Explore the vast range of titles available.

Background Studies of women of European ancestry have shown that the average familial relative risk for first-degree relatives of women with breast cancer is approximately twofold, but little is known for Asian women. We aimed to provide evidence for the association between family history and breast cancer risk for Asian women by systematically reviewing published literature. Methods Studies reporting the familial relative risk of breast cancer for Asian women were searched in three online databases and complemented by a manual search. Odds ratios (ORs) for the association between family history and breast cancer risk were pooled across all included studies and by subgroups in terms of the type of family history, age, menopausal status and geographical region. Results The pooled OR for women who have a first-degree relative with breast cancer was 2.46 (95% confidence interval [CI]: 2.03, 2.97). There was no evidence that the familial risk differed by the type of affected relative (mother versus sisters), the woman’s age (< 50 years versus ≥ 50 years), menopausal status (pre versus post) and geographical region (East and Southeast Asia versus other regions) (all P  > 0.3). The pooled ORs for women of Asian ancestry with a family history in any relative were similar for those living in non-Asian countries (2.26, 95% CI: 1.42, 3.59) compared with those living in Asian countries (2.18, 95% CI: 1.85, 2.58). Conclusions Family history of breast cancer is associated with an approximately twofold relative risk of breast cancer for Asian women, which is of similar magnitude to that observed for women of European ancestry. This implies that similar familial factors are implicated in breast cancer risk between women of European and Asian ancestries. Genetic factors are likely to play a substantial role in explaining the breast cancer familial risk for Asian women, as similar risks were observed across different living environments and cultures.

The evidence that measures of obesity and stature are associated with prostate cancer is weak and inconsistent. We performed a systematic review and meta-analysis of the relationship between body mass index (BMI), height, weight, waist circumference and waist-to-hips ratio (WHR) and the risk of prostate cancer. Study-specific dose-response slopes were obtained, and random effects rate ratios (RRs) were computed from linear meta-regression models. We included 55,521 cases identified among 2,818,767 men from 31 cohort studies, and 13,232 cases and 16,317 controls from 25 case-control studies. The overall RR for BMI was 1.05 per 5 kg/m² increment, 95% CI 1.01-1.08. For studies that reported results by stage of disease, the RRs were stronger for advanced disease (RR 1.12 per 5 kg/m² increment, 95% CI 1.01-1.23) compared with localized disease (RR 0.96 per 5 kg/m² increment, 95% CI 0.89-1.03), p = 0.02. Height was also positively associated with risk (RR 1.05 per 10 cm increment, 95% CI 1.02-1.09), but the evidence was weak for weight (RR 1.01 per 10 kg increment, 95% CI 0.97-1.04), waist circumference (RR 1.03 per 10 cm increment, 95% CI 0.99-1.07), and WHR (RR 1.11 per 0.1 unit increment, 95% CI 0.95-1.30). Stronger associations were observed among cohort studies compared with case-control studies for BMI (p = 0.006), height (p < 0.001) and weight (p = 0.02). This meta-analysis indicates that obesity is weakly associated with an increased risk of prostate cancer (particularly advanced stage tumors). While increased stature may also increase risk, there is little evidence for an association with central obesity.

BackgroundWe quantified the individual and joint contribution of contemporaneous causal behavioural exposures on the future burden of oesophageal and stomach cancers and their subtypes and assessed whether these burdens differ between population groups in Australia, as such estimates are currently lacking.MethodsWe combined hazard ratios from seven pooled Australian cohorts (N = 367,058) linked to national cancer and death registries with exposure prevalence from the 2017–2018 National Health Survey to estimate Population Attributable Fractions (PAFs) with 95% confidence intervals (CIs), accounting for competing risk of death.ResultsCurrent and past smoking explain 35.2% (95% CI = 11.7–52.4%), current alcohol consumption exceeding three drinks/day 15.7% (95% CI = 0.9–28.4%), and these exposures jointly 41.4% (95% CI = 19.8–57.3%) of oesophageal squamous cell carcinomas in Australia. Current and past smoking contribute 38.2% (95% CI = 9.4–57.9%), obesity 27.0% (95% CI = 0.6–46.4%), and these exposures jointly 54.4% (95% CI = 25.3–72.1%) of oesophageal adenocarcinomas. Overweight and obesity explain 36.1% (95% CI = 9.1–55.1%), current and past smoking 24.2% (95% CI = 4.2–40.0%), and these exposures jointly 51.2% (95% CI = 26.3–67.8%) of stomach cardia cancers. Several population groups had a significantly higher smoking-attributable oesophageal cancer burden, including men and those consuming excessive alcohol.ConclusionsSmoking is the leading preventable behavioural cause of oesophageal cancers and overweight/obesity of stomach cancers.

