past 10 years. NSAID use was categorized as non-users, low (<4 days/week or <4 years), and high (≥4 days/week and ≥4 years). 111 SCLC were identified through linkage to a population-based cancer registry. Multivariable-adjusted Cox proportional hazards models including strong adjustment for smoking were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI). Compared to non-use, high use of regular-strength aspirin was associated with an elevated risk of SCLC (HR 1.78, 95% CI: 1.05–3.02; P-trend=0.03). Findings for low-dose aspirin were elevated but did not reach statistical significance. Use of non-aspirin NSAIDs was not associated with SCLC risk. Our findings provide further indication of heterogeneity in the association between aspirin and lung cancer morphologies. Large, prospective studies with comprehensive assessments of NSAID use and smoking history and data on both men and women, are needed in order to better understand the association between use of aspirin and SCLC. [Copyright &y& Elsevier]

Laboratory data suggest that intake of vitamin A and carotenoids may have chemopreventive benefits against melanoma, but epidemiological studies examining the association have yielded conflicting results. We examined whether dietary and supplemental vitamin A and carotenoid intake was associated with melanoma risk among 69,635 men and women who were participants of the VITamins And Lifestyle (VITAL) cohort study in western Washington. After an average of 5.84 years of follow-up, 566 incident melanomas were identified. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for risk of melanoma associated with dietary, supplemental, and total vitamin A and carotenoid intake after adjusting for melanoma risk factors. Baseline use of individual retinol supplements was associated with a significant reduction in melanoma risk (HR: 0.60; 95% CI: 0.41-0.89). High-dose (>1,200 μg per day) supplemental retinol was also associated with reduced melanoma risk (HR: 0.74; 95% CI: 0.55-1.00), as compared with non-users. The reduction in melanoma risk was stronger in sun-exposed anatomic sites. There was no association of melanoma risk with dietary or total intake of vitamin A or carotenoids. Retinol supplementation may have a preventative role in melanoma among women. [ABSTRACT FROM AUTHOR]

Inflammation may be involved in prostate cancer development and progression. This study examined the associations between inflammation-related phospholipid fatty acids and the 7-year-period prevalence of prostate cancer in a nested case-control analysis of participants, aged 55–84 years, in the Prostate Cancer Prevention Trial during 1994–2003. Cases (n = 1,658) were frequency matched to controls (n = 1,803) on age, treatment, and prostate cancer family history. Phospholipid fatty acids were extracted from serum, and concentrations of ω-3, ω-6, and trans-fatty acids (TFAs) were expressed as proportions of the total. Logistic regression models estimated odds ratios and 95% confidence intervals of associations of fatty acids with prostate cancer by grade. No fatty acids were associated with low-grade prostate cancer risk. Docosahexaenoic acid was positively associated with high-grade disease (quartile 4 vs. 1: odds ratio (OR) = 2.50, 95% confidence interval (CI): 1.34, 4.65); TFA 18:1 and TFA 18:2 were linearly and inversely associated with risk of high-grade prostate cancer (quartile 4 vs. 1: TFA 18:1, OR = 0.55, 95% CI: 0.30, 0.98; TFA 18:2, OR = 0.48, 95% CI: 0.27, 0.84). The study findings are contrary to those expected from the pro- and antiinflammatory effects of these fatty acids and suggest a greater complexity of effects of these nutrients with regard to prostate cancer risk. [ABSTRACT FROM AUTHOR]

Background: National studies reporting the prevalence of cannabis use have focused on individuals with a history of cancer without distinction by their treatment status, which can impact symptom burden. While pain is a primary motivation to use cannabis in cancer, the magnitude of its association with cannabis use remains understudied. Methods: We examined cannabis use and pain management among 5523 respondents of the Behavioral Risk Factor Surveillance System with a cancer history. Survey-weighted prevalence proportions of respondents’ cannabis use are reported, stratified on cancer treatment status. Regression models estimated odds ratios (ORs) and 95% confidence intervals (CIs) of cancer-related pain and cannabis use. Results: Cannabis use was slightly more prevalent in those undergoing active treatment relative to those who were not undergoing active treatment (9.3% vs. 6.2%; P=0.05). Those under active treatment were more likely to use cannabis medicinally (71.6% vs. 50.0%; P=0.03). Relative to those without cancer-related pain, persons with pain under medical control (OR 2.1, 95% CI, 1.4–3.2) or uncontrolled pain were twice as likely to use cannabis (OR 2.0, 95% CI, 1.1–3.5). Conclusions: Use of cannabis among cancer patients may be related to their treatment and is positively associated with cancer-related pain. Future research should investigate the associations of cannabis use, symptom burden, and treatment regimens across the treatment spectrum to facilitate interventions. [ABSTRACT FROM AUTHOR]

