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ObjectivesTo characterise neighbourhood food environments in British Columbia (BC) and determine whether food environment characteristics are associated with fruit and vegetable (FV) intake.DesignA cross-sectional study using geospatial linkage of food environment measures within 1 km residential buffers, analysed with mixed-effects modelsSettingUrban neighbourhoods in BC, Canada.ParticipantsApproximately 25 000 adults aged 35–69 years from the BC Generations Project cohort.Outcome measuresFV intake as a continuous variable (servings/day) and as a binary measure (<5 or ≥5 servings/day).ResultsApproximately 50% of participants lived in neighbourhoods without chain grocery stores, fast-food outlets or convenience stores within walking distance. Neighbourhoods in the highest density category for fast-food outlets were associated with lower odds of consuming ≥5 servings of FV per day (OR=0.89, 95% CI 0.80 to 0.98). Associations between chain grocery stores, convenience stores and FV intake were attenuated after adjusting for neighbourhood characteristics including walkability, and material and social deprivation.ConclusionsThe findings suggest limited neighbourhood access to retail food outlets across urban areas in BC. Participants living in neighbourhoods with greater density of fast-food restaurants were less likely to consume >5 servings of FV per day. Further studies are needed to better understand the null findings and additional factors that may be associated with dietary intake.

PurposeAntihypertensive medications may impact colorectal cancer risk. We conducted a systematic review and meta-analysis of associations, with colorectal cancer risk, of five classes of antihypertensive medications: angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), beta-blockers (BBs), calcium channel blockers (CCBs), and diuretics.MethodsA systematic search was conducted in MEDLINE, Embase, Web of Science, and the Cochrane library to identify relevant studies evaluating associations of ACEIs, ARBs, BBs, CCBs, and diuretics with colorectal cancer risk. Meta-analytic risk ratios (RRs) and corresponding 95% confidence intervals (95% CIs) were calculated using the inverse variance method.ResultsNo overall significant associations with colorectal cancer risk were observed; ACEIs (5 studies) RR 1.05, 95% CI 0.91–1.23, ARBs (5 studies) RR 0.94, 95% CI 0.80–1.11, BBs (4 studies) RR 1.00, 95% CI 0.92–1.08, CCBs (4 studies) RR 1.02, 95% CI 0.88–1.18, and diuretics (6 studies) RR 1.02, 95% CI 0.90–1.17. There was considerable heterogeneity across studies, partly explained by differences in study design and location. When stratified by study location, there was significantly reduced colorectal cancer risk for ARB use in Asian populations (2 studies, RR 0.69, 95% CI 0.58–0.83).ConclusionNo significant colorectal cancer risk with ACEIs, BBs, CCBs, or diuretics was observed. ARB use may be associated with decreased risk of colorectal cancer in Asian populations, although additional studies in diverse populations are needed to confirm associations and help understand possible reasons for geographical differences.

Background Metabolomics offers a promising approach to identify biomarkers for timely intervention and enhanced screening of individuals at increased risk of developing breast cancer. Methods We conducted a study of 593 female breast cancer cases and 593 matched controls nested in two prospective cohort studies. Mass spectrometry, without liquid chromatography, was used to conduct untargeted metabolomics profiling of serum samples collected, on average, 5.3 years before cancer diagnosis. Logistic regression was used to estimate odds ratios (OR) for a one standard deviation increase of metabolite intensities. Partial least squares discriminant analyses were applied to those metabolites significantly associated with breast cancer to develop risk prediction models. Results Associations were evaluated with a total of 837 metabolites. Twenty-four metabolites were significantly associated with overall breast cancer risk, including 13 associated with decreased risk and 11 associated with increased risk. Putative identities of the metabolites included various amino acids ( n  = 3), dietary factors ( n  = 10), fatty acids ( n  = 2), phosplipids ( n  = 4), sex hormone derivatives ( n  = 2), and xenobiotics ( n  = 3). For example, a metabolite identified as acetyl tributyl citrate, a plasticizer in food wrappings, was associated with an increased risk of breast cancer (OR = 1.21; 95% CI: 1.07–1.37). Risk prediction models for overall breast cancer and the various subtypes were found to have modest levels of prediction accuracy (area under the curve ranged from 0.60 to 0.63). Conclusions Additional studies are needed to confirm the identities of the metabolites and validate their associations with breast cancer risk. Metabolomics should be evaluated in conjunction with other ‘omics’ technologies for creation of clinically useful risk prediction models.