Objective The performance of FFPE tissue-derived DNA on the MethylationEpicV1.0 array can be unpredictable as the protocol only has two quality checks; checkpoint 1 for DNA quantity and checkpoint 2 for DNA quality assessment. We sought to incorporate a third, previously developed bisulfite conversion quality check prior to processing 255 FFPE tissue derived DNA samples. Results FFPE tissue-derived DNAs were prepared for 255 prostate tumour specimens and four controls. Checkpoint 1 assessed all samples to have 500ng DNA available for analysis except for two samples that yielded 483 and 486ng. All DNA samples passed both the quality checkpoint 2 and the bisulfite conversion quality assessment checkpoint 3. Assessment of array performance showed one of the 259 (0.4%) DNA samples had less than 90% of probes detected at p  = 0.05. Controls and replicate showed reliable reproducibility with correlations of 0.981 and 0.994. High quantity and quality measures of the FFPE tissue-derived DNAs (assessed by checkpoint 1 and 2) were likely responsible for 99.6% of DNAs producing high quality EPIC array data. This report suggests that checkpoint 3 has limited value in a setting where the FFPE tissue derived DNA has high quantity and quality measures.

Background Mammogram risk scores based on texture and density defined by different brightness thresholds are associated with breast cancer risk differently and could reveal distinct information about breast cancer risk. We aimed to investigate causal relationships between these intercorrelated mammogram risk scores to determine their relevance to breast cancer aetiology. Methods We used digitised mammograms for 371 monozygotic twin pairs, aged 40–70 years without a prior diagnosis of breast cancer at the time of mammography, from the Australian Mammographic Density Twins and Sisters Study. We generated normalised, age-adjusted, and standardised risk scores based on textures using the Cirrus algorithm and on three spatially independent dense areas defined by increasing brightness threshold: light areas, bright areas, and brightest areas. Causal inference was made using the Inference about Causation from Examination of FAmilial CONfounding (ICE FALCON) method. Results The mammogram risk scores were correlated within twin pairs and with each other ( r  = 0.22–0.81; all P  < 0.005). We estimated that 28–92% of the associations between the risk scores could be attributed to causal relationships between the scores, with the rest attributed to familial confounders shared by the scores. There was consistent evidence for positive causal effects: of Cirrus, light areas, and bright areas on the brightest areas (accounting for 34%, 55%, and 85% of the associations, respectively); and of light areas and bright areas on Cirrus (accounting for 37% and 28%, respectively). Conclusions In a mammogram, the lighter (less dense) areas have a causal effect on the brightest (highly dense) areas, including through a causal pathway via textural features. These causal relationships help us gain insight into the relative aetiological importance of different mammographic features in breast cancer. For example our findings are consistent with the brightest areas being more aetiologically important than lighter areas for screen-detected breast cancer; conversely, light areas being more aetiologically important for interval breast cancer. Additionally, specific textural features capture aetiologically independent breast cancer risk information from dense areas. These findings highlight the utility of ICE FALCON and family data in decomposing the associations between intercorrelated disease biomarkers into distinct biological pathways.

ObjectiveLimited research has assessed the association between patterns of body mass index (BMI) change across adulthood and mortality. We aimed to identify groups of individuals who followed specific group-based BMI trajectories across adulthood, using weight collected on three occasions and recalled data from early adulthood, and to examine associations with all-cause and cause-specific mortality.DesignProspective cohort study.SettingMelbourne, Australia.ParticipantsAdults (n=29 881) enrolled in the Melbourne Collaborative Cohort Study, who were aged from 40 to 70 years between 1990 and 1994, and had BMI data for at least three time points.OutcomeDeaths from any cause before 31 March 2017 and deaths from obesity-related cancers, cardiovascular diseases (CVDs) and other causes before 31 December 2013.ResultsWe identified six group-based BMI trajectories: lower-normal stable (TR1), higher-normal stable (TR2), normal to overweight (TR3), chronic borderline obesity (TR4), normal to class I obesity (TR5) and overweight to class II obesity (TR6). Generally, compared with maintaining lower-normal BMI throughout adulthood, the lowest mortality was experienced by participants who maintained higher-normal BMI (HR 0.90; 95% CI 0.84 to 0.97); obesity during midlife was associated with higher all-cause mortality even when BMI was normal in early adulthood (HR 1.09; 95% CI 0.98 to 1.21) and prolonged borderline obesity from early adulthood was also associated with elevated mortality (HR 1.16; 95% CI 1.01 to 1.33). These associations were stronger for never-smokers and for death due to obesity-related cancers. Being overweight in early adulthood and becoming class II obese was associated with higher CVD mortality relative to maintaining lower-normal BMI (HR 2.27; 95% CI 1.34 to 3.87).ConclusionOur findings highlight the importance of weight management throughout adulthood to reduce mortality.