Background: Cigarette smoking and aging are the main risk factors for pulmonary diseases, including cancer. Epigenetic aging may explain the relationship between smoking, electronic cigarette vaping, and pulmonary health. No study has examined smoking and vaping-related epigenetic aging in relation to lung biomarkers. Methods: Lung epigenetic aging measured by DNA methylation (mAge) and its acceleration (mAA) was assessed in young (age 21–30) electronic cigarette vapers (EC, n = 14, including 3 never-smoking EC), smokers (SM, n = 16), and non-EC/non-SM (NS, n = 39). We investigated relationships of mAge estimates with chronological age (Horvath-mAge), lifespan/mortality (Grim-mAge), telomere length (TL-mAge), smoking/EC history, urinary biomarkers, lung cytokines, and transcriptome. Results: Compared to NS, EC and SM had significantly older Grim-mAge, shorter TL-mAge, significantly accelerated Grim-mAge and decelerated TL-mAge. Among SM, Grim-mAA was associated with nicotine intake and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL). For EC, Horvath-mAA was significantly correlated with puffs per day. Overall, cytokines (IL-1β, IL-6, and IL-8) and 759 transcripts (651 unique genes) were significantly associated with Grim-mAA. Grim-mAA-associated genes were highly enriched in immune-related pathways and genes that play a role in the morphology and structures of cells/tissues. Conclusions: Faster lung mAge for SM is consistent with prior studies of blood. Faster lung mAge for EC compared to NS indicates possible adverse pulmonary effects of EC on biological aging. Our findings support further research, particularly on epigenetic markers, on effects of smoking and vaping on pulmonary health. Given that most EC are former smokers, further study is needed to understand unique effects of electronic cigarettes on biological aging. [ABSTRACT FROM AUTHOR]

The article discusses research on the use of selenium supplements and the risk of prostate cancer death and biochemical recurrence among men diagnosed with prostate cancer in the Health Professionals Follow-up Study (HPFS). Topics discussed include a suggestion for prostate cancer patients to be cautioned against the use of selenium supplements, micronutrient and dietary supplement use in the U.S., and the inconsistent results of clinical trials of selenium supplementation.

A response from the author of the article related to an association between long chain omega-3 polyunsaturated fatty acids and increased prostate cancer risk, based on large cohort analysis of the Selenium and Vitamin E Cancer Prevention Trial in a previous issue is presented.

Proton pump inhibitors (PPIs) have off-target activity on fatty acid synthase (FASN), a critical enzyme in energy balance and cancer growth. We evaluated risk of common obesity-related cancers: breast, colorectal (CRC), and endometrial, with use of PPI and histamine-2 receptor antagonists (H2RA) in 124,931 postmenopausal women enrolled in the Women's Health Initiative. Incident cancer cases were physician-adjudicated. Cox proportional hazards models were used to estimate multivariable hazard ratios (HR) and 95% confidence intervals (CI) for cancer incidence after year 3. There were 7956 PPI ever users and 9398 H2RA only users. Ever use of either PPI or H2RA was not associated with risk of breast cancer (n = 9186) nor risk of endometrial cancer (n = 1231). The risk of CRC (n = 2280) was significantly lower in PPI users (HR = 0.75, 95% CI = 0.61–0.92), but not in H2RA users (HR = 1.13, 95% CI = 0.97–1.31). The association of PPI use with CRC was apparent regardless of BMI or NSAID use, and was stronger with longer PPI duration (p = 0.006) and potency (p = 0.005). The findings that PPI use, but not H2RA use, demonstrate an inverse dose-response relationship with risk of CRC is consistent with preclinical data showing FASN inhibition prevents colon cancer progression and supports a role of PPI in CRC prevention. [ABSTRACT FROM AUTHOR]