Background Insulin resistance (IR) is a well-established factor for breast cancer (BC) risk in postmenopausal women, but the interrelated molecular pathways on the methylome are not explicitly described. We conducted a population-level epigenome-wide association (EWA) study for DNA methylation (DNAm) probes that are associated with IR and prospectively correlated with BC development, both overall and in BC subtypes among postmenopausal women. Methods We used data from Women’s Health Initiative (WHI) ancillary studies for our EWA analyses and evaluated the associations of site-specific DNAm across the genome with IR phenotypes by multiple regressions adjusting for age and leukocyte heterogeneities. For our analysis of the top 20 IR-CpGs with BC risk, we used the WHI and the Cancer Genomic Atlas (TCGA), using multiple Cox proportional hazards and logit regressions, respectively, accounting for age, diabetes, obesity, leukocyte heterogeneities, and tumor purity (for TCGA). We further conducted a Gene Set Enrichment Analysis. Results We detected several EWA-CpGs in TXNIP, CPT1A, PHGDH, and ABCG1. In particular, cg19693031 in TXNIP was replicated in all IR phenotypes, measured by fasting levels of glucose, insulin, and homeostatic model assessment-IR. Of those replicated IR-genes, 3 genes ( CPT1A, PHGDH, and ABCG1 ) were further correlated with BC risk; and 1 individual CpG (cg01676795 in POR ) was commonly detected across the 2 cohorts. Conclusions Our study contributes to better understanding of the interconnected molecular pathways on the methylome between IR and BC carcinogenesis and suggests potential use of DNAm markers in the peripheral blood cells as preventive targets to detect an at-risk group for IR and BC in postmenopausal women.

Studies have causally linked external thyroid radiation exposure in childhood with thyroid cancer. In 1995, investigators conducted relative risk analyses of pooled data from seven epidemiologic studies. Doses were mostly <10 Gy, although childhood cancer therapies can result in thyroid doses >50 Gy. We pooled data from 12 studies of thyroid cancer patients who were exposed to radiation in childhood (ages <20 years), more than doubling the data, including 1,070 (927 exposed) thyroid cancers and 5.3 million (3.4 million exposed) person-years. Relative risks increased supralinearly through 2–4 Gy, leveled off between 10–30 Gy and declined thereafter, remaining significantly elevated above 50 Gy. There was a significant relative risk trend for doses <0.10 Gy (P < 0.01), with no departure from linearity (P = 0.36). We observed radiogenic effects for both papillary and nonpapillary tumors. Estimates of excess relative risk per Gy (ERR/Gy) were homogeneous by sex (P = 0.35) and number of radiation treatments (P = 0.84) and increased with decreasing age at the time of exposure. The ERR/Gy estimate was significant within ten years of radiation exposure, 2.76 (95% CI, 0.94–4.98), based on 42 exposed cases, and remained elevated 50 years and more after exposure. Finally, exposure to chemotherapy was significantly associated with thyroid cancer, with results supporting a nonsynergistic (additive) association with radiation.

Diabetes medications may modify the risk of certain cancers. We systematically searched MEDLINE, Embase, Web of Science, and Cochrane CENTRAL from 2011 to March 2021 for studies evaluating associations between diabetes medications and the risk of breast, lung, colorectal, prostate, liver, and pancreatic cancers. A total of 92 studies (3 randomized controlled trials, 64 cohort studies, and 25 case–control studies) were identified in the systematic review, involving 171 million participants. Inverse relationships with colorectal (n = 18; RR = 0.85; 95% CI = 0.78–0.92) and liver cancers (n = 10; RR = 0.55; 95% CI = 0.46–0.66) were observed in biguanide users. Thiazolidinediones were associated with lower risks of breast (n = 6; RR = 0.87; 95% CI = 0.80–0.95), lung (n = 6; RR = 0.77; 95% CI = 0.61–0.96) and liver (n = 8; RR = 0.83; 95% CI = 0.72–0.95) cancers. Insulins were negatively associated with breast (n = 15; RR = 0.90; 95% CI = 0.82–0.98) and prostate cancer risks (n = 7; RR = 0.74; 95% CI = 0.56–0.98). Positive associations were found between insulin secretagogues and pancreatic cancer (n = 5; RR = 1.26; 95% CI = 1.01–1.57), and between insulins and liver (n = 7; RR = 1.74; 95% CI = 1.08–2.80) and pancreatic cancers (n = 8; RR = 2.41; 95% CI = 1.08–5.36). Overall, biguanide and thiazolidinedione use carried no risk, or potentially lower risk of some cancers, while insulin secretagogue and insulin use were associated with increased pancreatic cancer risk.