The association between change in weight or body mass index, and mortality is widely reported, however, both measures fail to account for fat distribution. Change in waist circumference, a measure of central adiposity, in relation to mortality has not been studied extensively. We investigated the association between mortality and changes in directly measured waist circumference, hips circumference and weight from baseline (1990-1994) to wave 2 (2003-2007) in a prospective cohort study of people aged 40-69 years at baseline. Cox regression, with age as the time metric and follow-up starting at wave 2, adjusted for confounding variables, was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for change in body size in relation to mortality from all causes, cardiovascular disease and cancer. There were 1465 deaths (109 cancer, 242 cardiovascular disease) identified during an average 7.7 years of follow-up from 21 298 participants. Compared to minimal increase in body size, loss of waist circumference (HR: 1.26; 95% CI: 1.09-1.47), weight (1.80; 1.54-2.11), or hips circumference (1.35; 1.15-1.57) were associated with an increased risk of all-cause mortality, particularly for older adults. Weight loss was associated with cardiovascular disease mortality (2.40; 1.57-3.65) but change in body size was not associated with obesity-related cancer mortality. This study confirms the association between weight loss and increased mortality from all-causes for older adults. Based on evidence from observational cohort studies, weight stability may be the recommended option for most adults, especially older adults.

Background Physical activity reduces the risk of colorectal cancer (CRC), but the relevant evidence derives primarily from self-reported recreational and occupational activity. Less is known about the contribution of other domains of physical activity, such as transport and household. We examined associations between domain-specific physical activities and CRC risk within the Melbourne Collaborative Cohort Study. Methods Analyses included 23,586 participants who were free from invasive colorectal cancer and had completed the International Physical Activity Questionnaire-Long Form at follow-up 2 (2003–2007). Cox regression, with age as the time metric, was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for ordinal categories of each physical activity domain. Results Adjusted HRs for the highest versus the lowest categories of physical activity were 0.71 (95% CI: 0.51–0.98; p trend  = 0.03) for recreational activity; 0.80 (95% CI: 0.49–1.28; p trend  = 0.38) for occupational activity; 0.90 (95% CI: 0.68–1.19; p trend  = 0.20) for transport activity; and 1.07 (95% CI: 0.82–1.40; p trend  = 0.46) for household activity. Conclusions Recreational activity was associated with reduced CRC risk. A non-significant, inverse association was observed for occupational activity, whereas no association was found for transport or household domains.

Background Higher levels of time spent sitting (sedentary behavior) contribute to adverse health outcomes, including earlier death. This effect may be modified by other lifestyle factors. We examined the association of television viewing (TV), a common leisure-time sedentary behavior, with all-cause mortality, and whether this is modified by body mass index (BMI), physical activity, smoking, alcohol intake, soft drink consumption, or diet-associated inflammation. Methods Using data from participants in the Melbourne Collaborative Cohort Study, flexible parametric survival models assessed the time-dependent association of self-reported TV time (three categories: < 2 h/day, 2–3 h/day, > 3 h/day) with all-cause mortality. Interaction terms were fitted to test whether there was effect modification of TV time by the other risk factors. Results From 19,570 participants, 4,417 deaths were reported over a median follow up of 14.5 years. More TV time was associated with earlier mortality; however, this relationship diminished with increasing age. The hazard ratio (HR) and 95% confidence interval (95% CI) for > 3 h/day compared with < 2 h/day of TV time was 1.34 (1.16, 1.55) at 70 years, 1.14 (1.04, 1.23) at 80 years, and 0.95 (0.84, 1.06) at 90 years. The TV time/mortality relationship was more evident in participants who were physically inactive (compared with active; p for interaction < 0.01) or had a higher dietary inflammatory index score (compared with a lower score; p for interaction = 0.03). No interactions were detected between TV time and BMI, smoking, alcohol intake, nor soft-drink consumption (all p for interaction > 0.16). Conclusions The relationship between TV time and all-cause mortality may change with age. It may also be more pronounced in those who are otherwise inactive or who have a pro-inflammatory diet.

To assess differences in accelerometer-assessed moderate- to vigorous-intensity physical activity (MVPA), light-intensity physical activity, and sedentary time between cancer survivors and adults without cancer. Accelerometer data collected from 241 breast cancer survivors (ACCEL-Breast study, 2013) and 171 colon cancer survivors (ACCEL-Colon study, 2012-2013) were pooled with data collected from adults without cancer (Australian Diabetes, Obesity and Lifestyle accelerometer substudy, 2011-2012). Linear regression was used to estimate differences in physical activity and sedentary behavior levels between cancer survivors and adults without cancer, adjusted for potential confounding factors. The mean MVPA was significantly higher among breast cancer survivors than among females who had not had cancer (29 vs 22 min/d; P<.001). Colon cancer survivors had significantly lower levels of light activity than did adults without cancer (311 vs 338 min/d; P<.001), more sedentary time (532 vs 507 min/d; P=.003), and more prolonged sedentary time (210 vs 184 min/d; P=.002). Contrary to findings from previous research (based on self-reported physical activity), cancer survivors engaged in more (breast) or equivalent (colon) MVPA compared with adults without cancer. Differences between colon cancer survivors and adults without cancer for light activity and sedentary behavior highlight the importance of considering the full activity spectrum in the context of cancer control.