Research suggests that high intake of supplemental vitamin B12 may be associated with increased risk of cancer, with some evidence that this association may vary by gender and smoking status. This investigation evaluates if similar patterns in association are observed for data for 11,757 adults from the National Health and Nutrition Examination Survey (1999-2006). Survey-weighted multivariable-adjusted linear regression was used to evaluate the association between regular B12 supplement use and log-transformed serum B12 levels. Persons taking vitamin B12 through a multivitamin/multimineral (MVMM) had a median supplemental intake of 12 mcg/day (Q1: 6, Q3: 25), compared to 100 mcg/day (Q1: 22, Q3: 500) for persons reporting supplemental B12 intake through a MVMM-exclusive source. MVMM users had a geometric mean serum B12 26% (95% CI: 23%-30%) higher than nonusers, whereas MVMM-exclusive users' geometric mean was 61% (95% CI: 53%-70%) higher than nonusers (p-trend < 0.001). Although a positive trend (p-trend < 0.001) was observed for both men and women, the association was stronger among women (p-interaction < 0.001). No interaction was observed for smoking status (p-interaction = 0.45). B12 supplementation is associated with higher levels of serum B12, with significant interaction by gender but not smoking. Further work is needed to better understand the interplay of B12 and gender. [ABSTRACT FROM AUTHOR]

Use of smokeless tobacco products (STPs) is associated with oral cavity cancer and other health risks. Comprehensive analysis for chemical composition and toxicity is needed to compare conventional and newer STPs with lower tobacco-specific nitrosamines (TSNAs) yields. Seven conventional and 12 low-TSNA moist snuff products purchased in the U.S., Sweden, and South Africa were analyzed for 18 chemical constituents (International Agency for Research on Cancer classified carcinogens), pH, nicotine, and free nicotine. Chemicals were compared in each product using Wilcoxon rank-sum test and principle component analysis (PCA). Conventional compared to low-TSNA moist snuff products had higher ammonia, benzo[a]pyrene, cadmium, nickel, nicotine, nitrate, and TSNAs and had lower arsenic in dry weight content and per mg nicotine. Lead and chromium were significantly higher in low-TSNA moist snuff products. PCA showed a clear difference for constituents between conventional and low-TSNA moist snuff products. Differences among products were reduced when considered on a per mg nicotine basis. As one way to contextualize differences in constituent levels, probabilistic lifetime cancer risk was estimated for chemicals included in The University of California’s carcinogenic potency database (CPDB). Estimated probabilistic cancer risks were 3.77-fold or 3-fold higher in conventional compared to low-TSNA moist snuff products under dry weight or under per mg nicotine content, respectively. In vitro testing for the STPs indicated low level toxicity and no substantial differences. The comprehensive chemical characterization of both conventional and low-TSNA moist snuff products from this study provides a broader assessment of understanding differences in carcinogenic potential of the products. In addition, the high levels and probabilistic cancer risk estimates for certain chemical constituents of smokeless tobacco products will further inform regulatory decision makers and aid them in their efforts to reduce carcinogen exposure in smokeless tobacco products. [ABSTRACT FROM AUTHOR]

Alcohol consumption, breast folate concentration and variation in one-carbon metabolism genes may be determinants of p16INK4a promoter methylation and P16 protein expression in histologically normal breast tissues, and may influence early breast carcinogenic events.p16INK4a is a tumor suppressor gene, frequently hypermethylated in breast cancer; this epigenetic silencing of p16INK4a occurs early in carcinogenesis. The risk factors and functional consequences of p16INK4a methylation are unknown. Alcohol consumption, a breast cancer risk factor, impedes folate metabolism and may thereby alter gene methylation since folate plays a pivotal role in DNA methylation. In a cross-sectional study of 138 women with no history of breast cancer who underwent reduction mammoplasty, we studied breast cancer risk factors, plasma and breast folate concentrations, variation in one-carbon metabolism genes, p16INK4a promoter methylation and P16 protein expression. Logistic regression was used to estimate multivariable-adjusted odds ratios (OR) and 95% confidence intervals (CI). p16INK4a methylation was negatively correlated with P16 expression (r = −0.28; P = 0.002). Alcohol consumption was associated with lower breast folate (P = 0.03), higher p16INK4a promoter methylation (P = 0.007) and less P16 expression (P = 0.002). Higher breast folate concentrations were associated with lower p16INK4a promoter methylation (P = 0.06). Genetic variation in MTRR (rs1801394) and MTHFD1 (rs1950902) was associated with higher p16INK4a promoter methylation (OR = 2.66, 95% CI: 1.11–6.42 and OR = 2.72, 95% CI: 1.12–6.66, respectively), whereas variation in TYMS (rs502396) was associated with less P16 protein expression (OR = 0.22, 95% CI: 0.05–0.99). Given that this is the first study to indicate that alcohol consumption, breast folate and variation in one-carbon metabolism genes are associated with p16INK4a promoter methylation and P16 protein expression in healthy tissues; these findings require replication. [ABSTRACT FROM AUTHOR]