Introduction: There is conflicting evidence for the association between antihypertensive medications and colorectal cancer risk, possibly reflecting methodological limitations of previously conducted studies. Here, we aimed to clarify associations between commonly prescribed antihypertensive medication classes and colorectal cancer risk in a large, retrospective, cohort study. Methods: Using linked administrative data between 1996 and 2017 from British Columbia, we identified a cohort of 1,693,297 men and women who were 50 years of age or older, initially cancer-free and nonusers of antihypertensive medications. Medication use was parameterized as ever use, cumulative duration, and cumulative dose. Cox proportional hazard models were used to estimate hazard ratios (HRs) and associated 95% confidence intervals (95% CIs) for associations of time-varying medication use [angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), beta-blockers (BBs), calcium channel blockers (CCBs), and diuretics] with colorectal cancer risk. Results: There were 28,460 incident cases of colorectal cancer identified over the follow-up period (mean = 12.9 years). When medication use was assessed as ever/never, diuretics were associated with increased risk of colorectal cancer (HR 1.08, 95% CI 1.04–1.12). However, no similar association was observed with cumulative duration or cumulative dose of diuretics. No significant associations between the other four classes of medications and colorectal cancer risk were observed. Conclusion: No compelling evidence of associations between antihypertensive medications and colorectal cancer were observed.

BackgroundAlthough smoking is the primary risk factor for lung cancer, 15–25% of lung cancers occur in never smokers. Emerging evidence suggests lifestyle factors are associated with lung cancer risk, but few studies among never smokers exist.MethodsA case–control study of never smokers within the Canadian Partnership for Tomorrow’s Health was conducted. At recruitment, participants provided data on lifestyle, health history and sociodemographic factors. Incident lung cancers were identified through linkage with administrative health records. Cases (n = 190) were matched to controls (n = 760) on age, sex, and follow-up time. Logistic regression analyses, adjusted for matching factors and annual income, were used to identify associations between lifestyle factors and lung cancer risk.ResultsConsumption of < 5 servings of fruits and vegetables/day was associated with higher risk of lung cancer (OR  1.50, 95% CI 1.03–2.17). Short or long sleep (≤ 6 or > 9 h/night) was also associated with increased risk of lung cancer (OR 1.52, 95% CI 1.01–2.29). No associations were observed for obesity measures, alcohol consumption, or physical activity.ConclusionOur findings provide evidence of a potential role between sleep, fruits and vegetable consumption, and lung cancer risk in a pan-Canadian, non-smoking population. However, the sample size is modest, and further investigation is needed.

Objectives The association between shift work and cancer, which is thought to be mediated by effects on circulating melatonin levels, may be modified by chronotype (ie, the inherent preference for activity in the morning or the evening); however, few studies have examined the potential impact of chronotype on the carcinogenic effects of shift work. The authors analysed the impact of chronotype on previously reported differences in melatonin levels among healthcare workers that exclusively worked night or day shifts. Methods The cross-sectional study included 664 men and women (310 day shift and 354 night shift workers) from which urine samples were collected throughout work and sleep periods and were assayed for 6-sulfatoxymelatonin. Participants also completed the Composite Scale of Morningness, a questionnaire used to assess chronotype. Results Among both morning and evening-type night shift workers, 6-sulfatoxymelatonin levels were constitutively lower during daytime sleep, night-time sleep and night work compared with day shift workers during night-time sleep. However, morning-type night shift workers consistently showed 6-sulfatoxymelatonin levels that were closer to levels in day shift workers than did evening-type night shift workers. Differences in 6-sulfatoxymelatonin levels between morning-type and evening-type night shift workers relative to day shift workers were statistically significant in every instance (p<0.05). Conclusions These results suggest that morning-type night shift workers may be better able to maintain a ‘normal’ circadian pattern of melatonin production as compared with evening-type night shift workers. The impact of this chronotype effect on cancer risk among shift workers requires further study.

ObjectivesUnderstanding the mechanisms by which an exposure causes cancer can be critical to establishing causality and to developing successful prevention/intervention strategies. Multiple mechanisms underlying the carcinogenicity of night shift work have been proposed, including several novel ones in recent years, though specific mechanistic links remain uncertain.MethodsNovel mechanisms for the carcinogenicity of night shift work will be reviewed. In the context of these mechanisms, the methodologic limitations that continue to plague human mechanistic studies of night shift work will also be discussed.ResultsMultiple animal studies and some human mechanistic studies have pointed to suppressed DNA damage repair, epigenetic impacts and gut dysbiosis as novel mechanisms by which night shift work may cause cancer. Human mechanistic studies continue to suffer from multiple limitations such as small sample sizes, poorly defined shift schedules, inappropriate timing of biospecimen collection relative to conduct of night shift work and inadequate consideration of diurnal variation in biomarker measures.ConclusionsWhile there is compelling evidence for multiple novel mechanisms underlying the potential carcinogenicity of night shift work, additional high quality human mechanistic studies are needed to establish the relevance of these mechanisms.