Background: Oxidative stress causes damage to many components of human cells (ie, proteins, lipids, and DNA) and is involved in carcinogenesis. Nutrients with antioxidant properties may protect against oxidative stress. In this study, the authors examined the intake of antioxidants from diet and supplements in relation to pancreatic cancer risk among participants of the Vitamins and Lifestyle (VITAL) Study.Methods: The participants included 77,446 men and women ages 50 to 76 years who were residents of western Washington State and who completed a baseline questionnaire between 2000 and 2002. Participants reported usual diet over the past year and use of supplements over the past 10 years in addition to demographic and lifestyle factors. During a median follow-up of 7.1 years, 184 participants developed pancreatic adenocarcinoma. Cox proportional hazards models were used to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for 7 antioxidants: β-carotene, lutein plus zeaxanthin, lycopene, vitamin C, vitamin E, selenium, and zinc.Results: An inverse association was observed between dietary selenium and the risk of pancreatic cancer (medium vs low intake: HR, 0.58; 95% CI, 0.35-0.94; high vs low intake: HR, 0.44; 95% CI, 0.23-0.85; Ptrend = .01); however, when supplemental and dietary exposures were combined, the association was no longer statistically significant.Conclusions: Dietary selenium intake was inversely associated with the risk of pancreatic cancer, and the observed association was attenuated by selenium supplementation. [ABSTRACT FROM AUTHOR]

BACKGROUND: Oxidative stress causes damage to many components of human cells (ie, proteins, lipids, and DNA) and is involved in carcinogenesis. Nutrients with antioxidant properties may protect against oxidative stress. In this study, the authors examined the intake of antioxidants from diet and supplements in relation to pancreatic cancer risk among participants of the Vitamins and Lifestyle (VITAL) Study. METHODS: The participants included 77,446 men and women ages 50 to 76 years who were residents of western Washington State and who completed a baseline questionnaire between 2000 and 2002. Participants reported usual diet over the past year and use of supplements over the past 10 years in addition to demographic and lifestyle factors. During a median follow-up of 7.1 years, 184 participants developed pancreatic adenocarcinoma. Cox proportional hazards models were used to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for 7 antioxidants: β-carotene, lutein plus zeaxanthin, lycopene, vitamin C, vitamin E, selenium, and zinc. RESULTS: An inverse association was observed between dietary selenium and the risk of pancreatic cancer (medium vs low intake: HR, 0.58; 95% CI, 0.35-0.94; high vs low intake: HR, 0.44; 95% CI, 0.23-0.85; Ptrend = .01); however, when supplemental and dietary exposures were combined, the association was no longer statistically significant. CONCLUSIONS: Dietary selenium intake was inversely associated with the risk of pancreatic cancer, and the observed association was attenuated by selenium supplementation. Cancer 2013. © 2012 American Cancer Society. [ABSTRACT FROM AUTHOR]

The associations of types of fish and fish preparation methods with pancreatic cancer risk remain unknown. The authors conducted a prospective cohort study in western Washington State among 66,616 adults, aged 50–76 years, who participated in the VITamins And Lifestyle cohort study. Diet was assessed by a food frequency questionnaire. Pancreatic cancer cases were identified by linkage to the Surveillance, Epidemiology, and End Results cancer registry. During an average follow-up of 6.8 years, 151 participants developed pancreatic cancer (adenocarcinoma). Long-chain (n-3) polyunsaturated fatty acids (LC-PUFAs) and nonfried fish intake were inversely associated with pancreatic cancer incidence. When the highest and lowest tertiles of exposure were compared, the multivariable-adjusted hazard ratio of pancreatic cancer was 0.62 (95% confidence interval: 0.40, 0.98) (Ptrend = 0.08) for LC-PUFAs and 0.55 (95% confidence interval: 0.34, 0.88) (Ptrend = 0.045) for nonfried fish. Docosahexaenoic acid showed a greater inverse association with pancreatic cancer than eicosapentaenoic acid. No statistically significant associations were observed with fried fish and shellfish consumption. The potential health impact of fish consumption may depend on the types of fish consumed and fish preparation methods. LC-PUFAs, particularly docosahexaenoic acid, and nonfried fish, but not shellfish or fried fish, may be beneficial in the primary prevention of pancreatic cancer. [ABSTRACT FROM PUBLISHER]

Objective: The empirical dietary index for hyperinsulinemia (EDIH) and empirical dietary inflammatory pattern (EDIP) scores assess the insulinemic and inflammatory potentials of habitual dietary patterns, irrespective of the macronutrient content, and are based on plasma insulin response or inflammatory biomarkers, respectively. The glycemic index (GI) and glycemic load (GL) assess postprandial glycemic potential based on dietary carbohydrate content. We tested the hypothesis that dietary patterns promoting hyperinsulinemia, chronic inflammation, or hyperglycemia may influence type 2 diabetes risk.Research Design and Methods: We calculated dietary scores from baseline (1993-1998) food frequency questionnaires among 73,495 postmenopausal women in the Women's Health Initiative, followed through March 2019. We used multivariable-adjusted Cox regression to estimate hazard ratios (HRs) and 95% CIs for type 2 diabetes risk. We also estimated multivariable-adjusted absolute risk of type 2 diabetes.Results: During a median 13.3 years of follow-up, 11,009 incident cases of type 2 diabetes were diagnosed. Participants consuming the most hyperinsulinemic or proinflammatory dietary patterns experienced greater risk of type 2 diabetes; HRs (95% CI) comparing highest to lowest dietary index quintiles were EDIH 1.49 (1.32-1.68; Ptrend < 0.0001) and EDIP 1.45 (1.29-1.63; Ptrend < 0.0001). The absolute excess incidence for the same comparison was 220 (EDIH) and 271 (EDIP) cases per 100,000 person-years. GI and GL were not associated with type 2 diabetes risk: GI 0.99 (0.88-1.12; Ptrend = 0.46) and GL 1.01 (0.89-1.16; Ptrend = 0.30).Conclusions: Our findings in this diverse cohort of postmenopausal women suggest that lowering the insulinemic and inflammatory potentials of the diet may be more effective in preventing type 2 diabetes than focusing on glycemic foods. [ABSTRACT FROM AUTHOR]

Uterine leiomyomata (UL) are the leading indication for hysterectomy in the United States. Dietary supplementation with lycopene was associated with reduced size and incidence of oviduct leiomyoma in the Japanese quail. Two US prospective cohort studies of women reported little association between intake of lycopene, or other carotenoids, and UL incidence. However, these studies relied on self-reported physician-diagnosed UL, which is prone to misclassification. This study examines the association between dietary intake of carotenoids and UL incidence. Data were derived from the Study of the Environment, Lifestyle, and Fibroids, a prospective cohort study. Women completed self-administered baseline questionnaires on demographic characteristics, reproductive history, and lifestyle, including a 110-item validated food frequency questionnaire, from which dietary intakes of carotenoids—including alpha carotene, beta carotene, cryptoxanthin, lutein-zeaxanthin, and lycopene—and vitamin A were estimated. One thousand two hundred thirty Black women aged 23 to 35 years who did not have a previous diagnosis of UL, cancer, or autoimmune disease were eligible for enrollment (2010-2012). Participants were residents of the Detroit, MI, metropolitan area. Transvaginal ultrasound was used to assess UL at baseline and 20, 40, and 60 months of follow-up. Cox regression was used to estimate hazard ratios and 95% CIs, adjusted for energy intake, age at menarche, education, body mass index, parity, age at first birth, years since last birth, current use of oral contraceptives or progestin-only injectables, alcohol intake, and cigarette smoking. Among 1,230 women without prevalent UL at baseline, 301 incident UL cases during follow-up were identified. Intakes of lycopene, other carotenoids, and vitamin A were not appreciably associated with UL incidence. Hazard ratios comparing quartiles 2 (2,376 to 3,397 μg/day), 3 (3,398 to 4,817 μg/day), and 4 (≥4,818 μg/day) with quartile 1 (<2,376 μg/day) of lycopene intake were 1.03 (95% CI 0.72 to 1.47), 1.22 (95% CI 0.86 to 1.72), and 0.95 (95% CI 0.67 to 1.36), respectively. Study findings do not support the hypothesis that greater carotenoid intake is associated with reduced UL incidence. [ABSTRACT FROM AUTHOR]

Polychlorinated biphenyls (PCBs) are a class of lipophilic endocrine-disrupting chemicals with wide industrial use in the U.S. from the 1930s through 1977. Due to their environmental and biological persistence, low levels of PCBs remain detected in wildlife and humans. Although U.S. studies have shown higher serum PCB concentrations among Black women compared with White women, studies of correlates of PCB exposure among Black women are scarce. We examined predictors of plasma PCB concentrations in a cross-sectional analysis of baseline data from a prospective cohort study of 1693 premenopausal Black women aged 23-35 years from Detroit, Michigan (2010-2012). We collected demographic, behavioral, dietary, and medical data via self-administered questionnaires, telephone interviews, and in-person clinic visits, as well as non-fasting blood samples. We measured concentrations of 24 PCB congeners in baseline plasma from a subset of 762 participants. We used linear regression for log-transformed lipid-adjusted PCB concentrations to calculate percentage differences across levels of selected predictors. We did this separately for individual PCBs, sum of total PCBs, and sum of PCBs by degree of chlorination and hormonal activity. PCB concentrations were positively associated with age, duration of urban residence, cigarette smoking, heavy alcohol intake, and being breastfed in infancy, and inversely associated with body mass index (BMI) and lactation duration. The strength of some associations varied by degree of chlorination. For example, a 5-kg/m2 higher BMI corresponded to a 2.9% lower summed concentration of tri- and tetra-substituted PCBs (95% CI -4.6%, -1.2%), an 8.3% lower summed concentration of penta- and hexa-substituted PCBs (95% CI -10.0%, -6.5%), and a 12.1% lower summed concentration of hepta-, octa-, nona-, and deca-substituted PCBs (95% CI -13.7%, -10.4%). Likewise, associations for age and being breastfed in infancy were stronger for higher-chlorinated PCBs. Results agree with studies on predictors of PCB body burdens, few of which include large numbers of Black women. [ABSTRACT FROM AUTHOR]

Background: Aspirin use is associated with reduced risk of several cancers. A pooled analysis of 12 case-control studies showed a 10% decrease in ovarian cancer risk with regular aspirin use, which was stronger for daily and low-dose users. To prospectively investigate associations of analgesic use with ovarian cancer, we analyzed data from 13 studies in the Ovarian Cancer Cohort Consortium (OC3).Methods: The current study included 758 829 women who at study enrollment self-reported analgesic use, among whom 3514 developed ovarian cancer. Using Cox regression, we assessed associations between frequent medication use and risk of ovarian cancer. Dose and duration were also evaluated. All statistical tests were two-sided.Results: Women who used aspirin almost daily (≥6 days/wk) vs infrequent/nonuse experienced a 10% reduction in ovarian cancer risk (rate ratio [RR] = 0.90, 95% confidence interval [CI] = 0.82 to 1.00, P = .05). Frequent use (≥4 days/wk) of aspirin (RR = 0.95, 95% CI = 0.88 to 1.03), nonaspirin nonsteroidal anti-inflammatory drugs (NSAIDs; RR = 1.00, 95% CI = 0.90 to 1.11), or acetaminophen (RR = 1.05, 95% CI = 0.88 to 1.24) was not associated with risk. Daily acetaminophen use (RR = 1.28, 95% CI = 1.00 to 1.65, P = .05) was associated with elevated ovarian cancer risk. Risk estimates for frequent, long-term (10+ years) use of aspirin (RR = 1.15, 95% CI = 0.98 to 1.34) or nonaspirin NSAIDs (RR = 1.19, 95% CI = 0.84 to 1.68) were modestly elevated, although not statistically significantly so.Conclusions: This large, prospective analysis suggests that women who use aspirin daily have a slightly lower risk of developing ovarian cancer (∼10% lower than infrequent/nonuse)-similar to the risk reduction observed in case-control analyses. The observed potential elevated risks for 10+ years of frequent aspirin and NSAID use require further study but could be due to confounding by medical indications for use or variation in drug dosing. [ABSTRACT FROM AUTHOR]

Objectives: We examined the association between combustible tobacco product use and e-cigarette use motivations in dual-product and exclusive e-cigarette users. Methods: Adult urban and rural Ohioan exclusive (N = 131) and dual e-cigarette users (N = 114) enrolled in a cohort study rated 21 factors motivating e-cigarette use (eg, quitting combustible products) at baseline. Logistic regression stratified by user type and controlling for region (urban/rural) was used to evaluate associations between motivations for e-cigarette use and use of combustible tobacco products within 18-months. Results: Among exclusive e-cigarette users, endorsing, "using e-cigarettes helps people quit smoking cigarettes" and "using an e-cigarette feels like smoking regular cigarettes" showed lower odds of using a combustible product at least some days per week within 18 months. Among dual-users, no e-cigarette use motivations emerged statistically significant in terms of combustible product use within 18 months, though a few e-cigarette motivations were borderline statistically significant. Conclusions: Among exclusive and dual ecigarette users, motivations related to the value of e-cigarettes as a cigarette substitute were associated with combustible product use at follow-up. [ABSTRACT FROM AUTHOR]

Introduction: Rural Americans are particularly vulnerable to tobacco price reducing promotions are known to be directed to and used by vulnerable populations. Tobacco purchasing decisions, such as unit quantity purchased, may vary by rurality, by price promotion use, and possibly by the interaction between the two. Purchase decisions are likely to affect tobacco use behavior. Therefore, explanation of variation in tobacco purchase quantity by factors associated with rural vulnerability and factors that fall under the regulatory scope of the Tobacco Control Act (TCA) of 2009 could be of value to regulatory proposals intended to equitably benefit public health.Methods: Our sample included 54 combustible tobacco users (298 purchase events) and 27 smokeless tobacco users (112 purchase events), who were asked to report all tobacco purchases on a smartphone application. We used an ecological momentary assessment methodology to collect data about tobacco users' purchasing patterns, including products, quantity purchased, and use of price promotions. A parent cohort study provided relevant data for home-outlet distance calculation and covariates. Our analysis examined associations between our outcome-purchase quantity per purchase event-and distance from participant's home to the nearest outlet, whether a price reducing promotion was used, and the interaction of these two factors.Results: Combustible users showed an increased cigarette pack purchase quantity if they lived further from an outlet and used a price promotion (i.e., an interaction effect; RR = 1.70, 95% CI [1.11, 2.62]). Smokeless users purchased more units of snuff when they used price promotions (RR = 1.81, 95% CI [1.02, 3.20]).Conclusions: Regulatory action that imposes restrictions on the availability or use of price promotions could alter the purchasing behavior of rural Americans in such a way that makes it easier to reduce tobacco use or quit. Such action would also restrict flexibility in the price of tobacco products, which is known as a powerful tobacco control lever. [ABSTRACT FROM AUTHOR]

The role of acetylsalicylic acid (aspirin) as a chemo-preventive and adjuvant therapeutic agent for cancers is generating attention. Mounting evidence indicates that aspirin reduces the incidence and mortality of certain obesity-related cancers, particularly colorectal cancer. In endometrial cancer, previous studies examining the effect of aspirin remain inconsistent as to the reduction in the risk of endometrial cancer. While some evidence indicates protective effects in obese women, other studies have showed a potential deleterious effect of these medications on endometrial cancer outcomes. However, exposure measurement across studies has been inconsistent in recording dose, duration, and frequency of use; thus making comparisons difficult. In this article, we review the evidence for the association between endometrial cancer and obesity, the pharmacological differences between regular- and low-dose aspirin, as well as the potential anti-tumor mechanism of aspirin, supporting a possible therapeutic effect on endometrial cancer. A proposed mechanism behind decreased cancer mortality in endometrial cancer may be a result of inhibition of metastasis via platelet inactivation and possible prostaglandin E 2 suppression by aspirin. Additionally, aspirin use in particular may have a secondary benefit for obesity-related comorbidities including cardiovascular disease in women with endometrial cancer. Although aspirin-related bleeding needs to be considered as a possible adverse effect, the benefits of aspirin therapy may exceed the potential risk in women with endometrial cancer. The current evidence reviewed herein has resulted in conflicting findings regarding the potential effect on endometrial cancer outcomes, thus indicating that future studies in this area are needed to resolve the effects of aspirin on endometrial cancer survival, particularly to identify specific populations that might benefit from aspirin use. [ABSTRACT FROM AUTHOR]

The 2014 Surgeon General's Report on smoking and health concluded that changing cigarette designs have caused an increase in lung adenocarcinomas, implicating cigarette filter ventilation that lowers smoking machine tar yields. The Food and Drug Administration (FDA) now has the authority to regulate cigarette design if doing so would improve public health. To support a potential regulatory action, two weight-of-evidence reviews were applied for causally relating filter ventilation to lung adenocarcinoma. Published scientific literature (3284 citations) and internal tobacco company documents contributed to causation analysis evidence blocks and the identification of research gaps. Filter ventilation was adopted in the mid-1960s and was initially equated with making a cigarette safer. Since then, lung adenocarcinoma rates paradoxically increased relative to other lung cancer subtypes. Filter ventilation 1) alters tobacco combustion, increasing smoke toxicants; 2) allows for elasticity of use so that smokers inhale more smoke to maintain their nicotine intake; and 3) causes a false perception of lower health risk from "lighter" smoke. Seemingly not supportive of a causal relationship is that human exposure biomarker studies indicate no reduction in exposure, but these do not measure exposure in the lung or utilize known biomarkers of harm. Altered puffing and inhalation may make smoke available to lung cells prone to adenocarcinomas. The analysis strongly suggests that filter ventilation has contributed to the rise in lung adenocarcinomas among smokers. Thus, the FDA should consider regulating its use, up to and including a ban. Herein, we propose a research agenda to support such an effort. [ABSTRACT FROM AUTHOR]

Background Individual studies have suggested that some circulating fatty acids are associated with prostate cancer risk, but have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease. Methods Principal investigators of prospective studies on circulating fatty acids and prostate cancer were invited to collaborate. Investigators provided individual participant data on circulating fatty acids (weight percent) and other characteristics of prostate cancer cases and controls. Prostate cancer risk by study-specific fifths of 14 fatty acids was estimated using multivariable-adjusted conditional logistic regression. All statistical tests were two-sided. Results Five thousand and ninety-eight case patients and 6649 control patients from seven studies with an average follow-up of 5.1 (SD = 3.3) years were included. Stearic acid (18:0) was inversely associated with total prostate cancer (odds ratio [OR] Q5 vs Q1 = 0.88, 95% confidence interval [CI] = 0.78 to 1.00, Ptrend = .043). Prostate cancer risk was, respectively, 14% and 16% greater in the highest fifth of eicosapentaenoic acid (20:5n-3) (OR = 1.14, 95% CI = 1.01 to 1.29, Ptrend = .001) and docosapentaenoic acid (22:5n-3) (OR = 1.16, 95% CI = 1.02 to 1.33, Ptrend = .003), but in each case there was heterogeneity between studies (P = .022 and P < .001, respectively). There was heterogeneity in the association between docosapentaenoic acid and prostate cancer by grade of disease (P = .006); the association was statistically significant for low-grade disease but not high-grade disease. The remaining 11 fatty acids were not statistically associated with total prostate cancer risk. Conclusion There was no strong evidence that circulating fatty acids are important predictors of prostate cancer risk. It is not clear whether the modest associations of stearic, eicosapentaenoic, and docosapentaenoic acid are causal. [ABSTRACT FROM PUBLISHER]